An Analysis of Fifty Cases Treated by William Donald Kelley

Louise Lubetkin BDS, Peter Moran, M.B., B.S., B.Sc.(Med), F.R.A.C.S., F.R.C.S.(Eng)
February 14, 2020

(as presented by Nicholas Gonzalez, MD in his monograph “One Man Alone”)


In 1981, as an ex-journalist turned medical student, Nicholas Gonzalez, then in the second year of his medical studies, became intrigued by the work of William Donald Kelley, DDS, a Texas orthodontist. Kelley had devised a highly unorthodox, nutrition-based method of treating cancer, and claimed to have cured himself of advanced pancreatic cancer using this method alone. He had subsequently begun treating other cancer patients, perhaps most famous among whom was the actor Steve McQueen, who succumbed to mesothelioma in 1980.

In the hope of eventually having his method accepted by mainstream medicine, Kelley invited Gonzalez to visit his office in Dallas, TX, granting him unfettered access to his patient records. Over the ensuing several years, Gonzalez spent a considerable amount of time combing through them, eventually compiling a monograph whose central purpose was the presentation of the 50 cases that are analysed and discussed here.

The monograph was finished in early 1986. Gonzalez says that he tried hard at that time to get it published, but was unsuccessful. Indeed, it was not until 2010, a full 23 years after its completion, that Gonzalez decided to self-publish the monograph, now titled of One Man Alone: An Investigation of Nutrition, Cancer and William Donald Kelley. Gonzalez took advantage of its publication to add a fifteen-page preface in which he recounts in some detail the story of how the investigation began, and the subsequent unravelling of his relationship with Kelley.

The Kelley treatment is just one of a great many unconventional cancer treatments promoted in recent decades.  These treatments, which are often administered in various combinations, have two key attributes in common. First, they are based upon a variety of poorly supported or long-since discredited theories of cancer.   Second, they share a reliance upon collections of seemingly impressive case reports and testimonials: all the methods, no matter how unlikely, seem able to accumulate some. These testimonials are significant not only because it is largely through them that the methods continue to attract potential patients, but also because they mount a challenge, of sorts, to mainstream medicine.

It is therefore important that such cases be looked at carefully, and, if found wanting, that the reasons for such an opinion are spelled out.  It is possible that a sometimes too perfunctory dismissal of this type of anecdotal evidence in the past has contributed to accusations that orthodox medicine’s attitudes to alternative cancer methods are governed by unjustified biases or ignoble motives.

The mainstream might retort that it should not be too difficult to show that a treatment method can regularly cure otherwise incurable cancer, as per prevalent claims, there being a number of easily measurable and very predictable cancerous states upon which that could be demonstrated.

Recognizing that this is a recurring source of uncertainty for cancer patients, retired surgeon Peter J. Moran MB, BS, BSc (Med), FRCS, and medical writer Louise Lubetkin, evaluated the fifty case histories outlined by Nicholas Gonzalez in his book One Man Alone. Their analysis, presented here, was carried out with these three fundamental questions in mind:

  • Can the Kelley method cure cancer, or induce remission?
  • If not, can it prolong survival of cancer patients?
  • How should mainstream medicine react to this evidence?

Can the Kelley method cure cancer?

To be compelling, cases intended to demonstrate the cure of cancer would need a firm diagnosis of invasive cancer, in a measurable form and of a type having highly predictable behavior. Further, such cases would need to demonstrate that all manifestations of cancer abate with the use of the treatment being assessed, with that treatment alone, and within a time frame consistent with a causal relationship. Additionally, cases would need to show that patients stayed cancer-free for the rest of their life, or at least for a period which indicates cure in terms of the usual behavior of that cancer.  (For example, it is very rare for colorectal cancer to recur for the first time five years after treatment.)

Even a relatively few – a mere handful or less – well-documented and confirmable cases with these specifications within recent experience of a single practitioner would go some way towards establishing that an alternate cancer treatment was worth pursuing further. (Of course, the number of such documented cases would need to be proportionately greater in those types of cancer – e.g., certain lymphomas, renal cell cancer, melanoma, chronic lymphocytic leukemia and childhood neuroblastoma – that are known to undergo so-called spontaneous remission more frequently than others.

Demonstrating cancer remission follows similar rules, but of course remission may be partial and temporary.

While there are no cases here that fully meet these stringent criteria, there are certainly some that are suggestive of an effect (specifically, patients 671219203448). These are cases where many of the criteria are met to a reasonable standard and who we are advised lived on for a long time free, or apparently free, of cancer.  The term “reasonable standard” is used here because doubts concerning some aspects of the cases for the present purpose – that is, of being required to pronounce upon whether a cancer was likely to have been cured by the Kelley method – might have been resolved by the ability to review diagnostic or staging data , i.e., the means by which the diagnosis of cancer and its extent have been determined. For example in the case of Patient 34, a biopsy specimen definitely warrants review, and in Patient 48 the interpretation of an abdominal CT scan is crucial.  In other cases, small areas of doubt might have been avoided by the application of emergent new diagnostic and staging technology, such as minimally invasive methods of biopsy of difficult lesions (via endoscopy, fine needle aspiration, or CT and ultrasound-guided core biopsies), or by refinements in the identification and staging of cancer using newer imaging techniques (PET scanning, MRI) and cancer markers, both clinical and cytological.

 Residual doubt aside, is nevertheless easy to understand how many people, including Gonzalez as a junior medical student, might be impressed by these fifty cases.   Indeed, many lose force mainly through hindsight from the vantage point of subsequently published research (see comments on patients 221,1424), or from wider clinical experience than either Gonzalez or Kelley would have possessed.

 For present purposes, a major weakness in many cases is the lack of independent, objective confirmation of crucial aspects of the story (for example, see comment on Patient 31).    It is also not clear why we are provided with copies of some records, but not others of equal or greater importance from similar sources (e.g. Patient 39).

These fifty cases display a variety of other problems.   A few (e.g., Patient 38) are seriously undermined by the lack of biopsy proof of cancer in the lesions of most relevance to the treatment effect being claimed.  In others with no biopsy of metastatic disease there is sufficiently conclusive evidence from imaging and marker studies (e.g., Patient 43), but the case for a Kelley treatment effect is weak on other grounds.  Often the outcome being described is not as unusual as Kelley assumes, or the cancerous (or presumed cancerous) lesions may never have been independently shown to have resolved (e.g., Patient 10), or at least, not within a time frame that would justify its attribution to the Kelley treatment alone (e.g., Patient 19 and others).

In most patients, treatments with known cancericidal properties have also been used close to the time of initiation of the Kelley treatment, often in somewhat abbreviated courses, it is true, but with considerable potential significance to outcomes.   For example, research has confirmed an exquisite sensitivity of many cases of lymphoma to abbreviated courses of radiotherapy and chemotherapy (see comments on Patients 214, and 24).  This surely helps explain why cases of partially treated lymphoma figure so prominently here – 11 cases out of the 50. (Patient 2, described by Gonzalez as “brain cancer” was re-classified as a lymphoma on the final histology.)

This heavily confounding admixture of conventional methods is an unavoidable feature of unconventional cancer practice, contributing to the difficulties of interpretation of many testimonials and case reports. This is often apparent when looking at case histories and testimonials of Gerson, Revici, and other alternative cancer practitioners.

It is important to understand that there is little or no data available as to the minimum course of a cancericidal agent such as radiotherapy or chemotherapy that is capable of producing regular or occasional cures or remissions of cancer.  The dosages chosen for use in everyday clinical practice are based upon that which achieves maximal desired response rates in clinical trials with an acceptable level of side effects.   Rare and unexpected cures from treatment intended to be palliative might also not necessarily be widely publicized, since such cases, being so unusual, would not affect normal medical practice.   In consequence, doctors will always be inclined to attribute good outcomes to agents possessing known effects upon established human cancer rather than ones for which such activity has never been established.

The promoters of unconventional methods will argue otherwise, of course. Yet when faced with cancer that has not been recently treated by any other means, they exhibit what appears to be a disturbing lack of confidence in their methods. Untreated cancers of this kind would provide an excellent basis for a “best test” of their treatment method, yet there is very rarely any attempt to take advantage of the opportunity presented. Thus, it was apparently not thought worthwhile to take photographs of the visible cancerous deposits that we are told were ablated by the Kelley method alone in Patients 122528 and 30. Neither was it deemed useful in many other cases to take simple, obvious, necessary steps to establish the state of the cancer before starting the new treatment, nor to document its resolution thereafter, so as to be able to later more convincingly demonstrate the responses that we are led to believe were confidently anticipated in at least some such cases, and that we are indeed now being asked to trustingly accept on little more than someone’s say-so (see comments on Patient 31).

 It might be claimed that this apparent lack of foresight can be partly attributed to a severance of patient contact with mainstream investigative facilities and a general lack of emphasis on data collection and record keeping within alternative cancer practice.   Yet everyone has a camera.   This seeming unawareness of, or disregard for, the importance of the most conclusive possible evidence when making potentially life-dependent medical claims remains immensely damaging to the credibility of those promoting such methods. These very stories are calculated to arouse the expectation in prospective patients that established, even clearly visible, cancer has been made to regress permanently, yet without ever quite demonstrating that to the standard that such a claim would merit – and this despite the fact that very suitable patients for the demonstration of more conclusive results are being treated.

In other Kelley cases the presumption of the presence of an active cancerous state is extremely dubious (e.g., Patient 8 and several of the cases of supposed pancreatic cancer – see below).   In others, remission was already very likely to have occurred – or was explicitly stated in the medical notes to be already occurring – but the accompanying, usually undocumented, narrative by Gonzalez describes it as occurring subsequently, only after the Kelley treatment was begun (e.g., Patients 226313343).

Gonzalez very often supports his claims that the Kelley treatment was responsible for remissions by reference to improvement in patient symptoms.   This is risky.  In most of those stories the improvements could reasonably be attributed to the usual slow recovery from surgery, radiotherapy and/or chemotherapy, and to the remission that was already underway as a result of those treatments.   Also some of these case reports (e.g., Patients 3428) demonstrate the notoriously unreliable relationship between the level of symptoms experienced by highly stressed and anxious cancer patients and the known or likely state of their disease at the time.

We must also seriously doubt that the cases selected for presentation are as randomly representative of Kelley’s results as Gonzalez states.   It is unlikely that any convincing successes would have been omitted, given the initial intention of selecting cases most suggestive of an effect for the Kelley method.

Conclusion:  In the end, knowing that similarly unusual outcomes are not uncommonly encountered within everyday oncological experience, and that so many of the cases presented by Gonzalez depend upon dubious or uncertain assumptions concerning diagnosis, staging or prognosis, we cannot conclude that the Kelley treatment can regularly or reliably contribute to the cure of cancer.    True, we cannot exclude it as a rare event, but the same could be said of almost anything.  Certainly anyone deciding to use this treatment should not have high expectations of it.

Does the Kelley method prolong survival?

The above factors affect this question too, of course.

Very relevant here is the fact that well over half of these 50 cases involve cancers that can be very slowly progressing, or have variants that are very slowly progressing, or that are compatible with prolonged survival or cure with the treatments already provided.   Eleven cases involve lymphomas, as discussed above; 5 are cancers of the prostate – well known for indolent behavior.  Five cases are operable colorectal cancers with favorable prognoses; 5 are breast cancer, which can sometimes display prolonged survival, even when metastatic, when treated with conventional methods. Several are rarer neuroendocrine cancers that are well known for their indolent characteristics.  A further 2 cases involve testicular cancer, which has high permanent cure rates with conventional care.

In contrast, there are no instances of prolonged survival with biopsy-proven pancreatic (non-islet cell) adenocarcinoma (see below), and only one of prolonged survival with advanced non-small-cell lung cancer  (Patient 21 – the unusually favourable course of whose disease may possibly be attributed to radiotherapy), among the more common and notoriously poor prognosis cancers.

Also, while Gonzalez uses the phrase “metastatic cancer” liberally, and sometimes erroneously (e.g., Patients 8 and 22),  he is in most cases referring to local metastases to regional lymph nodes, which with many cancers (breast, colon, testis) is still compatible with good outcomes,  and not nearly as ominous as distant metastases in lung, liver, bone or elsewhere, which carry an almost universally bad prognosis with many types of cancer.   Indeed, cases with widespread distant metastases are also not represented here in any proportion to their usual frequency.

While an unconventional treatment might conceivably work better in less advanced and less aggressive cancers, it is going to be correspondingly difficult to demonstrate the possibility of benefit using cases that not uncommonly fare quite well without such treatment.

Gonzalez also makes much of the poor prognoses supposedly given to many of these patients by their doctors. In some cases (e.g. Patients 71011) these prognoses seem inexplicably grim when judged against the usual behavior of that particular kind of cancer.  Sometimes, also, the dire prognoses reported by Gonzalez contrast sharply with the tone of comments made in the contemporary medical notes (e.g., Patients 23640).

Of course, patients’ recollection of what they have been told can sometimes be incomplete and very shaky.  In a few of these cases (e.g. Patients 830) the doctors may themselves have been seriously misled as to the true state of the disease.  It is also possible that they may never have actually reached a final opinion on prognosis or management once there were indications that the patient was likely to reject further conventional care.   In a couple of cases the doctors express the intention of reviewing some of the initial findings, but no further records are supplied.

Conclusion: It can be very difficult to demonstrate any measurable effect on survival  without well-planned clinical studies. Given the data provided by Gonzalez, all we can say is that there is no clear evidence of the prolongation of survival from the Kelley treatment.

How should mainstream medicine react to such material?

The few better quality cases might arguably have carried more weight if they had been presented within a consecutive case series of, say, 100 or 200 patients with more certainly diagnosed and predictable cancer types, instead of being selected out of well over a thousand cases with such widely varying standards of investigation and documentation.   The general impression is that the few unusual outcomes among these 50 cases most likely derive from variables that are familiar within everyday oncological experience. For example, there is wide variation in the behavior of most cancers, and in their responsiveness to conventional treatment. Furthermore, within the medical profession it is widely known and understood that the diagnosis and staging of cancer is not error-proof Indeed, because it is critically dependent upon a single opinion – that of the pathologist reviewing biopsy material – small inaccuracies, discrepancies and inter-pathologist disagreements regularly occur. This is mainly only evident when more than one institution is involved. Studies have put the discrepant diagnosis rate in such situations at approximately 9 percent, and in anywhere from 2 to 9 percent of these cases, such discrepancies can have a profound impact on the treatment and prognosis of the patient.*

This interpretation will be greatly reinforced in the minds of the scientific medical community by other factors, such as the implausibility and lack of significant evidential support for Kelley’s theories of cancer; and also of the improbability of any useful effect upon cancer or human physiology from some of the methods being used, such as coffee enemas and skin brushing.    Nutritional supplements, including pancreatic enzymes, have now been fairly extensively tested on cancer in animal studies, and many supplements and dietary interventions also looked at in clinical studies without arousing any strong expectations of useful effects upon established human invasive cancer.    The epidemiology of cancer is also not suggestive of nutritional deficiencies as such, as opposed to the carcinogen content of the diet, having any general role in its causation in most populations, let alone any influence upon its behavior once established, despite widespread opinion to the contrary.  There is also little evidential support for Beard’s theories concerning the role of pancreatic enzymes in cancer, whatever similarities may exist between the cancerous state and trophoblast.

The Kelley treatment is also by no means cheap or easy for sick patients to follow (see below).     There are many reasons why considerably more solid evidence would be required before the mainstream might take any interest in this method.

*Abt AB, Abt LC, Olt GJ. The effect of interinstitution anatomic pathology consultation on patient care. Arch Pathol Lab Med. 1995; 119(6):514-7.

Kronz JD, Westra WH, Epstein JI. Mandatory Second Opinion Surgical Pathology at a Large Referral Hospital. Cancer 1999; 86: 2426-35.

Epstein JI, Walsh PC, Sanfilippo F. Clinical and cost impact of second opinion pathology. Review of prostate biopsy prior to radical prostatectomy. Am J Surg Pathol 1996;20;851-857.


The Kelley Treatment for Pancreatic Cancer

The Kelley treatment is most strongly associated with the treatment of pancreatic cancer.  Kelley claimed to have cured himself of this disease, but from his own account of his illness pancreatic cancer was an unlikely diagnosis which was never confirmed. It was based upon symptoms of improbably long duration that were more likely to have had other causes.

Contributing to the legend, and described by Dr Kelley himself in his book as  “the most outstanding study in medical history” and as adhering to  “ rigid standards — i.e., Biopsy diagnosed at a major medical institution,” Gonzalez performed a separate examination of Kelley’s patients with presumed pancreatic cancer.   The report is included in One Man Alone and describes how five pancreatic cancer patients believed to have adhered strictly to the prescribed protocol survived for a spectacular mean period of nine years (which would equate to cure with the standard diagnosis of adenocarcinoma of the pancreas), whereas those who did not follow the protocol at all died within a mean period of 67 days; and only marginally less quickly (233 days) if they partially followed the regime.

The very poor results in those not pursuing the treatment and the difference when partially applying it can surely be largely explained by the rapidity with which patients with genuine inoperable pancreatic adenocarcinoma typically deteriorate.   When required to treat recently diagnosed biopsy-proven pancreatic adenocarcinoma in the recent NIH-funded study of the Kelley method* (which largely disposed of the claim of any useful effect for it), Gonzalez complained bitterly that he was being required to treat many patients who were already too sick to pursue his somewhat arduous routines, or not for long enough for there to be any effect.

Other patients would be likely to abandon the routine at the first sign that they were continuing to decline.   There is no indication that Gonzalez was aware of these likely confounding factors.  He offers  “Too much trouble or physician opposition” as the main reasons for patients not following the regime, and describes only one of the not fully compliant patients as being too sick.

More importantly, it transpires that the five long-surviving patients are included in the 50 case histories described below (Patients 3435363738).  Helping to explain the above findings, and fatally for any validity for this study (notwithstanding Kelley’s admiration of it), it is now apparent that not one of these patients had biopsy proof of pancreatic adenocarcinoma, or findings creating any reasonable certainty of that diagnosis.  Three (Patients 353637) were actually biopsy-proven examples of relatively rare neuroendocrine tumors (NETs) which, as explained in their case summaries, are quite compatible with prolonged survival, even when metastatic.   Patient 35 presented with liver secondaries for which a primary site of the NET was never determined, and Patient 37 had a carcinoid variant of NET involving the small bowel mesentery for which no primary site was established.   The other, (Patient 36) had an operable islet cell tumor of the tail of the pancreas, a relatively good prognosis lesion, and significantly, the only one of the 5 cases in which a tumor of any kind in the pancreas was confirmable.

The other 2 had changes in the pancreas which were not biopsied and that are consistent with the generalised induration caused by chronic pancreatitis, a well-known diagnostic trap for surgeons.  One of these (Patient 34) had had a biopsy of a small nodule in the liver which on frozen section was suggestive of a metastasis from pancreatic cancer, but malignancy was never quite explicitly, or independently, confirmed on later more reliable paraffin section examination.

Subsequent studies* have failed to show any benefits from Kelley-type treatment in inoperable biopsy-proven adenocarcinoma of the pancreas, all patients with that confirmed diagnosis having succumbed to their disease within about the usual time period despite employing the Kelley treatment.

In the latter study, Gonzalez thought he had shown improved survival over conventional care but the comparison was corrupted by patient exclusions, and the prolonged survival was mainly manifested in 4 patients in whom the pathological diagnosis was uncertain.

*Chabot JA, Tsai WY, Fine RL, Chen C, Kumah CK, Antman KA, Grann VR. Pancreatic proteolytic enzyme therapy compared with gemcitabine-based chemotherapy for the treatment of pancreatic cancer. J Clin Oncol 2010; 28(12):2058-63

Gonzalez NJ, Isaacs LL. Evaluation of pancreatic proteolytic enzyme treatment of adenocarcinoma of the pancreas, with nutrition and detoxification support. Nutr Cancer 1999;33(2):117-24

The role of Dr Robert Good

In the introduction to his monograph, which Gonzalez added in 2010, the name of Dr Robert Good is frequently mentioned. It is easy to get the impression, reading this introduction, that Good was at the very least sympathetic to Gonzalez’ research, and perhaps even an enthusiastic supporter of the project. This would be a misapprehension.

Because he was still an enrolled medical student at the time he carried out the research for this monograph, Gonzalez’ “research detour” required the assent of his academic mentors, prominent among whom was Dr Good, who was then head of Sloan Kettering Cancer Center. Dr Good apparently had no objection in principle to Gonzalez pursuing the project, although he instructed Gonzalez that any work on the Kelley treatment had to be on Gonzalez’ own time, and would not be considered as a part of his official medical studies.

Dr Good’s cautious encouragement of Gonzalez in this project seems to have stemmed entirely from his wish to foster a heuristic approach to medical education. Gonzalez himself quotes Dr Good as saying that a student always learns best when pursuing a project of his own devising, rather than an assignment picked by someone else. Thus Good’s support of Gonzalez, at least at the inception of what turned out to be a long and increasingly time-consuming investigation, should be seen as stemming from a belief in the utility of students pursuing their strongest interests and cannot be construed as in any way as bestowing legitimacy or approval on Kelley’s protocol. To the contrary:  Dr Good, who died in 2003, went to considerable lengths in the final years of his life to distance himself from the perception that he had in any way endorsed Gonzalez’ study or Kelley’s methods. A collection of Good’s letters (here) written over the period 1988-1991, clearly reflect the deep concern he felt that his name might be used by Gonzalez in connection with the study, in order to imply support for the Kelley approach. Here, for example, is an excerpt from a 1991 letter to Dr John Renner of the Consumer Health Information Research Institute:

I have repeatedly implored Dr Gonzales by word of mouth and in writing, even by a notarized letter, that he must not use my name to promulgate treatment which I do not advocate, have not advocated, do not condone and cannot support at the present state of knowledge.

Dr Gonzales continues to imply that I have supported, do support or that my observations might be taken as support for this line of treatment. That conclusion is inappropriate and wholly unwarranted.”


Note to readers on the classification of lymphomas

The lymphomas represent a group of more than 50 distinct but related cancers of the lymphatic system. Broadly, the lymphomas fall into two main categories: Hodgkin lymphoma (or HL, formerly known as Hodgkin’s disease), which represents less than 12 percent of the total number of lymphomas diagnosed annually, and the non-Hodgkin lymphomas (or NHL), which represent the remainder. Thus, of the 79,990 new cases of lymphoma that will be diagnosed in 2014, 70,800 will be classified as NHL while 9,190 will be given a diagnosis of HL.

The incidence of lymphoma has been rising steadily over the past 30 years. The reasons for this are not entirely clear, but certainly the growing number of people in the general population living with immunodeficiency states is an important contributory factor. Immunodeficiency predisposes strongly towards the development of lymphoma: this is why people with HIV are at significantly higher risk of developing lymphoma, as are those whose immune system has been intentionally subdued in order to facilitate organ or tissue transplantation.

Correct identification of the specific type of lymphoma has direct implications for both treatment and outcome. Treatment of these diseases is far from monolithic, and the outlook and expectation of remission – or better yet, cure – of the disease varies widely by type.

Historically, classification of the different types of lymphoma depended largely on morphology – that is, the microscopic structure and predominant cellular characteristics as determined by a detailed visual examination of biopsied lymphoid tissue.  That was more or less the only tool available at the time Gonzalez was compiling his monograph. However, over the past 30 years the classification of the lymphomas has become much less reliant on pure morphology (although morphology still matters), and more concerned with identifying cell characteristics through immunophenotyping, cytogenetics and molecular biology.

Consequently, hand in hand with expanding knowledge of the lymphomas as a group, the system by which they are classified for diagnostic purposes has undergone repeated revisions. Even the names of specific subtypes have changed since the 1980s, sometimes more than once. For example, what we now term Hodgkin lymphoma used to be called Hodgkin’s disease, and several of the non-Hodgkin lymphomas have acquired new names. This can be extremely confusing: the constantly changing nomenclature and the lack of standardization across the medical literature spanning the past 30 years can make it very difficult to follow which particular disease one is reading about.

The latest classification of the lymphomas was drawn up by the World Health Organization (WHO) in 2008, replacing the many older systems that were in use, sometimes concurrently, until then.  The WHO system attempts to draw together all the important biological attributes of a particular type of lymphoma. Undoubtedly this system, too, will need to be revised and updated as ever more detailed understanding of the biology of this extraordinarily diverse group of diseases emerges, but this need not concern us here. For the purposes of understanding the clinical material presented by Gonzalez in this monograph it is important primarily to be aware of the constantly evolving state of knowledge, and the fact that terminology has changed significantly in the intervening years.

It is also important to bear in mind that there is now a substantially more nuanced understanding of the natural history of this group of diseases than there was in the 1980s. While the way we speak about the different types of lymphoma suggests that they are immutably entities, distinctly different from one another, the truth is that individual disease categories under the rubric of lymphoma are now known to be somewhat permeable. It is quite possible, for example, for one type of lymphoma to evolve, over time, into quite another type – Hodgkin lymphoma transforming into non-Hodgkin lymphoma, for example; or for that matter, for chronic lymphocytic leukemia/small cell lymphoma to undergo transformation to Hodgkin lymphoma (Richter’s transformation)*. Similarly, it is possible for two different types of NHL to coexist concurrently in the same patient – or even for a patient to have a composite of leukemia and lymphoma.  It should also be borne in mind when assessing the relevant histories that follow that many of the newly elucidated protean behaviors of this complex group of diseases, would have been unfamiliar to the doctors who treated some of the lymphoma patients in Gonzalez’ study.

Kirchner EM, Ebsen M, Kirchner J, Theegarten D, Voigtmann R. Transformation of Hodgkin’s disease to high-grade B-cell lymphoma: remission after Rituximab monotherapy. Ann Oncol 2001;12(8):1169-1171

Krause JR, Drinkard LC, Keglovits LC. Hodgkin lymphoma transformation of chronic lymphocytic leukemia/small cell lymphocytic lymphoma. Proc Bayl Univ Med Cent. 2013;(26)1:16-18


The Fifty Cases


Patient 1:  Possible cholangiocarcinoma

Gonzalez states that this patient “survived nearly six years after diagnosis of bile duct carcinoma.”

This 54 year-old man presented with jaundice and at operation on 20th Dec 1976 was found to have obstruction of the bile ducts due to hard mass “consistent with carcinoma” at the union of the right and left hepatic ducts, extending about 1 cm into the common hepatic duct. Attempts were made to obtain a biopsy of the mass but were unsuccessful.   A lymph node in the area was examined and reported as showing  “no evidence of disease.” A T-tube was inserted, but possibly distal to the obstruction.   There is no data in the operation notes or other documentation as to the size of the lesion, but Gonzalez refers to it as “large.”

According to hospital admission notes of 20th March, 1977 the lesion was treated with 500 rads radiotherapy post-operatively “over eight weeks”.   The 500 rads is likely to be a misprint, as 5000 rads would be a more usual dosage for treatment of a cholangiocarcinoma   and much more likely to be spread over such a long period.

The patient began the Kelley regime in “early March” 1977 but required readmission on 20th March with cholangitis and subsequent gastrointestinal haemorrhage. He was still “deeply jaundiced” at this stage.  Although his Hb (haemoglobin) fell to 4.8G%, it was decided not to intervene.  He was apparently regarded as terminal and his family decided to take him home.    During this admission his bilirubin fell from 20 to 7.6.

Next readmitted to hospital 30th August 1977 with massive ascites, presumably from portal vein thrombosis.  At this stage bilirubin was normal but alkaline phosphatase was very high, at 720, which would be consistent with persisting continuing biliary obstruction.  In view of his presumed terminal state, he was managed conservatively again.  He improved enough to go home after one week.

However he was readmitted 28th November 1977 for a peritoneo-venous shunt for his ascites: he had being requiring weekly abdominal paracenteses at which 4-7 L of fluid were removed.   Bilirubin levels not stated but alkaline phosphatase was 1280 at this stage.

Next documentation is dated 25th September 1978, when the patient’s alkaline phosphatase was extremely high at 1500 IU, but bilirubin was only 2.6. Liver scan showed “little change in last 10 months” with a large left lobe of liver, prominent porta hepatic area and “probable malignancy” in the porta hepatis.

Gonzalez states that over this period patient enjoyed a reasonably good quality of life despite frequent hospitalisations and gastrointestinal bleeding and what he terms “problems relating to his hepatic failure.”

On 28thMarch 1979 Patient 1 was admitted with upper gastrointestinal bleeding and was transfused on this occasion.

He died in May 1982 after lapsing into hepatic coma.


A complex case of purported moderately prolonged survival with probable cholangiocarcinoma, although there is unfortunately no certainty as to what the pathology was or how it responded to any of the treatments used.    The lack of biopsy leaves open the possibility of rarer forms of cancer for this location, ones that may be more responsive to radiotherapy, such as lymphoma.

There aren’t many likely benign causes of this man’s ultimately fatal biliary (and probably portal vein) obstruction but the absence of biopsy proof of malignancy is always a problem. A truly effective treatment should be able to demonstrate its worth in more clear-cut cases.

The medical literature contains reports of survivors of over five years with the combination of radiotherapy and chemotherapy with cholangiocarcinoma.

Patient 2: Primary central nervous system lymphoma


This 31 year-old patient survived five years after diagnosis of what was initially thought to be a glioma (an aggressive brain tumor) but was subsequently identified as a central nervous system lymphoma.

The patient had experienced a variety of fluctuating neurological symptoms over a period of about a year, starting in mid-1981. His symptoms included numbness and weakness of the lower extremities, and incontinence.  He was initially thought to have multiple sclerosis and was treated empirically with ACTH.  However, in September 1982 he was admitted to hospital with headaches and confusion, and a CT scan of his head revealed a large mass in the third ventricle region of the brain.   Exploratory surgery on 16th Sept 1982 revealed two brain tumors, both of which were bulging into the third ventricle.  The lesions were considered inoperable, a frozen section examination of biopsy tissue having been described as showing “high grade glioma.”

However, the final pathology report, after more reliable paraffin section examination, recorded a diagnosis of “small cell neoplasm consistent with lymphoma.”

The main concern at this point was marked weakness in the lower limbs with features suggesting spinal cord compression, a medical emergency.  A myleogram on 28th September 1982 confirmed the presence of a lesion at T5-T8 level.  The medical record states that he was to be referred to another institution for radiotherapy “as soon as possible” with the intention that
“after the patient’s [sic] received a sufficient radiation course he will be returned to the Ann Arbor VAMC where further staging work up shall proceed.”   (That further staging was planned conflicts somewhat with Gonzalez’ account, in which he states that “doctors informed his wife that he had four to six months to live – at most.”)

The patient was treated with 2200 rads to the brain and 2277 rads in 16 days to the spinal lesion – about half what was intended: on 15th October 1982 the patient chose to discontinue treatment and pursue the Kelley program.

The records of the original hospital state that the wife came to collect his records on 27th October.   It is recorded in the medical notes, presumably on the wife’s statement, that the patient’s memory had improved but that at this early stage after radiotherapy there was no detectable change in the neurological status of his lower extremities.

Gonzalez continues: “Patient 2’s first months on his nutritional regimen were difficult: at times he lapsed into such confusion that his wife had to force the supplements into his mouth.  Nevertheless, on the therapy he slowly began to improve to the point his mental status normalised and over a period of a year he progressed from a wheelchair to a cane.”

However, Gonzalez provides no further medical documentation of this case other than a CT brain scan report dated 21st April 1983 (about six months later) which is described as being of poor technical quality, but which showed post-surgical changes and was otherwise “grossly negative.” For some reason no hospital notes are provided for this consultation, nor for another consultation in June 1983 when doctors were said to have been “stunned” when he walked into the clinic unaided, and also “further surprised” when the CT scan of his brain showed no definite evidence of cancer.


Lymphoma is generally very radiosensitive and deposits can be definitely cured by radiotherapy.   The dosage recommended here was of the order of that used for cure rather than palliation.   In one study* of palliative radiotherapy for NHL deposits a dose of a mere 400 rads (4Gy) was found to produce a complete response rate of 49 percent with 50 percent freedom from local progression within 2 years.  It is to be expected that five times this dose would have had a dramatic effect on this man’s lymphoma deposits and have significant potential for producing long-term survival.

A CT scan performed six months after the patient had received radiation suggested that the tumor was now in remission. It is not clear what, if anything, the Kelley program contributed.

*Chan EK, Fung S, Gospodarowicz M, Hodgson D, Wells W et al., Palliation by low-dose local radiation therapy for indolent non-Hodgkin lymphoma. Int J Radiat Oncol Biol Phys 2011 Dec 1; 81(5):e781-6

Patient 3:  Metastatic breast cancer 

Dr Gonzalez describes this patient as: “a 62-year old woman from Iowa with a history of metastatic breast carcinoma, now alive more than ten years since her diagnosis.”

In late August 1976 a mammogram revealed a suspicious lesion in the patient’s left breast, which on biopsy proved to be an infiltrating ductal carcinoma, measuring 3cm, and with 10 of 17 axillary nodes involved. She underwent a modified radical mastectomy on September 2nd 1976, and received two months of 5-fluorouracil post-operatively.

Gonzalez’ summary states that “subsequent bone and liver scans showed no evidence of metastatic disease,” but no documentation is provided. Gonzalez goes on to state: “She reported to me that a series of follow-up chest x-rays at that time revealed lesions in her lungs consistent with metastatic malignancy.” However, this is also not documented in any way. Neither is it mentioned in the hospital discharge summary, which would be unusual if there were significant concern about possible metastatic lesions.   She would also not be normally considered for minimal adjuvant chemotherapy if she were suspected of having metastatic disease in her lungs.


The presence of distant metastases is not documented.

Gonzalez makes much of the patient’s  “rapid decline” a mere two months after surgery and after two cycles of 5FU, and states that she improved on the Kelley program, but her poor health status and slow recovery cannot be attributed to her breast cancer.  It is not so aggressive as to produce major decline so quickly from a starting point of minimal disease. Furthermore, Gonzales allows that there was no definitive evidence of active cancer when the patient began the Kelley protocol.

Gonzalez lays emphasis on the fact that there were areas of comedo-type ductal carcinoma in situ (DCIS) within the excised tissue, and also some focal areas of necrosis. He interprets the presence of these features as signs of the aggressive nature of the patient’s cancer. However, comedo and comedo-necrosis, are terms which describe only DCIS, the non-invasive premalignancy from which an invasive cancer can (and in this case, did) later develop. DCIS with these features may be considered more likely to undergo malignant change, but there is no evidence that an invasive cancer which arises from comedo-type DCIS will behave any more aggressively than one that arises out of a non-comedo DCIS.

Patient 4: Recurrent breast cancer


Gonzalez introduces this patient as “a 44 year old woman from Los Angeles with a history of recurrent breast cancer, alive 13 years since her original diagnosis.”

In July 1974 this lady underwent a modified radical mastectomy for a 2cm mucinous cancer of the breast.  The pathology report mentions “metastases to axillary lymph nodes adjacent to breast.” Other axillary (armpit) contents were not involved, and there was no evidence of distant spread on chest x-ray, bone scan or liver scan.

For reasons that are not quite clear, nor supported by any documentation, Gonzalez states that the patient was advised to undergo “a two years course of the drug Alkeran” which she duly began that summer (1974).

In October 1976, “only months after completing the regimen,” she developed a small nodule in her mastectomy scar that proved to be a local recurrence of breast cancer.

Again no documentation is provided, but according to Gonzalez, she was advised to undergo radiotherapy and further chemotherapy, but she declined, and instead she sought treatment at an “alternative” clinic in Mexico, there receiving a variety of treatments including Laetrile and the conventional chemotherapy drug cyclophosphamide (Cytoxan). No documentation, dates or details of the extent of this treatment are provided, Gonzalez says only: “when Patient 4 reacted badly to the treatment she left the clinic and returned home to California.”  Subsequently, in late 1976, she apparently began a series of injections of BCG vaccine.

In December 1977 she developed a new nodule “in the region of her mastectomy scar.” When surgically removed on 29th December 1977 at Cedars-Sinai Hospital in Los Angeles, the 0.7 cm lesion was described as showing  “dermal and subcutaneous metastatic breast ductal carcinoma.”

Less than nine months later a third nodule appeared, was excised, and was also described as “adenocarcinoma consistent with metastatic carcinoma of mammary gland origin.”

At this point, although her health had begun deteriorating, she is stated to have continued to refuse further chemotherapy – if indeed it was actually recommended: local radiotherapy would be a more usual approach to such localized disease. She chose instead to employ the Kelley regimen, which she began in February 1979.

“Within months,” Gonzalez states, “all her symptoms and problems – her fatigue, depression, weakness and weight loss – resolved, Today, eight years since beginning the Kelley regimen, Patient 4 is in excellent health.  During this time her once persistent malignancy has not recurred.”


This lady had several local recurrences in or close to her mastectomy scar excised over a period of two years.  Thirteen years later she was still alive with no further recurrences.  Gonzalez attributes her prolonged disease-free survival to the Kelley program.

While local recurrence of breast cancer is often associated with a poor prognosis, there are cases where cancers with low distant metastatic potential cause multiple local recurrences, either due to implantation at the time of surgery or from in–transit metastases in the lymphatic system, due to cells entrapped after removal of the draining lymph nodes. I personally [Dr Moran] have had such a case, a patient who was initially treated by another surgeon, and who developed innumerable local recurrences over very many years, without distant spread, before they finally stopped recurring.

Patient 4 is said to have been very ill at the time she commenced the Kelley regimen but there is no documentation of any cancer pathology at that time.  This kind of general decline would not be a typical accompaniment of minimal cancer; indeed, she did not apparently display it with prior recurrences.   She may well have had a depressive or stress-related illness as the result of the recurring problem, and the improvement in her outlook and energy level over a period in which no further recurrences arose is not surprising.

In conclusion, no clear effect of the Kelley treatment can be demonstrated here.

Patient 5: Metastatic breast cancer

Gonzalez introduces this patient as: “A 78-year old woman from Arkansas alive 13 years since diagnosed with metastatic breast cancer.”

On 21st June 1974, biopsy of a 5 cm breast mass revealed cancer and a left radical mastectomy was performed.  On examination of the specimen there were metastases in lymph nodes up to 2.5 cm in size “at all levels of axillary dissection.” The pathology report is, however, rather skimpy on detail and it is not clear how many of the nodes that were removed were actually involved with cancer, or whether the highest axillary node was involved.

She was advised to undergo “an aggressive course” of radiation to the chest wall, but the patient refused further conventional treatment.  As a nurse for 25 years, she reportedly told Dr Gonzalez that she had seen too many patients with cancer die after chemotherapy and radiation to have much faith in the standard approaches.


The patient was alive thirteen years following her mastectomy, and had experienced no recurrence.  The omitted radiotherapy would have made the risk of local recurrence of her cancer much less likely, but without having any other effect on her chances of survival.

While such heavy involvement of the axillary (armpit) lymphatics is generally associated with a poor prognosis, this is by no means certain.  I  [Dr Moran] have had a similar case in a much younger woman (who also refused radiotherapy) and who, at last review, had survived for a comparable period since first treated.  However, the likelihood of long-term disease-free survival for such a case may be as low as a few percent.

Patient 6Metastatic breast cancer

Gonzalez describes Patient 6 as “a 78-year-old-woman from Colorado with a history of metastatic breast carcinoma, alive 14 years since diagnosis.”

This lady underwent a radical mastectomy in May 1973 at the age of 64 for biopsy-established invasive intraductal carcinoma. The pathology notes describe a 1 cm lesion in the breast, apparently mostly composed of intraductal cancer (DCIS), and no involvement of axillary lymph nodes.  This should have been a good prognosis lesion.

In December 1974, Gonzalez states,  “a follow up bone scan and x-ray studies were completely clear.”

However, some 2.5 years later, in May 1977, she presented with worsening pain in her right ribcage, which, according to Gonzalez, had been present since “mid-1976” and was initially regarded as muscle strain.

Hospital notes of June 1st 1977 state:

“…she has noted some right upper abdominal or rib pain which has been intermittent over the last two years, but has recently become progressively more severe.  One week ago the patient had a repeat bone scan which had previously been negative and is now positive in the ribs and spine.  Rib x-rays confirmed metastatic disease.  A chest x-ray was negative.  Thus, this 68-year old female developed new changes on bone scan and x-rays confirming metastatic bone disease.

“Plan: Plan to review the patient’s hospital records including the x-rays and scans and obtain liver scan and mammogram. “

The oncologist went on to suggest the expectation of a good response to stilbestrol (a synthetic estrogen),  being “this far post-menopausal (and) with a long disease-free interval.”   (According to Gonzalez’ summary of the case, a hysterectomy and bilateral salpingo-oophorectomy had been performed before she developed breast cancer, but the date on which this occurred is not supplied.)

Unfortunately Gonzalez supplies none of the reports for the critical investigations and there is no comment on what was found on the planned review of them.

In June 1977 the patient was commenced on stilbestrol.   At this time she also began Kelley treatment.  “Within weeks on this combined regime,” Gonzalez reports, her bone pain improved.  Within a year her symptoms had completely resolved.”

In 1979, when commenting on the patient’s good progress despite having stopped taking stilbestrol six months previously, her oncologist said  “As time goes by without therapy I am more concerned that our original diagnosis of bone metastases was incorrect, but as you know, she did have confirmatory x-rays of her positive areas on bone scan.  She may just have long remission off of (sic) therapy, but only time will tell.”


Bone scans can be falsely positive, even with multiple lesions*, so that a review of all the imaging would be desirable in this case.  Metastatic disease is possible with the minimal cancer that this lady had originally, but less common.

It must also be said that it is most unusual for hormonal treatment to cure established metastatic cancer, although it does seem capable of controlling or eliminating occult cancer.

In summary, a fairly impressive case, weakened by an inability to examine original investigations, the small possibility of diagnostic error, and the possibility of an unusual response to conventional hormonal treatment.

Jacobson AF, Stomper PC, Jochelson MS, Ascol DM, Henderson IC et al. Association between number and sites of new bone scan abnormalities and presence of skeletal metastases in patients with breast cancer. J Nucl Med 1990;31(4):387-92

Patient 7: Breast cancer


Patient 7 is 53-year old woman who was alive 17 years after being diagnosed with breast cancer.

In 1970 she underwent R radical mastectomy for infiltrating carcinoma.  No adjuvant treatment (chemotherapy or radiation following surgery) was suggested, according to Gonzalez, and no documentation of the surgery or follow up is provided.

In 1973 she developed invasive cancer in the left breast and underwent left radical mastectomy. No details are provided about these procedures.

Gonzalez states that the patient’s health deteriorated gradually over the year following her second mastectomy, and by mid-1974 she also “developed pain along the length of the vertebral column and into the right shoulder that by late 1974 was so severe at times she was unable to dress herself or walk.”   She was also described by Gonzalez as suffering from “chronic fatigue, lethargy and bouts of depression persisting for months at a time.”

Gonzalez states that x-rays of the patient’s spine performed in May 1975 showed  “obvious abnormality” in the fifth lumbar segment, described as “indicative of osteolytic metastasis from breast carcinoma.”   While Gonzalez suggests that the patient was suffering from severe skeletal pain for a long time before her doctors did any investigations, this is rather unlikely in someone with a history of breast cancer.   It is more likely that previous investigations, perhaps forgotten by the patient when recounting her history, were negative.

 A bone scan on May 14th 1975 described “focal abnormal uptakes of skull and tip of right scapula.  Possibility of metastatic disease should be considered” Rather oddly, although “three areas of abnormal uptake” are described “over the skull” and the comment that “the possibility of metastatic disease should be considered” there is no mention of any abnormality in the fifth lumbar vertebra, where the x-rays had suggested a major osteolytic lesion.  This is one of the more poorly documented cases, where it would be helpful to be able to examine the original films, and have access to other investigations.

At any rate, it was assumed quite reasonably that she had metastatic breast cancer and on May 27th 1975 a bilateral oophorectomy was performed as intended palliation.   At the same time she began Dr Kelley’s treatment.   While the 4-5 year disease free interval and the presence of bone secondaries alone (and not visceral metastases) would arouse an expectation of a good remission from oophorectomy, Gonzalez tells us the patient was told “she would probably not live out the year.” She decided to pursue alternative therapies, beginning “the nutritional program in the summer of 1975.”

Gonzalez says: “She told me that within six months, her persistent pain and depression resolved.”   Yet he also states in his later summary, “Although she did undergo oophorectomy, Patient 7 continued to deteriorate after the procedure.”     According to the patient’s account several further bone scans showed complete regression of the skeletal lesions, though the reports are “no longer available.”   Twelve years after the oophorectomy she remained well.


 Another case where there is very strong suspicion of malignancy and modest expectations of the conventional treatments used in parallel with the Kelley treatment, but room for small doubts on both scores.

Patient 8:  carcinoma of cervix


This patient is described by Gonzalez as a“78-year old woman from Canada alive nine years since her diagnosis of metastatic cervical cancer.”

Patient 8 was 65 years old when diagnosed with cancer of the cervix, Stage Ib, in January 1978.  A biopsy was apparently carried out at that time but no biopsy reports are supplied.

At the urging of her physicians, the patient underwent two courses of radium insertion “to full dosage” and 1150 rads of external radiation to pelvis in late March 1978.  Against medical advice she decided to stop treatment at that point. The radiotherapist recorded in the notes that he had advised the relatives that there was “no more than 40%” chance that the disease would be controlled by the treatment already given.  She was at that time bothered by heartburn, severe abdominal pain and urinary difficulties“ which the oncologist attributed to the radiotherapy, rather than her cancer.

Gonzalez states that the cancer “grew unchecked” over the ensuing 6 months, and that in September 1978 she developed a partial urinary obstruction brought on by “the enlarging pelvic tumors.” A renogram is said to have shown declining function in both kidneys but no documentation is provided.   The patient “still refused all conventional intervention” and although Gonzalez states that she had earlier consulted Dr Kelley (no date for this consultation is given), she had not yet begun the Kelley treatment due to family opposition.  One wonders if this is entirely likely, given the ensuing five months of supposed decline.

She was finally admitted to a different hospital in late October 1978 because of recurring bleeding and weakness, strangury (bladder spasms) and “some bowel problems.” It is not clear whether the bleeding was vaginal or from the bladder, as there is reference to the urinary catheter becoming blocked by clots.   In either case most of her symptoms could be explained by local radiation changes from the vaginal inserts because of the proximity of the cervix to the bladder and rectum.

At this admission she was described as “terminal,” but there is no documentation of how that status was determined.  It seems likely that having limited familiarity with her case, and bearing in mind the fact that she was known to be adamantly refusing conventional treatment, no energetic assessment was made of what they describe as her “carcinoma of the uterus” (although it was actually of the cervix).  Thus, a mass is described as arising out of the pelvis – rather unlikely in a partially treated cervical cancer within this time frame, given the deep location of the cervix within the pelvis – despite the abdomen being described as bloated, the lower abdomen “tender,” and there being a suspicion also of urinary retention, which led to the insertion of a catheter.   Sometimes unreliable findings and assumptions of junior staff become enshrined in hospital notes and repeated without anyone checking them.

A “Dr F” (possibly a urologist) saw her in consultation and “noted” the “frozen pelvis with carcinoma” but there is no record of the results of either his internal or abdominal examination.   It is even stated that he was unable to examine her adequately rectally “because of haemorrhoids,” which suggests that per vaginam examination was being avoided. He, too,  may have been leaping to certain assumptions concerning the disease status.

She was readmitted a day after discharge because family could not cope and again abdomen “showed marked tenderness in the lower abdomen with a hard tumor mass rising out of the pelvis.”   Again she was discharged home with a urinary catheter.

There is no further documentation on this lady.  She is said to have at this point started Dr Kelley’s treatment, to have gradually improved over the following year with regression of what Gonzalez describes as  “her abdominal tumors,” and kidney function returning to normal.  Nine years later, we are told, she reports good health with no signs of cancer on Pap smear and ultrasound.


 The problem in this case is that there is no confirmation of the presence of cancer in November 1978.  In my opinion it is most unlikely that a partially treated and relatively early cervical cancer would grow to the massive size that would enable it to be palpable abdominally under difficult conditions within that time period, if ever, before causing death in other ways such as bilateral renal failure from ureteric obstruction.

It seems likely that she was assumed to be terminal by doctors unfamiliar with the patient but knowing her to be refusing medical care for her cancer, and over-reliant on the findings of junior doctors, coupled with presumptions based upon what they were told by the patient and family, and this diagnosis  was never doubted or questioned by Kelley, a dentist with limited relevant clinical expertise, or by Gonzalez, who was then a junior medical student.

The outcome of this case otherwise is reasonably explained by the radiotherapy and surgery.

There is also no evidence that this cancer was ever “metastatic,” as Dr Gonzalez described it.

Patient 9: Colon cancer


Gonzalez introduces this patient as  “a 74-year old woman from California alive more than ten years since her diagnosis of colon cancer.”

Surgery for carcinoma of the transverse colon was carried out on December 15th 1976.   An ulcerating lesion is described as partially circling the bowel wall and infiltrating through into the subserosa. It is reported as a moderately differentiated adenocarcinoma with involvement of two lymph nodes examined.  Her oncologist recommended no further treatment following surgery.

Throughout the following year (1977) she developed sharp pains in back, chest, and shoulders, fatigue, depression and bouts of abdominal discomfort, and was admitted to hospital in December 1977 at which time was requiring opiates for pain (admission not documented).  A discharge summary dated December 9th 1977 documents stable physical condition, no abnormalities and no suggestion or suspicion of cancer recurrence.

Following this, over the ensuing year she “continued to deteriorate” and by the end of 1978, according to Gonzalez, she had become bedridden.  He states that “in desperation” she turned to unconventional methods and started on the Kelley treatment in January 1979.   Within weeks her disabling pain abated and other symptoms resolved completely.

Ten years later at age of 74 she was well with no evidence of cancer.



 This lady’s illness is most unlikely to be due to cancer regardless of the small elevation in CEA (1.1 to 2.8) that was noted in November 1977, but not recorded thereafter despite supposed continued decline over a further year. There was no documentation of recurrent cancer at any stage.  Possibly a depressive illness.

This case cannot be regarded too seriously and Gonzalez himself allows that this is “ not a definite case.”   He concedes that five-year survival of “colorectal cancer with two positive nodes” has been documented in at least one study at 25 percent even without adjuvant treatment. Recurrence of colorectal cancer is rare after five years.

Patient 10:  Colon cancer


Gonzalez describes this patient as  “a 67-year old man from Iowa who has survived nearly 12 years since his diagnosis of metastatic colon cancer.”

In mid-1974 he noticed a change in bowel habit, but it was not until several months later that he consulted a family physician and was referred for evaluation at a local clinic. There he was found to have a suspicious lesion in the right colon.   A liver-spleen scan performed preoperatively showed a “suspicious defect in left lobe of liver” measuring approximately 2.5 cm in diameter.  Chest x-ray was clear.

 At operation on 8th July 1975 a large (10 cm) cancer of the caecum with invasion of the mesentery was discovered, along with “two lesions in liver, one in the right and one in the left lobe; the right one was larger than the left, measuring about 2×2 cm.” The consistency, color, etc., of these liver lesions were not described, and neither were they biopsied, but the five regional lymph nodes that were sampled showed that there was no lymph node involvement.

Gonzalez reports that the patient was given a prognosis of “three to six months,” which would itself be extremely pessimistic for someone with early hepatic secondaries from colorectal cancer.  Additionally, since they were not biopsied, we can have no certainty that these lesions were indeed cancerous, there being a number possible benign causes for liver lesions.

 Also unfortunate is the fact that no further imaging is presented for this patient. If it had been possible to show that the lesions had been present at the start of Kelley’s treatment, but had resolved during subsequent treatment, that might have been much stronger evidence of a treatment effect than the patient’s survival from what in any case has an excellent chance of being a curative operation.

Mistaken diagnoses are also common in this situation.  In one case series,* 7 percent of operations that were regarded as palliative actually proved to be curative.

*McLeish JA, Thursfield VJ, Giles GG. Survival From Colorectal Cancer in Victoria: 10-year follow up of the 1987 management survey. ANZ J. Surg. 2002,72: 352-356


No proof of cancer when Kelley treatment began, or evidence of a response of the lesions that the Kelley protocol was supposedly treating.

Patient 11: Colon cancer

Gonzalez describes Patient 11 as a “60-year old woman from Michigan who has survived over 17 years since diagnosed with carcinoma of the colon.”

This lady had a five-year history of abdominal pain, which, by the end of 1968, was said to have incapacitated her for several hours a day and several days a week.   She also experienced chronic constipation and rectal bleeding.   A barium enema and other tests performed in mid-1969 were  “largely unrevealing.” She was finally admitted to hospital in March 1970 with diagnosis of possible bowel obstruction, at which point a further barium enema revealed a stricture in the descending colon consistent with a carcinoma.

At surgery, on March19 1970, a 7cm mass in the descending colon was resected.  There was no evidence of extramural extension of tumor and no evidence distant spread.   The pathology report describes an intermediate-grade carcinoma involving the full thickness of the bowel wall, but with no lymphatic spread.

There is no documentation of her subsequent progress, and we are dependent upon Gonzalez’ account of what he was told.   According to Gonzalez, the patient states that she was advised that the cancer would probably recur.   It is not clear why she would be told that on the pathology described.  This may have had something to do with her subsequent progress.

After a minor traffic accident in December 1971 her health began to deteriorate again with the recurrence of severe abdominal pain, constipation and chronic nausea.  Her appetite declined and she lost 12 pounds in weight.   Gonzalez states that in January 1972 she saw a gastroenterologist and “underwent, as an outpatient, a complete evaluation including upper and lower GI series, sigmoidoscopy, and colonoscopy. “ These studies revealed a large, restricting recurrent tumor in the remnant of her descending colon.   “Although I do not have the records to confirm this,” Gonzalez continues, “Patient 11 claims her doctor told her the cancer had metastasized widely.”

There is no documentation of this and no mention of a biopsy, which would be routine if such a cancer was encountered at colonoscopy.   The patient says she was advised to undergo immediate surgery to prevent obstruction, but instead chose to consult Dr Kelley and “within days noticed an improvement.” Within a week “the bowel obstruction cleared and abdominal swelling lessened.” From that point onward, her appetite improved and she gained weight.  “Eleven months after beginning her protocol, she reports passing a large globular mass of tissue which she and Dr Kelley assume was the remnants of her tumor.”


If the facts were as stated then it would be hard to gainsay this case.  However, one cannot help wondering why neither any documentation of the colonoscopy findings is provided nor is there a biopsy report available.   It is also possible to identify this lady from versions of her story on the Internet*, and they provide no reassurance that the facts are as given.  For example, in one version of her story she states that she was told as an outpatient “that I could not live three weeks like I was, since my cancer had metastasized to the lymph glands.” No likely outpatient test could establish that, and in any case it is a ridiculously unlikely prognostication. The story of the cancer being passed per rectum is equally troubling for the trustworthiness of this material.

* See the following, taken from Pat Judson’s story:

“Despite that prediction, by the grace of God, I lived past the time the doctors had given me. In January 1972, almost two years after the original surgery, I experienced a recurrence of a blockage of the colon. I knew for a certainty that if I went back to my doctors who had done surgery on me, I would be immediately hospitalized. I looked for an understanding doctor. After he did what he could, he told me that I would have to return to my doctors for surgery; that I could not live three weeks like I was since my cancer had metastasized to the lymph glands. When I asked him how long he thought I could live with surgery, he expressed doubt and said “possibly three months.” After considerable thought, prayer and discussion with my family, I decided I could not endure another surgical ordeal. Surgery, for me, was no picnic. I chose instead to accept death, and trusted without question the judgement of the doctors who said nothing could be done to help me.”

Rethinking Cancer: Non-Traditional Approaches to the Theories, Treatments and Prevention of Cancer:

Gonzalez says “Clearly this patient’s apparent cure and current good health can only be attributed to her nutritional regimen. “    But in the absence of so much critical documentation such a claim cannot plausibly be made.  In addition, the very long and dramatic history of abdominal symptoms prior to the diagnosis of bowel cancer is clearly not likely to be due to cancer over that period, leaving grounds for doubt as to the significance of her later symptoms.

Patient 12: Hodgkin lymphoma (Hodgkin’s disease)


Patient 12 is described by Gonzalez as a  “44-year old man with a history of widely metastatic Hodgkin’s disease, alive five years since his original diagnosis. “

This man developed enlargement of neck lymph nodes in July 1971.  A biopsy was inconclusive and the glands subsided spontaneously.   In January 1982 he presented with full-blown Stage lV A Hodgkin lymphoma with enlarged lymph nodes in the neck, axillae (armpit) and inguinal (groin) regions. CT scan revealed further enlarged nodes in the chest and retroperitoneum, as well as suspicious nodules in both lungs.  A bone marrow biopsy revealed myeleofibrosis.

He went into remission with combination chemotherapy but relapsed in 1983 with enlargement of glands in a similar pattern.  After a further round of chemotherapy, completed in late October 1983, his disease seemed to be under control.

While this is not documented independently, Gonzalez describes the patient as experiencing drenching night sweats beginning in January 1984 –  “a characteristic sign of advancing Hodgkin’s disease,” as Gonzalez comments; but a CT scan on February 14th was said to show no sign of cancer and at oncological review on 10th May 1984 he was said to be “feeling reasonably well.” Furthermore, although some axillary nodes were noted bilaterally, and a 1.5 cm inguinal node was noted on the right, the oncological review notes state that there was “no clear-cut evidence of recurrent Hodgkin’s disease.”   The doctor records that Patient 12 was at this time on a vegetarian diet, taking megavitamins and had also (according to Gonzalez) begun using regular coffee enemas under the guidance of a former Kelley patient.

At a further review on 19th July 1984 the patient stated he was feeling “perfectly well” but he had noted some right-sided axillary nodes not noted previously.   On examination there were suspicious glands up to 2.5 cm in size in both axillae and the left femoral region.  He was advised to schedule an appointment for a right axillary node biopsy.

There is no further independent documentation of this man’s progress.  Gonzalez states that the nodes continued to enlarge, his night sweats and weight loss continued, and in September 1984 the patient’s left leg suddenly swelled.

He was reviewed by Dr Good and Dr Gonzalez on October 9th 1984 at which time he appeared “in the terminal stages of cancer,” with numerous lymph node enlargements including a 12 cm one in the left groin. He also displayed the distinctive skin rash of Hodgkin lymphoma.

It was at this point that the patient consulted Dr Kelley directly, and “began the full Kelley regimen.” When he returned to Dr Good’s clinic on January 19th 1985 he was “smiling, walking without a cane, looking not merely improved but healthy, with an added ten pounds on his frame and normal pink tone to his skin”.  The rash had disappeared and no nodes were now palpable.

He is said to have remained well except for a relapse when trying laetrile, until the spring of 1987.


It is not at all unusual patients to survive five years – and much longer – with Hodgkin lymphoma.

However this is one of the better cases, because of the very dramatic remission that apparently occurred over several months at the end of 1984 – unusual even for the Kelley treatment, there being no other cases with independent confirmation of such a dramatic and apparently objective change in cancer  in the absence of any conventional treatment.   Unfortunately Dr Good is no longer alive to confirm these events.  It does strain credulity a little that we are required to believe that this dramatic change in patient fortune arose as the result of a shift to a more “authentic” form of the Kelley regimen from one that closely mimicked it, including the use of many of its elements.

It would be interesting to know what happened to this man subsequently. Indeed, it is surprising that Gonzalez does not appear to have considered it useful to provide information as to the progress of any of these cases after the cut-off point in 1987, even though It is likely that he had ongoing contact with many of them.

So-called spontaneous remissions do occur in Hodgkin lymphoma but they are extremely uncommon (*see here, for example).   One would also be reluctant to confidently invoke that possibility without having more assured and more complete information about all circumstances surrounding this case than we can have from the supplied information.

*Mangel J, Barth D, Berinstein NL, et al. Spontaneous regression of Hodgkin’s disease: two case reports and a review of the literature. Hematology 2003;8(3):191-6

Patient 13:  Hodgkin lymphoma (Hodgkin’s disease)

Patient 13 is described as a “37-year-old man from Washington state, alive nine years since diagnosed with Hodgkin’s disease.”

This man presented in late 1977 with enlarged cervical and axillary lymph nodes, occasional night sweats and pruritus (itching).  ”Chest x-ray revealed mediastinal lymphadenopathy and a lymphangiogram demonstrated involvement of intra-abdominal lymph nodes.   A biopsy of a large neck lymph node confirmed Hodgkin lymphoma, predominantly nodular sclerosing variant, but the pathologist’s report noted that there were “areas of  “mixed cellularity, and large collections composed mainly of mailgnant reticulo-endothelial cells with lymphocyte a depletion…” Interestingly, the pathologist appended the comment: “and I do not understand the meaning of some of these patterns.”

A staging laparotomy was performed on 14th February 1978.  A biopsy of periaortic lymph node confirmed involvement.  Liver and spleen biopsies and bone marrow aspiration were negative.

He was given a diagnosis of Hodgkin lymphoma, nodular sclerosing type, Stage lll B.

It was decided to treat him with three cycles of combination of chemotherapy (MOPP) followed by radiation (4060 rads) given in a mantle configuration (i.e., to chest, neck and axillae) over a period of six weeks. After a 2-3 month rest period he would receive further radiation, this time in an “inverted Y” pattern, targeting the abdominal lymph nodes. This would be followed by more cycles of MOPP “if he can tolerate the chemotherapy after the radiation therapy.”

He received the initial 3 cycles of MOPP uneventfully and completed the mantle field radiation on July 14th 1978.  His Vancouver Hospital medical progress notes, dated 21st August, 1978, state that he “seems to be doing well, no problems.   He will return Sept 1th, 1978 and we will commence the inverted Y radiation at that time.”

However, Patient 13 was next seen on 3rd November 1978, at which time he refused further treatment, indicating that he was pursuing diet therapy instead.

While all this is well documented in the hospital notes, Dr Gonzalez’ account, which was presumably based upon the patient’s impressions, differs markedly.  For example, Gonzalez describes severe reactions to the chemotherapy – which is of course possible, but that having “struggled through [the third cycle of MOPP]…. he felt so debilitated he decided to discontinue chemotherapy.”

According to Dr Gonzalez the oncologist warned the patient that without finishing the suggested therapy, his disease could prove fatal.  “When he refused to give in,” writes Gonzalez, “his doctors then suggested a six-week course of radiation to the chest as an alternative.  Patient 13 agreed to the plan and in late May 1978 began the proposed regimen.  But in mid-July 1978, after receiving a total of 4060 rads to the chest and upper abdomen, Patient 13 reacted so badly to the treatment he refused to continue.  At the time he was not believed to be in remission. ”

There is no documentation of such an opinion, or of any findings that might have contributed to it.  Also, per the hospital notes, everything was proceeding smoothly according to the original plan, and in August 1978 the notes state: “he seems to be doing well; no problems.”  The question of further chemotherapy was intentionally left open to later reassessment: the original treatment plan was to give further MOPP only if “he can tolerate it.”

The patient began the Kelley treatment in July 1978 and followed the full regime for three years.  He is reported to be well 9 years after initial diagnosis.


A weak case.  We have no knowledge of the patient’s disease status when Kelley treatment started, and the favorable outcome can be reasonably explained by the standard treatment he received. Furthermore, Gonzalez himself allows that there are reported cases of patients with advanced Hodgkin lymphoma enjoying prolonged survival after incomplete courses of MOPP and it is feasible that this was responsible for suppression of less prominent disease in this man’s abdominal lymph nodes, despite the omission of the intended inverted Y radiation.

Patient 14:  Hodgkin lymphoma (Hodgkin’s disease)


Gonzalez introduces this patient as “a 36 year-old Canadian, alive 13 years since developing Hodgkin’s disease.”

The patient first noticed a lump on left side of his neck in January 1971, which fluctuated in size.  It enlarged dramatically in June 1972 and at operation (5th June 1972) to remove what was probably thought to be a branchial cyst he was found to have a matted collection of lymph nodes.  Supposedly, 15 lymph nodes were removed – an extremely unlikely number for such an excision biopsy. (It could be possible that a 1.5 cm gland was removed and that somehow this became garbled.)  Gonzalez reports that on examination, the biopsy specimen was found to contain typical nodular sclerosing Hodgkin lymphoma, although unfortunately the pathology report is not provided.

A hospital examination on July 1st 1972 revealed that there were still palpable nodes in the neck, 1-2 cm in size, including “under the scar.” Nodes were palpable in the axillae and groins but were not obviously abnormal.

Other investigations:  “Chest x-ray: no relevant abnormality.  Lymphangiogram showed changes typical of early Hodgkin lymphoma in the left para-aortic nodes.   Liver and spleen scan: suggestive of a space-occupying lesion in the anterior right lobe.  Poor concentration of medium in the left lobe suggesting an extensive infiltrating lesion.  The spleen is moderately enlarged measuring 8 by 13 cm.  Bone scan:  in the left side of the pelvis and the left sacroiliac joint.  “… possibility of an abnormality of this site.”

Patient 14 was commenced on chemotherapy with the intention of a six months course of MOPP.   According to Gonzalez’ account he tolerated the first cycle well, but after the second cycle he developed severe weakness, fatigue and anorexia.  When he fell ill again during a third cycle in late August 1972 he refused to continue.   Gonzalez states that the patient  “was told that he most probably would not live a year without proceeding with treatment,” but notes confirming this impression have not been provided.

Indeed, no further medical notes are provided, but we are told that he began the Kelley regime in September 1972.   While this again is not independently documented, Gonzalez states that after several months on the therapy the nodes in the axilla and groin “suddenly enlarged considerably” only to “resolve over several months.” He was told by Kelley that this “often happens before the disease regresses.”

Fluctuation in the size of lymph nodes is actually a very common patient complaint and as a surgeon I [Dr Moran] have had to biopsy many such only to find (benign) hyperplasia of unknown cause.  It is possible that this was such an event in someone disposed to be closely monitoring his nodes, and sensitive to any change.   If Kelley was truly not worried about this event it is likely that the lymph node enlargement was not striking, as I know of no evidence that such events are common either in Kelley’s experience, or with any kind of standard medical treatment of cancer, even in those treatment methods which are capable of causing very rapid cancer destruction with the possibility of liquefaction or generalized inflammatory response (tumor lysis syndrome).

Despite receiving no further conventional medical treatment the patient was last known well 15 years after his first diagnosis, still following the Kelley program.


 The critical issue here is the effect to be expected from three courses of MOPP.   Gonzalez states: “In a telephone conversation with me, the patient’s Princess Margaret Hospital oncologist confirmed that in his professional opinion, Patient 14 was not in remission when he stopped conventional treatment.”

Yet there is no evidence of any visits at a reasonable interval after the last cycle of chemotherapy at which the oncologist would have been able to determine whether or not the patient was in remission.   In fact Gonzalez describes how, after the completion of chemotherapy in late August 1972, the patient began  “a long automobile trip through the United States ‘to clear his mind’” and it was on that trip that he encountered information about Dr Kelley and transferred himself to his care.   At most, the Princess Margaret Hospital oncologist would have been unable to say that he was definitely in remission.

Furthermore, oncologists are now looking for, and placing considerable weight on, the complete response (CR) rates of patients with Hodgkin lymphoma, using highly sensitive PET scanning after just two cycles of chemotherapy – at least in cases treated with ABVD, which has about the same impact as MOPP on survival but with fewer ill effects.  It is likely that a few of these “CR2” patients, who show a complete response after two cycles of chemotherapy, will have very long remissions or actual cure, especially in younger patients (such as Patient 14), who usually respond better.

CR2 is used as a means to guide further treatment and to determine the dose intensity for subsequent treatment cycles so as to reduce exposure to chemotherapy or radiation in those who can get by with less.

One source (Abeloff’s Clinical Oncology, 5th edition) says:

 “The optimum number of cycles of chemotherapy is not defined for patients receiving chemotherapy alone. In the NCIC HD.6 study, 69/196 (35%) of patients treated with ABVD alone achieved CR by CT criteria after two cycles of ABVD.* Of these 69 CR patients, 57 received a total of four cycles of ABVD (per protocol) and 12 received six cycles (physician decision) with a 5-year freedom from disease progression of 95%, compared with 81% for the 113 patients not in radiographic CR after two cycles. ……Current studies are examining the use of early metabolic CR by PET/CT to determine the number of cycles of chemotherapy, the intensity of the chemotherapy regimen, and which patients should receive RT [radiation treatment].”

* Meyer RM, Gospodarowicz MK, Connors JM,et al: ABVD alone versus radiation-based therapy in limited-stage Hodgkin’s lymphoma. N Engl J Med 2012; 366: 399-408.

Patient 15:  Hodgkin lymphoma (Hodgkin’s disease)


Patient 15 is introduced by Gonzalez as “a 37 year-old woman from Ohio with a history of recurrent Hodgkin’s disease, alive 23 years since her original diagnosis.”

This is one of the older cases in the series, and there is little documentation of the half-century that has passed since her original diagnosis. Unless otherwise stated the following is taken directly from Gonzalez’ narrative.

In December 1963, at age of 14, this patient developed painless swelling in her right wrist that settled spontaneously.  A month later she developed a painful node in the left side of her neck, which settled after antibiotic treatment.  However, the lump recurred and in June 1964 a biopsy indicated Hodgkin’s disease. A chest x-ray revealed enlarged mediastinal nodes.  She was treated with radiation only – 4000 rads to the neck and 4000 to the chest.

She did well until November 1967 when rapidly enlarging masses became evident in the left axilla and right clavicular region.  “After multiple biopsies documented recurrent Hodgkin’s disease” she received a further 4200 rads to “the neck and chest,” with regression of her disease. (As noted above, no biopsy reports or progress notes are presented.)

She was again well until mid-January 1972, when she developed a swollen right arm, shortness of breath and “severe left rib pain.”

She was readmitted to M.D. Anderson hospital, where the hospital notes describe her as being initially diagnosed in 1964 as “Hodgkin’s disease, paragranuloma type involving the left supraclavicular region and mediastinum Stage ll A.” The notes continue:  “A chest x-ray demonstrated what appeared to be a pleural thickening on the left with evidence of involvement of the 7th, 8th and possibly 9th ribs posteriorly by destructive process.”

She was also noted to have a 5 cm node in the left axilla.   Biopsy reports of this and the left pleura both confirm the diagnosis of Hodgkin lymphoma with nodular sclerosis.

She was re-classed as Stage lV disease and commenced MOPP chemotherapy.   She became very ill with the chemotherapy and refused to continue with it after two cycles, the second one being on February 28, 1972.

She was apparently well enough to return to school at this time.  She learnt of the Kelley treatment and began it in “late spring” 1972.   There is no information as to her clinical status at that point.

 She remained well until mid-1986, when a slowly growing thyroid cancer was detected – a probable complication of her earlier mantle field radiotherapy.


There is no certainty as to the status of her cancer at the time when Kelley began treating her, and there is a reasonable likelihood that her response was due to the conventional treatment she had received. Patient 14 was another young patient with an apparently spectacular response to a short course of chemotherapy, and the same comments as for Patient 14 also apply to Patient 15, viz:

Oncologists are now looking for, and placing considerable weight on, the complete response (CR) rates of patients with Hodgkin lymphoma, using highly sensitive PET scanning after just two cycles of chemotherapy – at least in cases treated with ABVD, which has about the same impact as MOPP on survival but with fewer ill effects.  It is likely that a few of these “CR2” patients, who show a complete response after two cycles of chemotherapy, will have very long remissions, or actual cure, especially in younger patients (such as Patient 14), who usually respond better.

CR2 is used as a means to guide further treatment and to determine the dose intensity for subsequent treatment cycles so as to reduce exposure to chemotherapy or radiation in those who can get by with less.

One source (Abeloff’s Clinical Oncology, 5th edition) says:

 “The optimum number of cycles of chemotherapy is not defined for patients receiving chemotherapy alone. In the NCIC HD.6 study, 69/196 (35%) of patients treated with ABVD alone achieved CR by CT criteria after two cycles of ABVD.* Of these 69 CR patients, 57 received a total of four cycles of ABVD (per protocol) and 12 received six cycles (physician decision) with a 5-year freedom from disease progression of 95%, compared with 81% for the 113 patients not in radiographic CR after two cycles. ……Current studies are examining the use of early metabolic CR by PET/CT to determine the number of cycles of chemotherapy, the intensity of the chemotherapy regimen, and which patients should receive RT [radiation treatment].”

Meyer RM, Gospodarowicz MK, Connors JM,et al: ABVD alone versus radiation-based therapy in limited-stage Hodgkin’s lymphoma. N Engl J Med 2012; 366: 399-408.

Patient 16:  Acute lymphocytic leukemia (ALL)

This patient is described by Gonzalez as a “50-year old man from Texas who has survived nearly 13 years since his diagnosis of acute lymphocytic leukemia (ALL).”

Patient 16 presented in September 1974 with pallor, weakness, weight loss, and petechiae (small red spots caused by bleeding into the skin).   The hospital notes record that on examination the patient was pale, with palpable liver and spleen. His haemoglobin was 8.3, WCC (white cell count) 40,100; platelets 137,000, 38 blast forms.

Bone marrow examination was performed on 24th September 1974, and the pathology report describes highly cellular marrow with the predominant cell type an “immature-appearing mononuclear cell which is suggestive of lymphocytes…. Highly cellular marrow with acute lymphatic leukemia.“

Unfortunately no further hospital progress notes are provided, but according to Gonzalez the patient was recommended combination chemotherapy with a COAP regime, and he was told that his chances were “dim.” Chemotherapy was begun “in September 1974” (no precise date given).

A second cycle of COAP was administered in “early November 1974” and a repeat bone marrow was performed on 5th November 1974. On this occasion the marrow was hypocellular and the pathologist’s comment was “though the megakarocytes appear to be adequate and some erythrocytic cells (red blood cell forming) are present, the myleocytic cells appear to be really depleted.   The atypical cells suggest lymphocytic cells.”

Disappointed with the results, the patient investigated unconventional methods and began the Kelley regime in “late November.  ”However,” Gonzalez notes, “He also continued chemotherapy and “with this combined approach” his leukemia went into remission.

No further documentation is provided, but according to Gonzalez he received a total of ten cycles of COAP over a two-year period.   He “remained well” until 1979 when he stopped the Kelley program “primarily because of financial considerations.” He remained in good health for a further 8 years until early 1987 when he experienced a second bout of leukemia.  Gonzalez remarks: “Once again Patient 16 has chosen to combine chemotherapy with the Kelley program and currently appears of be improving.”


This patient’s survival is indeed unusual for those diagnosed with acute lymphatic leukemia in those times.  These days, cases are broken down into precursor B cell, mature B cell and precursor T cell types, and are subtyped by the various cytogenetic changes and surface markers that the abnormal cells express. These different categories carry different prognostic implications, and with modern forms of chemotherapy five-year survival rates of 40 percent are achieved in ALL. Some of these patients go on to long-term survival.

In order to make any sort of prognostic evaluation of the likely outcome in Patient 16’s case we would need to have tissue for cytometric, chromosomal and further histological examination; but even if that were possible we would still have to judge this case according to diagnostic and treatment standards of the times.

What happened?  It comes down to a somewhat subjective opinion on likelihoods. Was this patient’s good fortune due to an unknown major diagnostic or misclassification error, or perhaps a rare and unexpectedly favorable response to conventional treatment – or was Kelley’s treatment the reason for the good outcome? If the latter is to be considered, it remains an unusual case, since cessation of treatment, or even failure to stick to the detail of treatment,  is so commonly blamed for relapse in Kelley’s patients.

Patient 17: Acute myelocytic leukemia (AML)


 Gonzalez introduces Patient 17 as a man who “survived for seven years after his diagnosis of acute myelocytic leukemia (AML) in 1977, before succumbing in September 1984 from causes unrelated to cancer.”

This man has a complicated medical history mostly not of relevance to present interest.   He was first noted to have anemia and leukopenia in January 1977, which was initially blamed upon quinidine medication. (Quinidine is an anti-arrhythmic agent, used to correct disturbances in the contractility of the heart.)

He was admitted to hospital in August 1977, at the age of 61, with a scrotal abscess.  At that time anemia (Hb 7.1) and leukopenia (2000 per ml) were confirmed, with normal platelet count.

A bone marrow examination report dated 1st Sept 1977 includes the following:

“  —- There is a marked shift to the left in the granulocytic series.    Numerous myleocytes and promyelocytes are present.    The number of blasts varies from field to field, but in some areas they are remarkably abundant.  I believe that this represents an acute leukemia.    Since there is partially arrested maturation along the granulocytic line, I would favor this diagnosis.  This could possibly represent an acute myelomonocytic leukemia. …Diagnosis: acute leukemia (please note description above).”

He was discharged on antibiotics on 6th September and instructed to return in one week for chemotherapy  (Cytosar and thioguanine given over five days).

At readmission on 24th October for further chemotherapy he was described as doing well, although requiring blood and platelet transfusions about a week previously.  He was given a further course of Cytosar 400 mg/day as continuous infusion, and thioguanine 200 mg 12 hourly orally for five days.

Unfortunately there are no further medical notes other than the reports of two bone marrow examinations.  The first is dated 1st November 1977, but appears to be a second opinion on slides previously submitted to the Alton Ochsner Medical foundation by the Rapides General Hospital. It was reported as showing “Acute myelogenous leukemia in partial remission.” The second is a further bone marrow examination dated 26th July 1978, which was regarded as normal for the history of the patient, being reported as “Acute myelocytic leukemia in remission”

However, Gonzalez, presumably on the patient’s advice, gives a rather more dramatic account of these times.  Thus, he says, the patient “almost died” from congestive cardiac failure during the first of these admissions.

Also, Gonzalez states: “Patient 17 failed to enter remission even after a third course of treatment administered in late October 1977” – an assessment at odds with the information provided by the hospital records.  At his admission on 24th October for his second round of chemotherapy he is stated to have had a bone marrow examination “five days prior to admission which was interpreted as having increased percentage of blasts again, and it was felt that he is not in remission at this time and admitted for chemotherapy [sic].”

This is presumably the bone marrow examination being reported on by the Ochsner pathologists and thus performed after his first cycle of treatment and before the second.

Gonzalez goes on:  “At that point, the attending oncologist at Ochsner prescribed additional doses of oral thioguanine and cytosine arabinoside, to be taken every day, indefinitely.   But several weeks later, Patient 17 became so ill on the treatment he simply threw the medication away.”

 This is also not in accord with the patient’s records.   He was to have continued with his usual heart medicines (digoxin, Quinidex and Dyazide) but his usual five-day leukemia regime was complete at discharge.  The discharge diagnosis in his records was “Acute myelogenous leukemia, status post chemotherapy (just completed second course)“ and the instructions were that he was to return to his doctor for follow-up of blood results, and to Ochsner for follow-up of his leukemia.

According to Gonzalez “Patient 17 worsened clinically” and after some investigation of  “alternative” methods by his wife he ended up consulting Dr Kelley.  “Despite their misgivings, Patient 17 felt sufficiently encouraged after his consultation to begin the program – and refuse further chemotherapy.”

The patient can be identified as Thomas M. of Alexandria, Louisiana.  He gives a somewhat different account of this period, which suggests that he may have continued on  “maintenance therapy” until midsummer of 1978, when he stopped treatment, perhaps encouraged by the bone marrow examination of 26th July 1978, which stated that he was in remission.

This is what Thomas M. says at :

“ Following three courses of Cytosar and Thiogunine at the Clinic (from October 7, 1977 through about mid-December 1977), I fortunately had a remission. I was to continue with maintenance therapy, which the medics told me would, at best, improve the quality of life. There was slim, if any hope for recovery.

“About midsummer of 1978, it became apparent that to continue the chemotherapy would destroy any hope I had of bodybuilding. These shots would nauseate and disrupt me and would knock my blood count from near normal to complete disarray. My mind indicated that they be discontinued, despite advice to the contrary.”

While the health problems that Gonzalez states were bothering the patient in late 1977 are neither described nor documented, he apparently “experienced a gradual but steady improvement in general health.  In July 1978, he experienced recurrent fevers, but a repeat bone marrow biopsy (the second one described above) showed no evidence of leukemia.” He was also able to stop all his cardiac medications.

 Then, despite his supposed resurgence of health on the Kelley regime, he had a flare-up of osteomyelitis in his leg and died of sepsis in September 1984.   Gonzalez states: “…according to his wife, an autopsy revealed he was free of leukemia at the time of his death.“


Regardless of the conflicting accounts (not unusual when relying upon patients’ memory of their medical history) this is an unusual case and we are presented with choices similar to those posed by Patient 16.    Gonzalez quotes Dr Peter Wiernik, apparently a contemporary (mid-1980s) authority on leukemia:  “I do not know of any five year or longer survivors of acute granulocytic (myelocytic) leukemia treated only with cytosine arabinoside and 6-thioguanine.”  This does not prove it cannot occur, of course.

Patient 18:  Chronic myelogenous leukemia (CML)

This patient is introduced by Gonzalez as “a 55-year-old woman from Illinois, alive more than 12 years since diagnosed with chronic granulocytic leukemia.”  (The term “chronic granulocytic leukemia” has now been superseded by new terminology, under which the disease is known as chronic myeloid or chronic myelogenous leukemia.)

This lady presented with fatigue and depression, and painful fingers in the right hand that were thought to be exhibiting Raynaud’s phenomenon.   She was found to have an elevated WCC (white cell count) and an abnormal bone marrow examination, and was referred to the Mayo Clinic in December 1974.

According to a letter from the Mayo Clinic to her doctor dated 16th December 1974, her WCC was 89,000 with basophils 7%, metamyelocytes 4.5%, and myelocytes 14.5%.   Platelets increased at 686,000.   Bone marrow examination showed markedly hypercellular smears with an erythroid-granulocytic ratio of 1:20.  Leucocyte alkaline phosphatase score 1 (normal range 30-70).   The Mayo Clinic hematologist’s opinion was that “The marrow is quite consistent with chronic granulocytic leukemia.”  Cytogenetic studies on the aspirate also revealed the presence of the Philadelphia chromosome, another pointer to chronic myeloid leukemia (CML).

The advice of the Mayo Clinic was that she was an early case, and that treatment should be deferred while watching her white cell count, with the intention of low doses of Myleran (busulfan) when her leucocyte count doubled to about 160,000.

The only other medical documentation supplied is a bone marrow aspiration report dated 2nd February 1984, ten years later, which gives the diagnosis:  “Chronic granulocytic (chronic myelogenous) leukemia in relapse.”

 According to Gonzales she was treated with busulfan under the supervision of a local oncologist and “within months” the disease went into remission.    She also began the Kelley treatment towards the end of 1975, under the care of a local chiropractor trained by Dr Kelley, ceasing chemotherapy at about the same time.

She is said to have remained well for seven years, but in January 1984, after having “stopped the program only because she felt confident her disease was cured,” she was found to have WCC of 20,000 on a routine test.   This is when the bone marrow aspirate reported 2nd February was performed, confirming a “mild” recurrence.

On this occasion her physicians suggested maintenance with low dose hydroxyurea, to which she agreed. She also resumed the Kelley regime around that time.    “Today, three years after her relapse, and 12 years since her original diagnosis,” Gonzalez says,  “Patient 18 continues on both hydroxyurea and a nutritional regimen. “  Her recent white cell counts are “falling in the normal range.”


A moderately unusual outcome, although Gonzalez himself quotes statistics showing 2 percent survival of patients with this diagnosis beyond ten years.   Also similar considerations apply to this case as apply to cases 16 and 17 – i.e., do you favor an effect from treatments these patients received that are known to produce and maintain remission on their own (and also have anti-cancer effects in vitro and in animal studies), or one which is not known to have such any such effects?

It is also worth noting, too, that in this case, as in the case of Patient 16, chemotherapy continued whilst the patient was concurrently pursuing the Kelley regimen. It would be impossible therefore, to parse out the effect of the Kelley regimen, which is precisely why Dr Good stipulated, in his instructions to his eager student, that patients selected for this study should be those whose outcome could only be attributed to the Kelley regimen – i.e., not those who were simultaneously pursuing both approaches.


Patient 19: Carcinoma of Unknown Primary (CUP)


Gonzalez describes this patient as having “died in September 1980 at age 69 after surviving six years with carcinoma to the liver, metastatic from unknown cause.”

In mid-1973 this lady noticed a painless mass in the right side of her abdomen.  Since she otherwise felt well she did not seek attention until October 1974 when she had lost weight and had begun to feel fatigued.

 On ultrasound she was found to have a 12cm mass in L lobe of liver and some internal echoes in the right lobe. At operation in October 1974 a “liver full of metastatic disease was discovered.”

The biopsy report is succinct: “ Section contains liver with undifferentiated malignant neoplasm.”

According to the hospital discharge summary dated 25th October 1974 she was given a five-day course of 5-fluorouracil injections, 1000mg each.  The summary states: “She will be followed up as an outpatient.  Chemotherapy will be maintained then prednisone and  [space left blank] added if no response to the fluorouracil.”

A primary site was never determined.  The only imaging records provided refer to a preoperative barium enema that showed no evidence of cancer.  Presumably other sources for possible primary were looked for at her operation, but none were found.

We only have Gonzalez’ narrative from that point on.

Sometime after her discharge from the hospital in late October, 1974, Patient 19 decided to pursue “alternative” treatments rather than continue chemotherapy.  Gonzales implies, without supplying details, that the Kelley treatment was begun in November 1974 and that no chemotherapy was given after then.

“Patient 19 responded very quickly to her regimen with improved energy and appetite, and within months her husband reported to me [that] the large abdominal masses [had] regressed completely.  Subsequently, Patient 19 followed the Kelley regimen for five years until 1980, when she discontinued her prescribed diet and supplements because she believed herself cured.  Although she never again became overtly ill, Patient 19 passed away peacefully in her sleep in September 1980, six years after diagnosis of terminal disease.”


An impressive case on the surface, but there are a number of lingering questions.    The hospital discharge notes, dated October 25th 1974, state that Patient 19 had “known of the mass for a long time,” and Gonzalez’ account echoes this, stating that the then-painless mass was first noted by the patient over a year before medical assessment in October 1974. This suggests that the tumor must have been present for a lot longer than that, in turn raising the possibility of a very slowly progressing cancer (for example, perhaps one of the rarer neuroendocrine tumors) which can have little propensity to produce symptoms.  Liver secondaries from such cancers are compatible with quite prolonged survival.  A review of the histology would be thus be desirable – indeed, with any case of CUP it would be of great importance, since it would offer the strongest chance of identifying the possible site of origin. Unfortunately, though, none is provided

It would have been useful to know the effect of the 5-FU chemotherapy that she received before she commenced the Kelley treatment. Could her apparent response to the Kelley treatment in fact have been a response to the chemotherapy she had been receiving? For example, I [Dr Moran] had a patient whose liver secondaries from colon cancer, which is mostly regarded as not a very good candidate for chemotherapy, unexpectedly shrivelled up and even calcified after treatment with 5-FU, a drug that is usually very well tolerated.

 It would also have been useful to have some confirmation of exactly when she stopped chemotherapy. As it is, Gonzalez’ narrative description provides only very general information, telling us, for example, that “she consulted Kelley in November 1974 and began the nutritional program, thereafter declining further conventional treatment.” He does not actually specify the actual date to which the word “thereafter” refers.  There is also no independent documentation at all as to what happened to her large liver mass, or as to the fact that she stayed cancer free until death in 1980.

Most liver metastases have a very poor prognosis, including those with unknown primary source, although the prognosis is a little better when this is the only known source of cancer; and there are exceptions, as described above.

Patient 20: Metastatic lung cancer


Dr Gonzalez tells us that Patient 20 “was 59-years old when in November 1986 she died from complications resulting from bronchoscopy.   At the time she had survived nearly 12 years after being diagnosed with metastatic, recurrent lung carcinoma.”

This lady was a smoker with chronic cough and a previous history of pneumonia in 1955 that was, according to Gonzalez, “so severe her doctors prescribed a course of radiation to clear her lungs.” (*See note below.)

In 1974 she developed bloody sputum, fever and was thought at first to have a possible abscess in the left lower lung, although chest x-ray was more suggestive of a neoplastic process.  Liver and brain scans showed no evidence of cancer.  A bronchoscopy was “inconclusive.”

The patient underwent an exploratory thoracotomy on March 6th 1975 and a left lower lobectomy was performed for a large mass that proved to be a mucinous bronchogenic carcinoma.   The pathology report describes a 9.5 cm tumor extending to, but not through, the pleura, and involving two out of seven broncho-pulmonary lymph nodes, but not the hilar nodes.

No further hospital notes are provided, but Gonzalez states “because of the nodal involvement, her doctors recommended additional surgery, so on March 17, 1975, only 11 days after her first operation, Patient 20 underwent a left pneumonectomy (removal of the entire left lung).”

A course of adjuvant chemotherapy was apparently recommended but the patient declined.  She decided to follow the Kelley treatment as described in the book One Answer to Cancer, giving up cigarettes, alcohol, junk food and tranquilizers.  She found sources of supplements and vitamins, gave herself coffee enemas, and began her own “cancer diet.”   “To her own surprise,” Gonzalez reports, “she noticed an almost daily improvement in health”.

She is stated to have continued the Kelley program for two years before tapering off and reverting to a “junk food” diet, when she became unwell again with depression, fatigue and general ill health.  She became hypothyroid, having stopped her thyroid medication, but remained unwell, with vague aches and pains even after resuming thyroid medication.  In September 1978 she was admitted to hospital for “through re-evaluation” and “after extensive testing she appeared to be cancer free.”

In October 1979, a year later, “she consulted her doctor again” for unstated reasons.  On 15th October 1979, a chest x-ray was performed, revealing “a 1 cm nodule right mid-lung with questionable second nodule overlying the proximal end of the fifth rib.”  Tomography was suggested, and that examination on 10th December 1979 confirmed the presence of two lesions in the right lung “compatible with metastatic disease.”

 No action was taken at that time and a further chest x-ray on 10th March 1980 showed the same lesions, but apparently larger, with the largest now 1.5 cm in diameter.

No further medical records are provided.   “At that point,” reports Gonzalez,  “Patient 20 resumed her nutritional protocol under the guidance of a former Kelley patient whom he had trained as a counsellor to administer his therapy. On the treatment, Patient 20’s multiple health problems improved and the lung masses gradually regressed.  Thereafter, Patient 20 remained in excellent health until November 1986, when, after developing influenza complicated by pneumonia, she was admitted to a local hospital for bronchoscopy.  During the procedure Patient 20 began to hemorrhage profusely after her physicians punctured one of the pulmonary arteries, and within an hour she had bled to death. ”


No proof of cancer is provided in the form of a biopsy of the lung lesions, in a patient with a checkered history of lung problems including pulmonary radiation. Also, four and a half years is quite a long time after surgery for such metastases to first appear.  While cancer cannot be ruled out on the facts given, other lesions such as (benign) granulomata of several kinds are possible.

Also, we are provided with photocopies of several x-ray reports, but, crucially, not the more recent ones purporting to show the resolution of these lesions with the Kelley treatment.   If these lesions were still at all evident in 1986 that would call into question the diagnosis of secondary carcinoma.

Otherwise the case is not extraordinary.

* Historically, chest irradiation was occasionally used to treat pneumonia and tuberculosis.

 Patient 21:   Advanced lung cancer (squamous cell carcinoma)


Patient 21 is “a 52-year old man from Ohio, {who] has survived 13 years since his diagnosis of metastatic squamous cell carcinoma of the lung.”

This man was a heavy smoker who was found to have a 3 cm mass in the upper lobe of the right lung on chest x-ray when he presented with persistent cough.

On April 7th 1974 a thoracotomy was performed at which, according to the operative record,  “tumor approximately 4 cm in greatest diameter was found in the periphery of the posterior segment of the right upper lobe. In the area below the azygos vein were multiple nodes which extend posteriorly up along the vena cava and acquire a maximum diameter of about 3.5 cm. On frozen section the tissue was positive for epidermoid carcinoma… Because of massive involvement of the mediastinum curative resection obviously was not feasible.”

Patient 21 was given a poor prognosis but commenced radiation treatment (“cobalt therapy”) while an in-patient and was to continue this as an outpatient.

No further medical notes are provided.

According to Gonzalez’ account:

 “Patient 21 completed the suggested regimen of 5000 rads to the lungs as an outpatient, but when the tumors continued to grow despite radiation, his doctors proposed a course of intensive chemotherapy.  Since his disease appeared to be incurable, Patient 21 refused all further orthodox treatment, instead choosing to investigate unconventional cancer therapies.   He soon learned of Dr Kelley, consulted with him and began the full program in late spring of 1974.

“Subsequently, over a several month period his persistent respiratory symptoms resolved, and within a year Patient 21 says he felt better than he had for a decade. Today, 13 years after his diagnosis, Patient 21 still follows his nutritional protocol and remains in excellent health with no sign of his once metastatic disease.”


It is a serious omission that no documentation is provided in support of the statement that “the tumors continued to grow despite radiation.” SCC is a radiosensitive type of cancer and disease progression would be unusual after the dosage said to have been applied.  Nor is any evidence provided that the cancer subsequently responded in any way to the Kelley treatment, in a time frame that might suggest a response to that approach.

Squamous cell carcinoma of the lung falls into the category of “non-small cell lung cancer” (NSCLC) and while the prognosis is poor with non-resectable disease, there are cases in the medical literature* of even ten-year survival with NSCLC after lower doses of radiotherapy given as palliation (see here and here).

 *MacManus MP, Matthews JP, Morikatsu W, Wirth W, Worotniuk V, Ball DL. Unexpected long-term survival after low-dose palliative radiotherapy for non-small cell lung cancer. Cancer 2006; 106(5):1110-6

Quddus AM, Kerr GR, Price A, Gregor A. Long-term survival in patients with non-small cell lung cancer treated with palliative radiotherapy Clin Oncol 2001: 13:95-98

Patient 22: Non-Hodgkin lymphoma


Dr Gonzalez states that Patient 22 “died in November 1986 at the age of 63 from renal failure and other complications of cancer, after surviving nearly seven years with a diagnosis of widely metastatic diffuse histiocytic lymphoma.”

In late 1979 this man presented with fatigue and an enlarged abdomen. He was found to have a mass in the upper abdomen. An ultrasound scan report is quoted: “a large bulky mass within the left side of the abdomen, measuring of the order of 13 to 14 cm’s [sic] in diameter …“

 On April 13th, 1980, at an exploratory operation, a large, inoperable retroperitoneal mass was confirmed and biopsied.  No operation notes or other investigations are provided, so there is no documented evidence of disease elsewhere.   Thus, the basis for the use of the term “widely metastatic” in Gonzalez’ description of the case is not apparent.

A very detailed pathology report provides a diagnosis of “malignant lymphoma, histiocytic type, (Rappaport) associated with extensive sclerosis.” This would nowadays be classified as a diffuse large (probably B, but possibly T) cell lymphoma. The pathology report remarks that in many ways this case was more typical of Hodgkin’s disease than NHL, even though there were apparently no identifiable Reed-Sternberg cells present. The case was uncharacteristic, also, in that while there was extensive sclerosis present (more typical of indolent NHL), microscopically the tissue exhibited many of the hallmarks of an aggressive lymphoma.

Gonzalez’ account states that the patient began CHOP chemotherapy on 2nd May 1980. However, the drugs listed included procarbazine, which is not an ingredient of classical CHOP. As in some of the other cases reviewed here, there is no independent confirmation that this is the only chemotherapy received. The first cycle was uneventful but according to Gonzalez the patient, upon returning home, decided against further chemotherapy and instead pursued the Kelley regimen.

By August 1980, apparently, the patient had had an ultrasound indicating that the tumor had “stabilized,” but the report is not provided. However, two further ultrasounds were performed subsequently, one more than a year later, in December 1981, and another in August 1982, more than 2 years after the initial diagnosis.  Reports of these are included, and confirm tumor shrinkage to about 7 X 6 cm in the last examination.

No other independent information is provided as to his medical status until his death in 1986. Death was apparently due to his cancer, but, according to Gonzalez, it was attributed by Dr Kelley to the patient’s switching to a vegetarian diet (Kelley is quoted as saying that lymphoma patients invariably worsen if they do not eat red meat regularly); and also to the somewhat inferior quality of the available supplements during the year 1985.    An alternative explanation might be that the patient deciding to go against Kelley’s previously apparently effective (and likely adamant) advice was more likely to have been due to an awareness of declining health in spite of the treatment.  There is no evidence supplied in support of either one of Kelley’s doubtful propositions.


 The fact that this tumor, despite its impressive size, appears to have been localized is compatible with quite prolonged survival, especially if the chemotherapy received had led to a partial regression.  There are also quite a number of cases in the literature of spontaneous remission in solitary large cell lymphomas. The somewhat erratic behavior of lymphomata in general, and the intricacy and shifting parameters of their classification, perhaps predisposes them to feature as prominently as they do in the testimonials and case reports of the “alternative” cancer scene.

Interestingly, both of the pathologists reviewing the slides of Patient 22’s biopsy mention the possibility of this being a T-cell lymphoma. At that time it was not considered necessary or routine practice to identify lineage or cell surface markers, since diagnostic classification was based primarily on morphology (size, shape and tissue characteristics of a particular sample) rather than on molecular biology, cytogenetics and immunohistochemistry, as is now the fundamental basis of lymphoma diagnosis.  Had Patient 22’s lymphoma been clearly identified as T-cell it would have perhaps had a bearing on the outcome of this case, since large cell lymphomas of the anaplastic type (ALCL) that express the protein ALK have a markedly better prognosis than those that do not. About 60 percent of patients with ALCL are ALK-positive, and up to 80 percent of those with ALK-positive ALCL have very long disease-free survival after standard chemotherapy.

Patient 23: Non-Hodgkin lymphoma


Patient 23 is introduced by Gonzalez as  “a 67-year old woman from Minnesota alive more than ten years since her diagnosis of diffuse mixed histiocytic and lymphocytic lymphoma.”

This lady had a past history of right-sided breast cancer with involved axillary lymph nodes, treated in 1957 with a right radical mastectomy followed by radiotherapy.

 In January 1976 she became unwell with fatigue, frequent colds and shingles.  In the spring of that year she noted several enlarged lymph nodes in her left neck.  She was referred to the Mayo clinic where an excision biopsy of two lymph nodes was performed on 6th October 1976.

The pathology report is not supplied but was summarized in the hospital notes as “Malignant Lymphoma, diffuse (partially nodular) mixed lymphocytic histiocytic type. “

There was no sign of residual disease on physical examination.  Chest x-ray was normal as were bone scan and IVP, but a lymphangiogram revealed “suspicious nodes in the region of the L2 interspace.”  Additionally,  “Bone marrow aspiration revealed several focal aggregates of lymphocytes suggesting bone marrow involvement by lymphoma.  Bone marrow biopsy, however, was interpreted as showing no definite evidence of malignant lymphoma.”

According to the hospital letter dated October 13th 1976:

“On the basis of the lymphangiogram and the histologic pattern of the lymphoma, we felt that [the patient] most likely had disseminated disease.   Because she is asymptomatic and has no sign of impending complications from her lymphoma, we have not advised initiation of specific therapy at this time.

We have arranged for a complete re-evaluation in approximately six weeks.  We do intend to initiate active treatment at the first sign of symptomatic progression of her disease.”

Gonzalez’ account, however, is more dramatic:  “The Mayo physicians painted a grim picture, telling Patient 23 her cancer would most likely ultimately prove terminal. Nonetheless, initially they recommended no therapy, wishing to hold off treatment until her disease worsened, but when her tumors grew more rapidly than expected, in January 1977 she returned to Mayo for palliative radiation.”

And after her radiotherapy:

“…Her doctors then suggested a course of intensive chemotherapy, which Patient 23 refused, instead choosing to investigate unconventional cancer therapies.  Within weeks she learned of Dr Kelley, visited him, and in late January 1977 began the full nutritional program.”

 A letter to her doctor dated January 14, 1977 confirms that there had been local progression of her malignant lymphoma in the left supraclavicular region and that in consequence she had now “completed a course of radiation therapy to the left supraclavicular, left axillary and mediastinal region.  She has developed mild dysphagia and cutaneous inflammation related to the radiation treatments…. Physical examination revealed no evidence of progression of lymphoma in other sites.”

The dose of radiation is not stated but appears not to have been trivial, and there is no hint in the medical notes that the radiotherapy was “palliative,” as suggested by Gonzalez, or intended to be so.  There is also no mention of the chemotherapy that he says was also advised.

 The only remaining documentation is a letter from the Mayo clinic dated 10th May 1979, over two years later, stating that she has been free of disease since that time and was experiencing no relevant symptoms.   Gonzalez states that “today, more than ten years after her diagnosis, Patient 23 is in good health with no sign of her metastatic malignancy.”


The remarks on Patient 2 are relevant here, showing how even quite small doses of radiotherapy can produce complete remission with reasonable relapse-free periods in lymphoma.  There is no further documentation regarding the “suspicious” lymph nodes seen on lymphangiography and on its own that report provides a tenuous basis on which to hang the success of the Kelley program.

Patient 24: Non-Hodgkin lymphoma

Patient 24 is introduced by Gonzalez as a “64-year old man from North Dakota, alive nine years since his diagnosis of diffuse poorly differentiated lymphocytic lymphoma.”

In late 1977 this man developed fatigue, loss of appetite and weight loss and late that year developed enlarged lymph nodes in the left side of his neck.  He was admitted to hospital where he was found to have enlarged lymph nodes in the right side of the neck, both axillae and the groin. The liver and spleen were also slightly enlarged.

Lymph node biopsy was reported thus: “Malignant Lymphoma, diffuse poorly-differentiated lymphocytic type, involving cervical lymph node.”

Bone scan was negative but bone marrow aspirates and biopsies “revealed malignant lymphoma in all bone marrow smears.”

 Lymphangiogram revealed “grossly abnormal external and common iliac nodes bilaterally, involvement of small periaortic and venous nodes.”

This patient was given a diagnosis of diffuse poorly differentiated lymphocytic lymphoma, which under subsequent taxonomic revisions (and currently the WHO 2008 system) would have been classified as a diffuse small cleaved cell lymphoma (DSCL).

The patient entered an Eastern Cooperative Oncology Group clinical trial and was randomized to receive a combination regimen of Cytoxan, bleomycin, vincristine and prednisone.  The clinical notes describe him as having taken the first cycle relatively uneventfully.

There are no further medical notes.   According to Gonzalez he became “extremely ill” after the first treatment in early February 1978 and even more violently ill after a second round of drugs in March 1978, at which point he decided to discontinue therapy,  “although his doctor warned him the disease was not yet in remission.”  He began the Kelley treatment in March 1978 and “within months the many swollen lymph nodes regressed completely.”    Crucially for these claims, no medical notes are provided as to his clinical status following truncated chemotherapy treatment, although such shortened courses are commonly sufficient to produce complete remission (see below*).

 Nine years later he is said to have remained well.


There is no independent documentation of the amount of chemotherapy this man received, however similar considerations apply here as to some of the Kelley cases of Hodgkin lymphoma (reviewed earlier) who also received brief or truncated courses of chemotherapy.  The lymphomas are peculiarly sensitive to both radiotherapy and chemotherapy.

*Foreshortened courses of chemotherapy not uncommonly induce durable remissions in NHL. In the following study, for example, PET scanning was negative in 50 out of 120 patients after “two or three cycles” of chemotherapy for high-grade NHL, and this was very strongly correlated with long term survival.

Mikhaeel NG, Hutchings M, Fields PA, O”Doherty MJ, Timothy AR. FDG PET after two to three cycles of chemotherapy predicts progression-free and overall survival in high-grade Hodgkin lymphoma. Ann Oncol 2005; 16(9):1514-23

Patient 25: Non-Hodgkin lymphoma


This patient is introduced as “a 63-year old woman from Florida who has survived more than 11 years since her diagnosis of diffuse poorly differentiated lymphocytic lymphoma.”

She developed cutaneous nodules on the left upper chest in May 1975, described as follows by an attending surgeon: “a firm nodule 1 cm in diameter was noted in the left subacromial (shoulder) area, and an area of subcutaneous nodularity and thickening radiated from this area towards the breast.”

A punch biopsy was diagnosed as “lymphoma cutis” In May 1975.   Further nodules were excised 24th September 1975, with a total area of skin 6.5 X 2 X 1.5 cm being removed.   A report from Mount Sinai Medical Centre described it as  “Diffuse malignant lymphoma intermediate cell type, left shoulder.”    An apparent review of these slides at Memorial Hospital stated  “Malignant lymphoma, poorly differentiated lymphocytic type, diffuse (lymphoma cutis).  Cannot predict behavior of solitary lesion of this type.”

At oncological review on 21st October 1975 physical examination was unremarkable, there being at this time only some very fine subcutaneous nodularity in the left chest.  Chest x-ray was normal, as was bone marrow aspiration.

The hospital notes state: “We will obtain a lymphangiogram to rule out retroperitoneal disease, but I would not be surprised if this was negative. She may indeed be under control at this point in time, with local radiation to the involved areas and then to observe her for future problems.”

The comment was also made that her VDRL (a screening test for syphilis) was 2 + positive and that she had been treated for syphilis in 1950 and “also relatively recently.”

The planned lymphangiogram was apparently never performed.  A hospital note made as the result of a chance encounter with the patient later in October 1975 records that she was not intending to return for further evaluation but was pursuing a “nutritional” treatment.

Gonzalez presents a somewhat contrasting account, describing her disease as “a very aggressive malignancy” and that she was advised to “proceed with both radiation and aggressive chemotherapy” (this last advice is not mentioned anywhere else).    According to him she sought a further opinion at Memorial Sloan-Kettering Cancer Center where a similar opinion was obtained – lymphangiogram with radiotherapy to the chest wall, if, as expected, there was no other evident area of involvement.

There is no independent documentation of her subsequent progress.  Gonzalez states that there was progression of the disease to involve a large area of her chest wall while on a trial of Laetrile, but that after commencing on Kelley’s “ nutritional protocol” the disease subsided over some months. She was known to be in good health 11 years after diagnosis.


While Gonzalez attempts to portray this condition as liable to “metastasize rapidly” if untreated, in a contemporary study six out of sixteen cases diagnosed as lymphoma cutis on the standards of the times remained confined to the skin for long periods (2-25 years) and in one untreated case “nodules and plaques” resolved spontaneously*.

Also it should be pointed out that lymphoma does not spread or “metastasize” from a central origin in the same fashion as, for example, the “solid” (epithelial) cancers.

The critical factor here is not the prolonged survival, which is not unusual in lymphoma cutis, but the supposed remission of previously progressive disease coinciding  with Kelley’s treatment, after apparent progression of the disease from the  minimal  state  described when last examined by a doctor.

This is case where the taking of simple and obvious steps such as photography might have greatly supported subsequent claims.  The absence of such fundamental record-keeping creates frustration and further doubts in the minds of those being asked to accept therapeutic claims.

This lady also has had syphilis,  “recently treated.” There are cases (see below) in which syphilitic involvement of the skin has been wrongly diagnosed histologically as lymphoma.  If this was the true diagnosis almost any course of antibiotics, for any reason, would have had a dramatic effect.

Bergman R. Pseudolymphoma and cutaneous lymphoma: facts and controversies. Clin Dermatol 2010;28(5):568-74  

Erfurt C, Luefti M, Simon M Jr, Schuler G, Schultz ES. Late syphilis mimicking a pseudolymphoma of the skin. Eur J Dermatol 2006;  16(4):431-4

Moon HS, Park K, Lee JH, Son SJ. A nodular syphilid presenting as a pseudolymphoma: mimicking a cutaneous marginal zone B-cell lymphoma. Am J Dermatopathol 2009;31(8):84608

*Wolk BH. Primary malignant lymphoma cutis. Can Med Assoc J 1977;117(7): 750-753


Patient 26: Non-Hodgkin lymphoma

 Patient 26 is introduced as “a 45 -year old man from Pittsburgh, alive nearly ten years since his diagnosis of nodular poorly differentiated lymphocytic lymphoma. “

He developed a painless lump in the left groin in August 1977, and at lymph node biopsy 11th October 1977 the diagnosis of Non-Hodgkin lymphoma. (The pathology report assigns the Rappaport classification of nodular poorly differentiated lymphocytic lymphoma (NPDL) – a type of Non-Hodgkin lymphoma that would now be viewed as a grade I (or possibly grade 2) follicular lymphoma).

A month later a node in the right side of the neck was excised and on examination this also contained “lymphocytic lymphoma”.   A liver-spleen scan was negative for further disease, as was a bone marrow examination, but a CT scan following a lymphangiogram revealed many abnormal lymph nodes in the retroperitoneal region.    The radiologist comments that the findings observed have been seen in glands displaying “fibrous hyperplasia” but opines that “in this case the changes are related to the patient’s lymphoma.”    Chest x-ray findings are not stated anywhere, which is a little odd.

 A staging laparotomy was considered but not proceeded with as the patient was a Jehovah’s Witness and refused blood transfusion.

It was decided to treat him via radiotherapy, but the planned fields and dosage are not defined in the notes provided.  In any case, after receiving approximately 1500 rads to “both ilioinguinal-femoral regions as well as to the retroperitoneal lymph node chain” the patient decided to seek another opinion at Sloan–Kettering hospital.   The radiotherapist states that “this dosage is not adequate to destroy lymphoma  (NB: contrary data is provided elsewhere in the present report)  but the palpable nodes disappeared very quickly during the short course of treatment.”

A letter from the oncologist at Sloan–Kettering dated 18th November1977 agreed with his classification as “NPDL stage lll with disseminated nodal involvement only” and the plan of management.   On examination at that time there were no obviously pathological nodes to be felt.   The follow-up notes contain the personal, handwritten note addressed to the attending physician: “This looks fairly straightforward.”

There are no further medical notes.   Gonzalez says: “Patient 26 instead opted to investigate unconventional approaches to cancer, learned of Dr Kelley, and in March 1978 began the full regimen.   He reported to me that within months, all his enlarged lymph nodes regressed completely.”

He was known to be still in remission nearly ten years after diagnosis, having pursued the Kelley regime for three years only.


There is no documentation of the state of the disease when the patient began the Kelley treatment, nor any documentation of the remission described by Gonzalez.   The oncologist stated his nodes had already “disappeared very quickly.”

However, the main problem with this case is the good prognosis of NPDL in terms of survival rates, whether treated or not, and Gonzalez does allude to this in his account.     Even with Stage lV disease most patients survive for ten years and many undergo spontaneous remission.  (See, for example, Horning SJ, Rosenberg SA. Natural history of initially untreated low-grade lymphomas. N Engl J Med 1984; 311(23 1471-5)

Patient 27: Non-Hodgkin lymphoma

Gonzalez describes this patient as “a 55-year old man from Washington State alive ten years since his diagnosis of nodular poorly differentiated lymphocytic lymphoma.”

In mid-1976 this man developed enlarged lymph nodes in his left groin and over a period of several months these gradually grew, to be then accompanied by “fatigue, insomnia and occasional flu-like symptoms.”

In March 1977, a lymph node biopsy was reported by Stanford University Medical “Nodular lymphoma, poorly differentiated lymphocytic type – Rappaport (which would now be classified as follicular lymphoma, small lymphoid type.)

 A lymphangiogram in “late March” 1977 revealed changes “consistent with involvement of the peri-aortic, iliac and femoral nodes by lymphoma.”

 The only documentation of this case is the reports on these two examinations.  No medical notes are provided.  Gonzalez states that “both chemotherapy and radiotherapy were then recommended, but Patient 27, who already knew of Dr Kelley …began the full program in the spring of 1977.  Patient 27 reported to me that within months, the enlarged groin nodes regressed, and his persistent symptoms resolved.”

Gonzales goes on to describe how in 1980 the groin nodes swelled again “after discontinuing the prescribed supplements.” The patient was said to have been advised “aggressive” chemotherapy by his oncologist but instead remission was reportedly achieved by resuming the Kelley regimen.

 He is said to have been in good health ten years later and claiming to be able to regulate his disease at will, causing nodes to swell or subside according to his diligence with the treatment.


Again, inadequate documentation of critical claims.  Refer also to comments following the previous case (Patient 26) regarding the generally good prognosis for untreated follicular lymphoma of this type and its propensity to spontaneous remission.

Patient 28: Malignant melanoma


Gonzalez presents Patient 28 as “a 42-year old man from Montana with a five-year history of recurrent malignant melanoma.”

In February 1982 this man had an inflamed, bleeding mole excised from his back.   The histology report is not supplied, but it was classed as a Clark’s level ll melanoma penetrating the skin to a 4 mm depth.

A re-excision of the area was performed.  A liver-spleen scan showed a vague abnormality on the right lobe of the liver such that “the possibility of a space occupying lesion in this area cannot be absolutely excluded.”

Despite this, and the worrying thickness (4 mm) of this lesion, the patient’s doctors were said to have, rather improbably, pronounced him “cured.”.

Within weeks we are told his general health began to deteriorate with fatigue, loss of appetite and rapid weight loss.  In May 1982 he noticed a nodule in his “left axillary region.”  He was referred to the Mayo clinic.  No relevant hospital notes are provided, but Gonzalez reports that the nodule was excised and an axillary lymph node dissection performed.  The superficial nodule (presumably an “in transit” lymphatic deposit) was confirmed to be melanomatous and five of 16 axillary lymph nodes were also infiltrated by melanoma – according to Gonzalez “a very ominous prognostic sign.”   No further treatment was recommended at this time

In September 1982 the patient noticed “a new subcutaneous mass [sic] in the area of his previous surgery” and he returned to the Mayo clinic.  A hospital letter records that he felt well, but had a “small 3-4 mm firm subcutaneous nodule above the lateral end of the left axillary scar”.   A chest x-ray was unremarkable.   The nodule was excised and described in a later letter as 0.9 cm in size and consisting of melanoma.

While the patient was informed of “the possibility or even probability of further recurrence” the opinion of the Mayo clinic was that “With no evidence of other disease, there would appear to be no role for either systemic chemotherapy or for local radiation to the axilla at this time”.   At this stage he would be regarded as having Stage lllC disease, which has a five-year survival rate of about 40 percent and a ten-year survival rate of about 24 percent.  This contrasts with Gonzalez’ later statement that melanoma, when metastatic to regional lymph nodes “usually kills quickly” (which is not always true).

There are no further medical notes. Gonzalez says that after a brief respite the patient developed worsening fatigue and anorexia, although his local doctor could find no evidence of active cancer.  A liver-spleen scan in November 1982 revealed no new lesions (perhaps the liver abnormality was now regarded as most likely a hamartoma — a benign lesion — of some kind).

However in March 1983, the patient is said to have discovered a new nodule on his right forehead. At that point, he decided to investigate unconventional approaches to cancer, and in April 1983 he began Kelley’s nutritional program.

According to Gonzalez, Patient 28 “responded quickly,” with symptoms abating, and “within several months” the nodule on his forehead regressed completely.  In support of this narrative Gonzalez referred to a doctor’s letter written in summary of his case to an insurance group stating that he had been seen “at frequent intervals” with no evidence of disease recurrence and when examined on Monday April 23rd 1984, physical examination was unremarkable.   There is no reference to a forehead recurrence in that letter.   It is a rather unlikely (but not impossible) site for recurrent disease in this man, but it seems a little unlikely that the patient would not have had a worrying lesion excised or biopsied when he was also taking the trouble to attend the Mayo clinic at frequent intervals.

He apparently continued to attend the Mayo clinic until last seen April 1986 when he is described as being in excellent health with no sign of cancer.


Gonzalez makes a number of statements in this case that reveal limited acquaintance with melanoma, its staging, and usual prognosis.

There is nothing unusual about this man’s progress other than the undocumented, unconfirmed, and somewhat unlikely development of a presumed melanomatous deposit on his forehead and the ensuing supposed cure by the Kelley regime.  The most likely site for a recurrence in this man would be in the scar or as further “in transit” deposits in local lymphatics, or in internal organs.   And again, why so little documentation of what could have been a triumphant demonstration of the effectiveness of Kelley’s methods on visible cancer?

Patient 29: Malignant melanoma

This patient is introduced as “a 50-year old woman from New York with a history of metastatic malignant melanoma.”

In July 1979 she had a biopsy of a changing “mole” on her left calf biopsied and diagnosed as malignant melanoma.

In Gonzalez’ words: “Patient 29 was then admitted to NYU Medical Center on November 11 1979 for wide local excision in the area of the original cancer, as well as sampling of the left inguinal lymph nodes.  As it turns out, two of the nodes were found to be infiltrated with melanoma, a very ominous finding that warranted, her doctors insisted aggressive adjuvant treatment.”

According to Gonzalez, but not supported by any medical records, she was to begin chemotherapy as an outpatient.  This was by no means a standard of care, since in those days melanoma was considered by most centers to be resistant to chemotherapy.

His description of the operation as “sampling” of the inguinal nodes is also questionable.   The limited hospital notes provided refer to a left “groin dissection” – a highly skilled, systematic technique that is still the primary treatment modality for metastatic melanoma involving the groin – and a pathology report is provided which describes “secondary malignant melanoma in two inferior nodes out of 19 inguinal lymph nodes.”     The “ominous finding” is also an overstatement.  This is Stage lllA melanoma, which has a five-year survival rate of around 78 percent. The ten-year survival is around 68 percent.*

The patient is said to be cancer-free eight years after her diagnosis.

*American Cancer Society



Not an unusual outcome.

Patient 30: Malignant melanoma


Gonzalez introduces Patient 30 as “a 66-year old man from New York alive 17 years since his diagnosis of recurrent malignant melanoma.”

This man had been aware of a pigmented lesion on his right instep for many years but had it removed as a precaution in March 1970.   It was reported by pathologists at the Wyckoff Heights Hospital in Brooklyn, NY, as a malignant melanoma with involvement to a depth of 2/3rds of the dermis.

Two weeks later he was reoperated upon.  A wide local excision of the original site was performed with an ipsilateral (same-sided) groin dissection.   The pathology report is not provided, but Gonzalez advises that all specimens including lymph nodes were “negative for tumor”.    A chest x-ray and liver scan showed no evidence of metastases.

The patient did well until August 1970, when he noted a new pinkish nodule in the area of the original malignancy on his right foot.  His dermatologist removed the lesion, which was classified as recurrent melanoma.

However, a month later, in mid-September 1970, Gonzalez writes, “after several new nodules appeared along the length of his leg, his dermatologist excised a right groin lesion, identified as metastatic malignant melanoma.“

The original report on only the first of these excisions  is provided, but a later discharge summary from Sloan-Kettering roughly confirms these events, although as we will see later, the diagnosis of “metastatic melanoma” in the usual sense is not established.

He was referred to the Sloan-Kettering Cancer Center and admitted on 18th October 1970.    Chest x-ray was normal, as were liver and brain scans.    It seems to have been accepted that this man was experiencing repeated in-transit metastases in the right leg, and as per rather aggressive policies adopted in those days for what can sometimes be rather indolent variety of melanoma a hemipelvectomy (very aggressive leg amputation) was advised.

 There is no description as to the state of his leg at this time in the hospital notes despite Gonzalez’ statement that “on physical exam multiple suspicious lesions were noted on Patient 30’s right leg.”  Additionally, in a pathology report dated 15th October 1970, there are no lesions displaying the features one would expect from in-transit metastases or “satellite” lesions. Instead, the report, which appears to be a Sloan-Kettering review of slides submitted from Wyckoff Heights Hospital from examination of  the original dermatologist’s excision(s), identifies:

  1. Malignant melanoma with junctional activity and showing extensive invasion into upper one half of dermis.
  2. Sclerosing hemangioma of skin
  3. Senile keratosis with hyperkeratosis

There are three different slide identifying numbers associated with the “A” diagnosis, one of which corresponds to that attached to the original excision.   The other two presumably relate to the two other melanomatous deposits excised, yet all are strongly suggestive of primary melanoma.  The B and C lesions are benign, although sclerosing hemangioma is commonly heavily pigmented and can have an appearance closely resembling an in-transit melanoma deposit.  There are no dates or sites given for these last two excisions, but they could mean that the patient’s dermatologist had removed all suspicious lesions (Gonzalez’  “several new nodules”) by the time he arrived at Sloan Kettering.  There is nothing in the material provided to suggest otherwise.

The first “recurrence” would normally be classed as a local recurrence, which can indicate a poor prognosis but does not of itself necessitate aggressive surgery.   Was the second “recurrence” (in the groin) another primary melanoma (multiple primaries are not uncommon)?   It is certainly not a “satellite” lesion as described in the hospital discharge summary, being too far away from the region of any other known site of melanoma. (Remember, the groin nodes were clear, which itself reduces the likelihood of in-transit disease).

The assumption that this man was doomed to further recurrence of melanoma in this limb is highly questionable. Despite the panicked reaction of the oncologists (as was not uncommon in those days with this much-feared disease) no pathology reports are provided which would suggest definite metastatic disease.

It is obviously fortunate for this man that he refused the advised amputation.  We are told that after a trial of the “alternative” cancer treatment Krebiozen, which caused a serious reaction, he began the Kelley program under the care of a trained counsellor.  “He reported to me that shortly after the beginning the treatment, the remaining lesions on his leg crusted over and fell off”.  This is (again) not supported by any documentation such as photography.


Unclear pathology on the information provided.  No proof of metastatic melanoma or of the state of the disease when treated by Kelley.

Patient 31: Multiple myeloma


Patient 31 is described by Gonzalez as:  “a 74-year old woman form California who has survived 11 years since her original diagnosis of advanced multiple myeloma.”

 This lady was diagnosed with multiple myeloma in “early 1976.” She presented with back pain, and a bone scan revealed erosive lesions in the skull, lumbar spine and right foot.   Serum electrophoretic pattern demonstrated a “gamma spike” characteristic of multiple myeloma.

She was treated with vincristine and prednisone.  According to the history given in the hospital notes of 3rd October 1981, she stopped the prednisone after a several days because of side effects, and the vincristine after eight months, again because of side effects, including nose bleeds.  From the same source, x-rays were said to have at some point showed healing of the back and she was told she was in remission.

Gonzalez’ story, however, has her stopping treatment after eight months because “she still showed signs of active disease,” choosing instead to investigate “nontoxic” approaches to cancer,  and states that she only went into remission with them.  She consulted Dr Kelley in “early spring of 1977” and “Within months, her fatigue, back pain and other symptoms resolved and x-ray studies confirmed that the formerly extensive disease had healed.”

However, she developed increasing back pain from January 1981 after, according to Gonzalez, she “discontinued her nutritional program,” and from May 1981 she experienced increasing fatigue, back pain loss of appetite and weight loss.

A bone marrow at this time showed “approximately 60% replacement of of haematopoietic elements by plasma cells consistent with multiple myeloma” and x-rays revealed multiple lytic lesions in her lumbosacral spine and pelvis, with a number of spinal compression fractures.

She was admitted to Loma Linda University Medical Center on 28th September 1981 and commenced on Alkeran and prednisone again “without side effects.” (per Loma Linda’s discharge summary dated October 3 1981).  There are no other medical records.

Gonzalez states: “When she failed to enter remission after eight months, Patient 31 discontinued the drugs, choosing instead to resume the full Kelley program.“

“As before, her bone pain, fatigue, and other symptoms quickly improved.  Even the multiple compression fractures of her spine, which have never been surgically treated, appeared to heal.” This is an odd statement: when myeloma is effectively controlled, lesions such as those in Patient 31’s spine will heal without surgical intervention.

 “Today,” Gonzalez concludes,  “11 years after her initial diagnosis and six years since her recurrence…she reports excellent health with no clinical sign of cancer.”


 As Gonzalez says, this lady’s “long-term survival is unusual,” but ten-year survival from myeloma was by no means unknown in the 1970s, even with the relatively unsophisticated treatments available at that time. (See tables below, courtesy of Cancer Research UK)

Gonzalez claims that neither of her two episodes of disease responded to the conventional treatment given and “each time her disease regressed only after she began the Kelley regime.”

 Yet there is no documentation supporting this claim, not in any hospital records, nor in any contemporary records that Kelley himself is said to have kept, nor from any other data that Gonzalez might have sought out so as to confirm such a claim from the patient, if that is what this is.  This adds to an expanding series of cases where the events  pertinent to crucial claims are occurring “off stage,” so to speak.  We are being asked to accept critical matters on what amounts to hearsay.

Gonzalez has expressed some frustration, even certain suspicions, concerning the fact that no medical journal would accept this work, into which he has obviously invested a great deal of time and effort.   If he is still thinking along those lines, he might look here for the true reasons why this material does not measure up the standards normally expected of scientific inquiry, especially in relation to such important claims.

Myeloma (C90): 1971-2009  Five-Year Relative Survival, England
Relative Survival (%)
Period of Diagnosis Male Female
1971-1975 11.1 12.1
1976-1980 12.9 14.5
1981-1985 16 18.4
1986-1990 19.2 21.6
1991-1995 19.9 21.8
1996-2000 26 26.7
2001-2005 31.4 32.2
2005-2009 37.1 37.1
Myeloma (C90): 1971-2007
Ten-Year Relative Survival, England
Relative Survival (%)
Period of Diagnosis Male Female
1971-1975 5.3 4.8
1976-1980 5.0 6.1
1981-1985 7.1 7.6
1986-1990 9.2 9.8
1991-1995 8.9 9.8
1996-2000 12.6 12.7
2007* 19.0 14.9
*2007 survival is a predicted survival rate for England and Wales. Data for 1971-2000 is for England only.

Patient 32: Ovarian cancer


Patient 32 is introduced as “a 40-year old woman from Olkahoma alive more than 13 years since diagnosed with ovarian cancer.”

This lady was found at a routine exam found to have painless 6 cm left ovarian mass.  At operation June 18th 1974 she was found to have a “6-8 cm left ovarian mass and a 4 cm right ovarian mass.”   There was free mucin in the abdomen and papillary areas of mucus- secreting tumor on the pelvic peritoneum.  Exploration of the abdomen revealed no other disease.

The pathology report describes the right ovary as measuring  5 X  4 X 4 cm (2 inches) in diameter and containing  several cysts.  The larger cyst proved to be a dermoid but a smaller 1 cm cyst had some papillary “fragments protruding from the wall” and this presumably is the one reported as demonstrating papillary cystadenocarcinoma.

The left ovary was at this time 3 X 2 X 2 cm, having presumably collapsed after being incised to obtain the specimen for frozen section analysis. It was reported as also displaying “papillary cystadenocarcinoma (mucinous)” as a well as a corpus luteum cyst and a follicular cyst.

The final diagnosis was  —

  1. Stage lll papillary mucinous cystadenocarcinoma of the ovary.
  2. Dermoid cyst of the left ovary.

While the medical notes go no further, Gonzales states that Patient 32 received “cobalt treatment to the pelvis, along with a course of the chemotherapeutic drug chlorambucil.”  The latter was continued until “fall” of 1975.  Shortly after discharge she also consulted Dr Kelley, following his protocol for seven and a half years.  13 years since her diagnosis she is described as in excellent health.


Relatively early case of ovarian cancer found at an incidental examination.  A somewhat unusual case without being overly convincing in view of the extensive conventional treatment also received.

Patient 33: Ovarian cancer


 This patient is described as “a 46-year old woman from Minnesota who has now survived 15 years since her diagnosis of metastatic ovarian carcinoma.”

This lady presented with abdominal discomfort and her physician detected a mass in the region of the right ovary.

At operation on 4th April 1972 she was found to have dense pelvic adhesions (presumably from pelvic inflammatory disease) and bilateral ovarian masses.  There was no discernible spread outside the pelvis, nor were the bowel or omentum involved, but there were papillary excrescences on both ovaries and the uterus.  A total abdominal hysterectomy and bilateral salpingo-oophorectomy was performed.

The pathology report states:

  1. Bilateral serous cystadenocarcinoma extending to peritoneal surface with peritoneal seeding and stromal infiltration.
  2. Acute and chronic cervicitis with abscess formation
  3. Intracanalicular tumor metastasis in the right tube.

She was discharged on 15th April 1972 after commencing a course of 4000 rads of radiotherapy to “the abdomen with chimney up the aorta” (to treat aortic lymph nodes).

 According to Gonzalez, Patient 33 was readmitted to hospital on 26 April because of a falling white cell count.   There is no documentation of this admission but Gonzalez states that after several days the patient stabilised to the point where the radiotherapy could be completed on an inpatient basis.   Gonzalez continues: “despite the treatment, doctors detected a rapidly growing pelvic tumor shortly before her discharge from Ramsay Hospital in late May 1972.   However, her physician decided to observe her progress for several weeks, before recommending additional therapy.”

Gonzalez, presumably in his clinical inexperience, assumes this mass to be recurrent cancer, but this would have been impossible within the time frame.  It is far more likely that any pelvic mass developing this quickly after surgery was a postoperative hematoma, or abscess, or matted bowel  after extensive  dissection of adhesions.   Also at an outpatient examination on 15th June, a mere 2-3 weeks after discharge from hospital on May 25th, there was no abdominal mass and only two 1-3cm areas of induration palpable on pelvic examination, consistent with normal post-operative findings post-hysterectomy at this stage, and a further deeper mass about 3cm on the left, possibly the residue of the abdominal mass described above.

So her pelvic masses had all but disappeared before she saw Dr Kelley in “late June 1972” and began “the full nutritional program.”  Nevertheless Gonzalez goes on to say “only months after she began treatment, the large pelvic mass regressed completely.”

 She is said to be well and cancer free 15 years after diagnosis.


It is not clear what the Kelley treatment contributed.   It seems likely that adhesions from pre-existing pelvic inflammatory disease helped confine this lady’s ovarian cancer to the pelvis and that the good outcome is due to the combination of surgery followed by radiotherapy to mop up any residual cancer.

Patient 34: Pancreatic cancer

This patient is introduced as “a 51-year old woman from Wisconsin alive nearly five years since diagnosis of metastatic adenocarcinoma of pancreas.”

In 1980 Patient 34 began having attacks of sharp mid-abdominal pain lasting hours at a time.

On August 18th 1982, while otherwise in perfectly good health, she was awakened by severe abdominal pain, nausea and vomiting.  She was noted to be extremely tender over the pancreas, with a high white cell count and elevated serum amylase.

Ultrasound scan the next day showed gallstones.

On August 26th 1982 underwent exploratory surgery and cholecystectomy.  Her pancreas, which was not biopsied, was found to be enlarged, with induration extending into the small bowel mesentery

During abdominal exploration a single small 1 cm nodule could be felt high up on the dome of the liver.   A frozen section examination reported “adenocarcinoma consistent with pancreatic or biliary origin.”

Post-operatively she did well.  The final pathology report on the liver lesion describes a specimen composed of “tumor which in turn is composed of irregular ductal structures lined by columnar to cuboidal cells.  Biliary tract or pancreas are suggested as possible primary.”

 No treatment was offered.

In September 1982, she was still quite well and seeking another opinion at Mayo Clinic.   CT scan confirmed “an enlarged pancreas but no localised mass lesion” which was considered to be “more suggestive of pancreatitis “ than cancer.

“Since she is feeling well at the present time,” the consulting Mayo oncologist offered no chemotherapy.

Patient 34 began Kelley treatment in December 1982 and “responded very quickly” according to Gonzalez – but he fails to say exactly how she responded, especially since she was reportedly well in September, a mere 3 months earlier.

She remained in excellent health five years later.


This lady’s clinical picture is consistent with severe acute gallstone pancreatitis.

The incidental finding of a small, single nodule in the right lobe of the liver, along with the frozen section report, is the main suggestion of cancer.  There is no mention in the Mayo clinic’s report that the pathology findings at the referral hospital were ever reviewed – and that is a great pity because this is what this case sorely needs.

In a small percentage of cases, in many anatomical sites, the histological diagnosis of cancer will be reversed by later review.  Also the “tumor” described in a rather muted  final pathology report in this case, after more reliable “paraffin section” histological analysis, mentions no cytological features specific for malignancy (such as those described in the quotation below) , heightening  concern that this lady became  labelled in everyone’s mind as incurable cancer of pancreas  at a very early stage, even during the operation,  and the diagnosis was never seriously reconsidered thereafter,.    We cannot, for example, be sure that the lesion biopsied was not a bile duct hamartoma*:

“ Bile duct hamartomas need to be distinguished from malignant neoplasms in the liver such as metastatic adenocarcinoma or cholangiocarcinoma (CC), especially during frozen section consultation. [my emphasis]  They are often multiple and draw the surgeon’s attention during laparotomy that prompts the intraoperative consultation. The typical luminal dilatation with bile is a helpful feature that distinguishes bile duct hamartomas from metastatic adenocarcinoma. In addition, the epithelial cells of bile duct hamartoma are typically bland and lack the malignant features seen in adenocarcinoma, including pleomorphism, hyperchromasia, and mitoses.”

*Practical Hepatic Pathology: A Diagnostic Approach. Romil Saxena. Ist edition. Elsevier. Ch 36: Benign tumors or tumor-like lesions

Patient 35: Pancreatic cancer (islet cell)


 Gonzalez describes this patient as “a 64-year old man from Minnesota with a history of metastatic islet cell carcinoma of pancreas.”

This man became ill “in the summer” of 1980 with abdominal swelling, fatigue and fever. He was found to have a tender mass under the right rib cage.  In “late July” 1980 an empyema (abscess) of the gallbladder was drained.   No operation notes are provided but Gonzalez states that a “small tumor discovered along the liver edge was biopsied and reported as being a benign hamartoma.”   A review of the biopsy slides at the Mayo Clinic agreed that this was a benign condition.

It was decided that the gallbladder should be removed once all the infection had settled but at operation on 19th January 1981 Patient 35 was found to have gross liver pathology with the liver being “virtually studded” with tumors varying from 1-3 cm in size, involving both lobes of liver.  Two lesions were biopsied and the gallbladder removed.

The pathology report is as follows:

“The liver tissue is almost totally replaced by tumor which shows uniform appearing smaller cells showing no prominent nucleoli, slightly eosinophilic cytoplasm with evidence of ribboning in some areas. Some haemorrhage into the tumor is present and slight necrosis is seen. The slides were reviewed again at Mayo Clinic. It is suggested that serum gastrin and insulin studies be performed to ascertain function of the tumor.”

Diagnosis:  Metastatic islet cell carcinoma.”

A CT scan on 27th January 1981 was reported as confirming multiple intrahepatic metastases.  Somewhat oddly, the report does not mention the pancreas, the usual location of islet cell cancers.  It states “etiology [of the metastases] not clear from scan”.

Patient 35 was entered into a clinical trial and randomised to receive streptozotocin and 5-FU, over 5 days out of every 5-6 weeks.   Hospital records show that he had a course in late January, another in late March, presumably continuing until his last recorded chemotherapy administration commencing 28th June 1981.

A CT scan report dated 18th June 1981 is provided and reports that multiple metastases seemed to have increased slightly in number and slightly in size since the examination in January.   On this occasion the pancreas was “well visualised and appears to be normal.”

There is then a gap in his records until 9th April 1982, when a photocopied hospital outpatient sheet indicates that he had had an episode of gastrointestinal bleeding.  In November and December 1983 he attended for a refill of Percodan prescription and finally on 13th January 1984 there is a note saying that he is working on his farm and that “his cancer remains in remission.”

According to Gonzalez there was an argument with his oncologist about his use of “alternative” treatments at his visit in June 1981, and he did not return for further chemotherapy, commencing “the full Kelley program” at this time.

“Subsequently he did well, with apparent regression of his once extensive disease.”      There is no documentation of regression of the liver tumors other than the comment in the 13th January 1984 note   (possibly from hearsay) that  “his cancer remains in remission.”   It is not clear otherwise how the hospital would know this.   Gonzalez apparently had access to this man’s hospital records and these would surely have contained any investigations that demonstrated cancer remission if they existed.

Somewhat unnecessarily, and hinting that he may have been experiencing disease progression by 1987, he is said by Gonzalez to have “… thereafter become careless, gradually dropping off therapy, thinking himself cured. When last contacted in late spring of 1987, six years after his original diagnosis, he intended to resume his nutritional program.”


Islet cell tumors can be asymptomatic, and so slowly progressing and indolent as to not warrant aggressive treatment.  C.G. Moertel, whose results are quoted by Gonzalez , says the following in one of his papers:*

“Advanced carcinoma of the islet cells of the pancreas, although rare, presents a kaleidoscope of clinical challenges. In addition to the usual problems associated with primary and metastatic tumor bulk, patients with islet-cell carcinoma may have evidence of a variety of hormonal excesses – sometimes sub-clinical, sometimes life-threatening. A special feature of islet-cell carcinomas, which should be weighed in any treatment decision, is the frequently indolent progression of disease even after metastasis has occurred. “

The decision to offer this man chemotherapy was said to have been because of “rapid progression of this process.” Yet the patient was described as “feeling well apart from tiredness” when admitted for his cholecystectomy, and physical examination was “unremarkable.” It seems to have been assumed that the extensive liver metastases had developed over the 4-5 months since his previous surgery.  It is equally likely that when confronted by an abscess at that operation the surgeon did not explore too widely at that time for fear of disrupting inflammatory adhesions and spreading infection.   It is thus feasible that this man had a particularly indolent form of hepatic metastases encountered only by chance, because of coincident gall-bladder disease.

This is another case where the subsequent progress of the patient might have been interesting and illuminating.

*Moertel CG, Lefkopoulo M, Lipsitz S, Hahn RG, Klaassen D. Streptozocin-Doxorubicin, Streptozpcin-Fluorouracil, or Chlorozototocin in the treatment of advanced islet-cell carcinoma. New Engl J Med. 1992 ;326(8):519-23

Patient 36:  Pancreatic cancer


Gonzalez introduces this patient as “a 59-year old man from Vermont alive nine years since his diagnosis of metastatic pancreatic carcinoma.”

According to the hospital inpatient summary this man was admitted to hospital for further investigation of a mass in the liver.  Cancer could not be ruled out and a possible partial hepatectomy was planned.  According to Gonzales Patient 36 had a history of chronic abdominal pain, fatigue and diarrhea with the passage of frequent black, watery stools.

At operation on 15thMarch 1978 the liver lesion was found to be a benign haemangioma.  However an incidental finding was an apparently well-localised mass in the tail of the pancreas with associated enlarged lymph nodes.  A portion of pancreas was removed containing these lesions.  Frozen section of the tumor suggested adenocarcinoma.    While Gonzalez states that “the surgeon resected as much of the pancreatic tumor as possible” there is nothing in the operating notes to suggest partial removal; it is even stated that “one surface of the pancreatic tissue was removed with the pancreatic tumor,” which suggests an attempt  to keep clear of cancerous tissue.

The final pathology report was of “islet cell carcinoma with metastasis to peripancreatic lymph nodes.”

There is no further documentation regarding this patient.   It would be interesting to know whether his diarrhea and other symptoms settled after his surgery.  If so, this would strongly suggest the likelihood of a VIPoma , a variant of islet cell tumor in which the secretion of vasoactive intestinal peptide (VIP) causes the kind of symptoms this patient experienced.  These tumors have an excellent prognosis after resection. If Patient 36 did indeed have a VIPoma, there would be nothing unusual about this case.

However, Gonzalez presents a more dismal scene. While not documented anywhere, and  an improbably poor prognosis for the patient to be given on the basis of the pathology encountered, his doctor is said to have suggested “… he might live six months and recommending no further treatment.”  (This last because they thought him likely to be cured?    There is nothing in the material provided to indicate otherwise).

We are also told that Dr Good reviewed this man’s slides and thought they were consistent with a “very primitive, very aggressive adenocarcinoma… though mimicking a variety of cell types including endocrine.”.  This seems an unlikely recollection.    Recognizable endocrine architecture is not a likely feature of a “primitive and aggressive.”  i.e., poorly differentiated, anaplastic cancer.



An completely unconvincing case, very misleadingly described by Gonzalez as “metastatic pancreatic carcinoma.” Islet cell tumors have a far better prognosis than ordinary adenocarcinomata of the pancreas especially if resectable, as in this case.

Patient 37:  Carcinoid


We are told that Patient 37 is “a 62 year old man from Missouri who has survived nearly ten years since his diagnosis of inoperable pancreatic carcinoma and carcinoid.”

This man had adult onset diabetes and developed chronic upper abdominal pain, worse after meals, in early 1977.   An oral cholecystogram was negative at that time.

In “the spring of 1977,” after a period of declining appetite and weight loss, he became jaundiced and he was admitted to hospital on June 22nd 1977 for further investigation, culminating in exploratory surgery on June 30 1977.

At operation the findings were consistent with biliary obstruction.  There was a 5 X 3 cm mass in the head of the pancreas and some lymph nodes observed in the distal portion of the porta hepatis. “ Two areas of metastasis were found on the small bowel mesentery with marked thickening and foreshortening of the mesentery. Frozen section examination of biopsies of these areas was reported as “metastatic adenocarcinoma.”

In view of this finding the lesion in the head of the pancreas was considered inoperable and neither the main mass nor the lymph nodes were biopsied. A cholecysto-jejunostomy was performed to bypass the biliary obstruction.

The final pathology report altered the diagnosis to carcinoid tumor.

We don’t have any further documentation of those times.  Gonzalez says that his doctors thought he might have two distinct cancers.  They gave him a poor prognosis, yet “strongly” advising both radiotherapy and chemotherapy while also informing him that the treatment would offer little benefit (?).

The patient instead sought out “alternative” methods, first laetrile and then consulting Dr Kelley.  We are told that he responded quickly – within a year feeling better than he had ever done in his life.  A follow-up CT scan at some stage “confirmed that the once “large” [actually only 5cm] pancreatic tumor had completely regressed. “

According to Gonzalez Patient 37 remained well until early 1983, i.e., six years later, when he developed cramping abdominal pain, anorexia and weight loss.  He was diagnosed with an incomplete small bowel obstruction and at operation on 10th October 1983, abdominal organs including the pancreas were apparently normal apart from a massive “ball” of small bowel matted together by adhesions.  A “massive adhesiolysis” (division of adhesions) was carried out and eventually a hard mass was encountered at what appeared to be the root of the small bowel mesentery.   A frozen section examination was reported as containing malignant tissue “with some type of endocrine producing tumor present”.     After further dissection it was found that the area of involved mesentery and small intestine could be resected, and this was achieved with re-anastomosis of the small bowel.  The appendix was also removed.

Regrettably, and for unclear reasons, the pathology report on the resected specimen is not provided leaving us wondering whether a primary source of carcinoid was found in either the resected small bowel or appendix, which are quite common sites for this kind of tumor.

While Gonzalez classes this case as unusually prolonged survival from “inoperable metastatic pancreatic cancer” the only proven diagnosis is of carcinoid tumor, which, like other neuroendocrine tumors, can be a remarkably indolent condition.  Localised pancreatitis has fooled many surgeons into thinking they are dealing with pancreatic cancer as a cause of biliary obstruction.

Ten years after original diagnosis he is said to be in good health.


 An unusual case, but an outcome consistent with the behavior of some cases of carcinoid tumor.  The mistaken diagnosis of pancreatic cancer when hard pancreatic masses are not biopsied is a matter of legend among surgeons, although these days a needle or core biopsy can  be employed with less risk of fatal pancreatitis or fistula.  These were once major deterrents to the incision biopsy of pancreatic masses, explaining why two or three of Kelley’s cases, including patient 38, may well be based upon this kind of misdiagnosis.

The above is a far more likely explanation for events than that the Kelley treatment was able to cure this man’s pancreatic cancer, but not his carcinoid, because, we are told, poor circulation in scar tissue “provides protection from circulating enzymes.”    Adhesions do not usually affect the blood supply to the small bowel mesentery.

Patient 38: Pancreatic cancer


Patient 38, says Gonzalez,  “died of Alzheimer’s disease at age 77, 12 years after being diagnosed with unresectable carcinoma of pancreas. “

This man is said to have developed chronic fatigue and depression in mid-1973, and later that year he experienced episodes of nausea, abdominal pain, and anorexia “that persisted during the first half of 1974.” He lost 50 pounds in weight.  He finally became jaundiced in August 1974 and was admitted for evaluation.

An exploratory operation took place on August 20th 1974. While the operation report is somewhat disjointed and contains many curious expressions (for example,  “…mass extending downwards over the posterior mesenteric muscles… “,  “…and below this level also there was mesenteria … [? sic]”) it seems that the entire head, body and tail of the pancreas was involved in a nodular mass with adherence to surrounding tissues.  The findings described are as consistent with a resolving or subacute pancreatitis as with pancreatic cancer, and this would fit the clinical history.  Pancreatic cancer usually presents as painless jaundice and as a more localised mass.

The reference to liver metastases is an off-hand portion of a single sentence:  “The liver was smooth, there was evident metastatic spread and no gross lesions of the hepato-duodenal ligament was [sic] noted except for slight enlargement of the common bile duct.”   One wonders whether assumptions as to the nature of the pancreatic lesion led to a rather perfunctory consideration of the nature of any abnormality in the liver.  No biopsies were taken, perhaps because of the same assumptions.   It was common practice not to biopsy the pancreas, because of the risks of pancreatitis or fistula, but there was no reason not to biopsy any obvious liver metastases.

The patient was nevertheless informed that he most likely would not live beyond several months.

However, his symptoms resolved on the Kelley regime (reduced alcohol intake would be helpful if that was a factor in the pancreatitis) and he died in April 1986 after developing Alzheimer’s disease.


While Gonzalez says “by any standards of medical science this man’s progress and long-term survival are unusual,” the absence of biopsy proof of pancreatic cancer is a serious problem because of the frequency with which mistakes are known to be made both in the diagnosis of pancreatic cancer by palpation alone, and also, scarcely less frequently, in the diagnosis of hepatic secondaries from appearance alone.   That there have also been no comparable results in cases of biopsy-proven pancreatic cancer treated by Gonzalez after the fashion of Kelley and published in recent studies seriously challenges any other interpretation of this case (see introduction).

Patient 39: Prostate cancer


Patient 39 is described as “a 67-year old man from California alive eight years since first diagnosed with metastatic prostate cancer.”

This man presented in January 1979 with urinary symptoms initially attributed to prostatitis but with only temporary relief by antibiotics.  Because of relapsing symptoms a needle biopsy was performed in May 1979, and this contained moderately differentiated (Grade ll of lll) adenocarcinoma.  A bone scan and chest x-ray showed no evidence of metastases.

While operation notes are not provided, he apparently came to surgery on 7th June 1979 after considerable discussion as to the various possible approaches, including radiotherapy.

It was apparently intended to perform a radical prostatectomy with lymph node dissections, and the latter were performed first.   It appears that once heavy nodal involvement was demonstrated by frozen section examination of some nodes, it was decided not to go ahead with radical prostatectomy but to treat the prostate by other means (which would have fewer potential complications and side effects).

While Gonzalez describes the surgeons as having only excised “several cancerous nodes” it is clear from the pathology report provided that full lymph node dissections were performed with well-differentiated micrometastases being found in only 1 of 16 right pelvic nodes, and well-differentiated adenocarcinoma in 4 of 24 left pelvic nodes.

There is no documentation thereafter.  According to Gonzalez the Scripps Clinic doctors proposed an “intensive program consisting of radiation, chemotherapy and estrogen but Patient 39 decided to refuse all further conventional treatment, and in late June 1979 began the full nutritional program.  Within months all his symptoms resolved.”

He is reported as having remained in good health until 1984 when he again developed “urinary tract obstruction” requiring surgery for correction of what proved to be a ureter blocked by scar tissue.  “During the procedure, no evidence of the previously noted metastatic cancer could be found”  (not surprisingly in view of the thoroughness of the previous procedure).

“Today, eight years after his diagnosis, he is in excellent health and cancer-free.”


This case is desperately in need of further information about the 1984 episode.   It is baffling that Gonzalez should provide such skimpy details when the examinations and investigations performed at this time should have shed light upon the current state of a prostate gland known to contain cancer and purportedly only treated via the Kelley program for the last five years.   The ureteric obstruction described could well have been silent and only found on an intravenous pyelogram performed for other reasons (such as prostatic “obstruction”?).  It is hard to avoid the conclusion that we are not being told the whole story here.

Gonzalez states: “Untreated prostate cancer is usually rapidly fatal…despite aggressive treatment with surgery, radiation and/or hormones… ” and he presents some studies in support of that contention. However, the studies he cites concern aggressive variants of prostate cancer, and while aggressive prostate cancers certainly, do occur, they are represent a minority of the overall number of new cases diagnosed each year. This cancer is in fact renowned for being often so slowly progressive that many patients, even with advanced disease, live on to die of other causes. From 2001 to 2007, the five-year survival rate for men diagnosed with local or regional prostate cancer in the US was 100 percent. For patients with metastatic disease, the five-year survival rate over the same period was 28.7 percent. For all stages combined, the five-year survival rate is 99 percent*

We know that this man’s prostate cancer was at an early stage (localized) since there was some delay before prostate cancer was diagnosed, and also because he was being considered for radical prostatectomy.  We also know that it was well differentiated, which suggests a slowly progressing type of cancer.  So it is just conceivable, in the absence of any evidence supplied to the contrary, that his prostate cancer might have been still grumbling away even eight years later, and that his earlier prostatic symptoms were partly due to prostatitis, as his doctors suspected.

There is a disturbing lack of detail regarding the 1984 episode. There needs to be absolute clarity that there was not a transurethral resection of the prostate in there somewhere.

I [Dr Moran] have also encountered patients who claimed to have produced remission in their prostate cancer “without any conventional methods,” but who were in fact taking hormonal agents, either as prescribed pharmaceuticals or as dietary supplements (sometimes adulterated), that are very capable of producing prolonged remission.  Patients seem not to regard hormonal pills – especially those purchased over-the-counter, claiming to be “natural” – as a “serious” treatment, on a par with methods like chemotherapy and radiotherapy. Yet such products are not without significant risk, as exemplified by the now-withdrawn “supplement” PCSpes, which was found to contain dangerous levels of undeclared drugs including the estrogenic drug diethylstilbestrol (DES), the anticoagulant warfarin, and the non-steroidal anti-inflammatory drug indomethacin. Even some of the naturally occurring plant flavonoids such as genistein may have sufficient estrogenic activity to exert a significant therapeutic effect.  (See citations below)

So we need reassurance that this patient (and any other for whom prolongation of survival is claimed for prostate cancer) was not self-medicating with any estrogenic supplements during that time.  Information as to his subsequent progress beyond 1986-7 would also be helpful.

*Data provided by SEER (Surveillance, Epidemiology and End Results program of the National Cancer Institute).      


Sovak M, Seligson AL, Konas M, Hajduch M, et al. J Natl Cancer Inst 2002; 94(17):1275-80Herbal Composition PCSpes for Management of Prostate Cancer: Identification of Active Principles.and

PCSpes: A Lesson for Future Dietary Supplement Research. J Natl Cancer Inst 2002; 94(17):1261-2

Patient 40: Prostate cancer


Patient 40 is “a 65-year-old man from Colorado alive nearly nine years since diagnosis of metastatic prostate carcinoma.”

This man developed urinary difficulties in early 1978. He was found at that time to have an enlarged prostate and elevated serum acid phosphatase.   A transurethral resection of the prostate was performed 18th September 1978.

Histological examination of the tissue revealed moderately differentiated carcinoma of prostate.

Bone scan showed multiple abnormal areas of uptake – highly suggestive of bony metastases – in sternum, ribs, lumbar spine, pelvis and cervical spine.

According to Gonzalez, “The patient’s physicians then recommended orchidectomy as well as aggressive radiation therapy, though they informed him that even with such treatment he would probably live only a year.”

This does not ring true.  Even without treatment metastatic prostate cancer is often very slowly progressing with many patients surviving for ten years or more*. It is also not clear why “aggressive” radiation therapy  (as opposed to palliative radiotherapy for localized symptomatic secondaries) would have been recommended for someone who already has metastatic disease.  There must  be some misunderstanding somewhere.

The patient rejected orchidectomy but did agree to oral stilbestrol with radiation to the breasts to avoid the gynecomastia (enlargement of the breasts) that is common in males when taking estrogens.

According to Gonzalez, the patient began Kelley treatment in early 1979, “ after which he pursued hormonal therapy only intermittently before discontinuing the medication for good.” It is not stated when he discontinued hormonal therapy. Moreover, even intermittent estrogen therapy would have lingering effects through testicular atrophy and pituitary suppression.  Some studies are offered below suggesting that intermittent hormonal therapy works as well as continuous treatment.

The patient’s urinary symptoms settled and “bone scans over a two year period” showed some healing of the multiple lesions.   This would be expected from the stilbestrol alone.

“Today, nearly nine years after his diagnosis he is in good health and appears cancer-free.”

*Tangen CM, Faulkner JR, Crawford Ed, Thompson IM, et al. Ten-year survival in patients with metastatic prostate cancer. Clin Prostate Cancer 2003; 2(1):41-5.


Survival such as this is not surprising in prostate cancer. Furthermore there is no documentation as to his status when last reviewed.

Gonzalez cites two references, Kane and DeVita.  “Kane describes a median survival of only 4.5 weeks in patients with skeletal involvement even when aggressively treated.” However, this study refers to hormonally unresponsive forms of prostate cancer, This is not relevant to this case. Patients in this study, unlike Patient 40, had failed to respond to hormonal therapy.

(Kane RD, Stocks LH, Paulson DF, Multiple drug chemotherapy regimen for patients with hormonally unresponsive carcinoma of the prostate: a preliminary report. J Urol 1977;117(4):467-71)

The second reference is to DeVita’s textbook where he states that estrogen therapy has not been shown to prolong life once the disease invades bone. This is in accord with some studies, but it is attributable to an excess of deaths from cardiac disease from this now out-dated treatment method.

References on intermittent vs continuous hormonal treatment:

Crook JM, O’Callaghan CJ, Duncan G, et al. Intermittent Androgen Suppression for Rising PSA Level After Radiotherapy. New England Journal of Medicine 2012;367(10):895–903. PMID: 22931259.

Salonen AJ, Taari K, Ala-Opas M, et al. The FinnProstate Study VII: Intermittent Versus Continuous Androgen Deprivation in Patients with Advanced Prostate Cancer. Journal of Urology 2012;187(6):2074–781. PMID: 22498230.Sartor O.

Patient 41: Prostate cancer


This patient, Gonzalez tells us, “died at age 83 after surviving nearly nine years with widely metastatic prostate cancer.”

 In early 1978 he experienced symptoms of urinary tract obstruction and was found to have an enlarged prostate gland.

In May 1978 a bone scan and x-rays showed “abnormalities in eighth vertebral body consistent with metastatic disease.” (Unfortunately no report is provided.)   A trans-urethral resection (TUR) of the prostate was performed on 18th May 1978, and according to the urologist’s letter he was diagnosed as stage D, Grade ll adenocarcinoma of the prostate

He was treated with stilboestrol 3 mg daily and a repeat bone scan was planned in about three months with the intention of considering orchidectomy “if there is more neoplastic involvement” (i.e., if the metastatic cancer had progressed).

Again the report is not provided but Gonzalez states that a follow-up scan in August 1978 showed that the metastatic lesions “had not improved” and in “early fall of 1978” his urinary symptoms returned.

According to Gonzalez’ narrative, his physicians now recommended orchidectomy “followed by radiation and chemotherapy.” (improbably aggressive treatment recommendations and not documented.)  However, the patient refused all further conventional treatment.  Instead, in early November 1978 he consulted Dr Kelley and “at the same time” stopped taking stilbestrol.

“Within months on his unconventional treatment and off hormones, all his symptoms resolved,” we are told,  “but after a year on the program – against Dr Kelley’s advice  – Patient 41 strayed from the prescribed diet and supplements. “   He did well for a while, Gonzalez states, but in early 1980 he once again developed chronic abdominal pain and urinary obstruction.

He was admitted for re-evaluation, and a bone scan on 18th February 1980 again showed uptake only in the thoracic spine at about the level of the ninth vertebra which the radiologist reported as representing “either trauma or metastasis,” although x-rays of dorsal spine revealed only “spondylotic lipping anteriorly of many of the vertebral bodies.” A second TUR was performed.  At this examination the cancer was found to extend beyond the prostatic capsule.  Histology again showed grade ll adenocarcinoma of prostate.

According to the hospital notes “the patient was advised that his best chances for survival would be to undergo treatment with estrogens and to undergo orchidectomy.” Gonzalez differs, saying that the patient “refused orchidectomy, radiation and chemotherapy, although he did agree to restart stilbestrol.  Six months later, he [once again] discontinued the hormonal therapy, thereafter pursuing only the Kelley regimen for treatment.”

No further medical records are provided.  We are told that he remained in good health for six years and that “a series of x-rays and bone scans [which are not provided] confirmed gradual healing of the previously noted metastatic lesions.  After stopping the Kelley program in mid 1986 [why?], his disease recurred within several months and he eventually died in February 1987 – at a time when Dr Kelley was no longer seeing patients – nearly nine years after his original diagnosis.”


Survival for nine years is by no means exceptional with prostate cancer. (Please refer to the previous cases of prostate cancer for further notes and citations on prostate cancer survival.)

 Although Gonzalez again states that prostate cancer metastatic to bone “usually kills quickly” this man’s progress is not exceptional for more indolent varieties of the disease – partially treated hormonally.

This man only ever had one area of abnormal uptake in his spine and the radiologists were unsure of its nature.   It is a little unusual for prostate cancer to produce a single metastasis to bone while progressing in other respects. It is also unusual for metastatic disease to be not seen on plain x-rays for so long  (x-ray of the dorsal spine at last admission in 1980 showed only spondylotic lipping of many of the vertebral bodies), nor to have resulted in some significant elevation of acid phosphatase at the time of his admission in 1980.  So there is also a little doubt as to the nature of the skeletal lesion.

Patient 42: Prostate cancer


This patient is described by Gonzalez as a “74 year old man from California who has now survived nine years since his diagnosis of prostate cancer.”

At a routine exam at age 65, Patient 42 was found to have an enlarged, tender prostate.  On May 24 1978, a prostatic biopsy revealed “very well-differentiated adenocarcinoma”  in the left lobe, with only benign prostatic hyperplasia on biopsies of the right lobe.   A bone scan was suggestive of an osteoblastic lesion in the right 6th rib, but this was not confirmed by x-ray.  Chest x-rays showed evidence of pneumonitis and this was also thought to be suspicious enough to need following up.

According to the hospital notes he was advised to consider radiation or surgery, perhaps preceded by staging laparotomy.  This suggests that there was no certainty regarding the presence of metastatic disease in either the bone or lung.

 However, the patient refused all treatment and began the Kelley regime shortly after June 19th 1978.

Gonzalez sums up Patient 41’s history thus: “Within weeks he noticed an improvement in his general health” and when last contacted nearly nine years after his diagnosis he was still following his nutritional regime and showing no signs of cancer.”


Even if this patient had early metastatic disease, living for nine years without major problems is not unusual.   If he did not have metastases, the following figures from one study * give an idea of the excellent prognosis from simply leaving localised prostate cancer alone:

“Median survival 12.4 years, at 12 years, only 43.9% of patients will have died, at 12 years only 10% of patients will have developed bony metastases” (the usual distant spread)*.

*Wilt TJ, Brawer MK, Jones KM, Barry MJ, Aronson WJ, et al. Radical Prostatectomy versus Observation for Localized Prostate Cancer. N Engl J Med 2012;367(3):203-13

Patient 43: Prostate cancer

 Patient 43 is introduced as “an 81 year old chiropractor from Arizona, alive 11 years since his diagnosis of metastatic prostate cancer. “

In November 1975, Patient 43 experienced pain in the right shoulder blade region.  X-rays revealed compression fractures of T7 and T8 vertebrae, believed to be a result of osteoporosis.

His condition worsened, and at hospital admission in June 1976, at age 70, he was found to have raised alkaline phosphatase and very high acid phosphatase of 302 units (normal 0-10), strongly suggesting metastatic prostate cancer.  Bone scan and x-rays of chest and spine confirmed multiple skeletal metastases.

 Needle biopsy of prostate confirmed adenocarcinoma.

Patient 43 underwent bilateral orchidectomy 8th June 1976, and soon afterward began stilbestrol therapy, as well as radiotherapy to the painful area of the spine.

He was discharged June 26, continuing radiotherapy as an outpatient, but according to Gonzalez,  “he failed to improve.”  On 12th July 1976 he was readmitted, and at that time  his hospital notes stated that he had been doing well until the last few days when he developed photophobia and dizziness, had trouble with speaking and was noted to be somewhat depressed, lethargic and drowsy.  By this time his acid phosphatase was already  “within normal limits,” indicating a dramatic response to the hormonal interventions.

The actual reports are not supplied, but according to the discharge summary x-rays still showed widespread lytic and blastic lesions suggestive of prostate cancer.    We would not expect much change in radiological appearances of those within this time frame, even with remission.   There was concern about the development of bilateral pleural effusions on chest x-ray and “increased marking suggestive of lymphatic metastases “ since previous x-rays.    Such metastases would be rare with prostate cancer and unlikely within this time frame, if not also made exceptionally unlikely by the dramatic change in acid phosphatase levels.  The presence of pitting edema in the legs was almost certainly due to fluid retention from the stilbestrol and perhaps from associated cardiac failure, which would also explain the pleural effusions and some of his other symptoms.  A brain scan was normal.

He was given more radiation to the spine during this admission, and after five weeks in hospital he had improved enough to go home on August 26 1976.

“In desperation” Gonzalez tells us, but without explaining why – was it perhaps from a mistaken perception that treatment had failed? –  he decided to investigate unconventional approaches to cancer and he began Dr Kelley’s regime in September 1976, “at the same time discontinuing hormone medication” (stilbestrol may contribute little after orchidectomy anyway).

Within several months all of his symptoms “bone pain, fatigue, lethargy and malaise” resolved (as might be expected from normal convalescence after such an illness, radiotherapy and with cancer remission already in progress from his orchidectomy) and “he says within two years he felt better than at any time in his life.”   He was said to have remained well 11 years after diagnosis.


Gonzalez’ assertion that this is an unusual patient, that his cancer “failed to respond” to the conventional treatments given, and that it responded only to the Kelley regime does not stand up to scrutiny.  The changes in acid phosphatase are completely inconsistent with that assertion, and the clinical and radiological features have other explanations.

As discussed in relation to previous prostate cancer cases, 11-year survival with metastatic cancer of the prostate is not exceptional.

Patient 44: Rectal cancer

Patient 44 is introduced as a “62 year old woman who has survived more than five years since diagnosed with metastatic rectal cancer.”

After a typical presentation (change in bowel habits) this lady was found to have a rectal carcinoma In January 1982.

On February 10 1982 an anterior resection of the rectum with primary anastomosis was performed.  Pathological examination revealed moderately differentiated adenocarcinoma invading through the muscle to the serosa.   Margins of resection clear but 18 of 32 lymph nodes resected with the colon were involved with cancer.

The operation notes are not provided, but presumably there was no evidence of distant spread at operation, and we don’t know whether the highest nodes along the resected inferior mesenteric artery were involved, which carries the worst  (but still survivable) prognosis with nodal spread.  That four nodes (described, curiously, as “distal far”) contained no evidence of cancer may suggest that they were not involved, but the terminology is unusual and open to interpretation.

She was apparently given a guarded prognosis and advised adjuvant chemotherapy, some forms of which have been shown to improve survival rates in patients with more advanced colorectal cancers.

She rejected this in favor of the Kelley treatment.

Remained well until an operation for adhesive obstruction in April 1987 at which time there was no evidence of cancer.


While Gonzalez says that the prognosis for rectal cancer involving multiple nodes is “dismal,” this is an exaggeration.   This patient was at worst a Stage lllC cancer, which has a 28 percent five-year survival rate and those surviving that long are very likely to be permanently cured*.

*American Cancer Society

Patient 45: Colorectal cancer


Patient 45 is described as a “47 year old man from Pennsylvania alive nearly ten years since his diagnosis of locally metastatic rectosigmoid cancer.”

Diagnosed with a large rectal tumor in September 1977.  On 29th September 1977 he underwent anterior resection of the rectum.

The pathology report describes a 5cm diameter encircling mass consisting of poorly differentiated adenocarcinoma.  Seven lymph nodes were described as “isolated,”  and these contained metastatic carcinoma.   The report is very skimpy, and there is no indication as to whether this means that the highest possible lymph nodes were involved or that all the nodes removed were examined.

As his prognosis would be somewhat guarded, he was given a course of chemotherapy with 5-FU post-operatively, but he chose to cease this in late December 1977 in favor of Dr Kelley’s nutritional regime.

Ten years later he was said to have remained well.


While there are some factors pointing to an unfavorable prognosis here this is another Stage lll case where cure rates are significant with surgery alone.  Adjuvant 5-FU does improve survival rates and ultimate cure rates a little*.

* Sargent D, Sobrero A, O’Connell MJ, Buyse M, Antre T, et al. Evidence for cure by adjuvant therapy in colon cancer: observations based on individual patient data from 20,898 patients on 18 randomized trials. J Clin Oncol 2009;27(6):872-7.

Patient 46: Renal cell carcinoma (kidney cancer)

Patient 46, Gonzalez tells us, “died at age 64 from lung cancer nearly eight years after being diagnosed with metastatic renal cell carcinoma.”

This is a complex case and difficult to reconstruct from the data provided.  The patient presented with fever and right sided back pain.  He was thought to have kidney infection but did not settle with antibiotics.  Investigations then revealed right upper ureteric obstruction.

On 15th May 1978 he underwent exploratory surgery.  The entire right kidney, renal pelvis and upper third of the right ureter were found to be encased in dense fibrosis and multiple blood vessels.    The findings were considered consistent with retroperitoneal fibrosis.   A ureterolysis was performed but the patient did not improve, remaining in pain and febrile.

On 27 June 1978 because of continued symptoms, poor renal function, and evidence of urinary extravasation from a “repaired ureter,” a right nephrectomy was performed with great difficulty.   There was a previously unsuspected 4.5cm tumor in the lower pole of the kidney.  The widespread intense fibrosis made the operation difficult.

The pathology report states that histologically, this was a clear cell carcinoma of the right kidney. The right renal vein was occluded by thrombus and there was evidence of acute and chronic pyelonephritis.  The perinephric fat showed some necrosis.

Post-operatively, the patient developed edema of both legs, mainly the right, and venograms revealed inferior vena caval obstruction.

While there was no evidence of distant metastasis, this was considered to be Stage III because of the renal vein involvement, and the consulting physician recommended adjuvant chemotherapy “because of the patient’s 25% likelihood of five year survival.”

He was discharged form hospital on July 21 1978 and began treatment with vinblastine and CCNU, along with Depo-Provera.

Despite the therapy, in late 1978 he developed severe low back pain.  A CT scan in November 1978   (report not supplied) was said to show a “new large tumor in the right side of the abdomen beneath the liver, with evidence of malignant disease in multiple abdominal lymph nodes and in multiple vertebral bodies. The records summarize these findings:  retroperitoneal adenopathy with infrahepatic mass with destruction of L-2 (one of the lumbar vertebrae} on the right side.”

The patient then had radiotherapy in the form of 3000 rads “to his spine for pain control.”  He also began Kelley treatment January 1979 along with his continued chemotherapy.   He was said by Gonzalez to have been very ill at this time, but there is no independent documentation of his status.  Gonzalez reports that “…with this combined approach gradually regained his strength, appetite and weight.”

The only remaining documentation of this period is a further CT scan of 24th May 1979 which seems to suggest that the mass noted on previous scans was a grossly dilated inferior vena cava, perhaps caused by tumor, and also that what were previously thought to be enlarged lymph nodes were in fact dilated azygos veins (collateral circulation following venous obstruction).  The patient was refusing intravenous contrast, which would have enabled clarification of the nature of these abnormalities.   “In any case, “ the reviewing radiologist wrote, “these densities are no longer present. “   This report mentions two previous scans in November and December of 1978, the reports of which are not provided.  There is no direct documentation of bone metastases, as per Gonzalez’ reference to malignant disease “in multiple vertebral bodies.”

The patient recovered from all this and at an operation for a ruptured gallbladder in October 1982 no cancer was found.

He lived on until he was diagnosed with a squamous cell carcinoma of the lung (attributed to becoming careless with his prescribed diet).  Despite radiotherapy and the continuation of a  “nutritional program in Dallas promoted as the “Kelley Program” though not authorised by Dr Kelley, he died January 1986.”

 Gonzalez says:  “When discussed with Dr Kelley, he repeated what he has said many times before: the many imitation “Kelley Programs” currently available are ineffective at best and often dangerous.”


There is no certainty that this patient had metastatic, as opposed to locally advanced, but potentially curable, renal cancer, which was also heavily treated by surgery, radiotherapy, chemotherapy and hormonal interventions.

Patient 47: Gastric cancer

Patient 47 is described as “a 47-year old woman from New Jersey alive ten years since her diagnosis of metastatic stomach cancer.”

This lady had a long history of dyspeptic symptoms and three years history of severe pain between meals, relieved by eating.   Barium meal 1977 revealed “suspicious lesion in the fundus and cardia of stomach.” A repeat x-ray was more suggestive of a benign myoma.

An endoscopy was performed on 10th March 1977.  The macroscopic appearances are not described, but a biopsy is reported as showing “tissue consistent with gastric polypoid tissue containing foci suspicious for malignancy.”

Surgery (radical subtotal gastrectomy) was carried out on April 17 1977.   Operation findings not described, and no pathology report is presented.  However the discharge summary described “adenocarcinoma of the stomach with metastases to gastrocolic nodes and omentum.”

There are indications that this could have been a more slowly growing well-differentiated type of cancer. The unusually long history of symptoms before diagnosis; the initial biopsies describing “gastric polypoidal tissue,” and the x-ray findings mentioning myoma raise the possibility of cancer arising within a benign gastric polyp, or a polypoidal cancer.   These are normally well-differentiated and associated with a better prognosis than the more common ulcerating or infiltrating types of cancer.   This might explain why a subtotal gastrectomy was performed for a proximal gastric cancer rather than total gastrectomy, although there were probably geographical differences in usual practice in this regard.

The “gastrocolic nodes” are actually within the attachment of the greater omentum to the stomach and the omentum is normally completely removed during such an operation.  If there were separate omental metastases, however, that would carry a more unfavorable prognosis.

While not documented, and presumably based upon the patient’s recollection, she told Gonzalez that she was informed post-operatively that she would most likely not survive a year.  It is doubtful that she would have been told this when she appears to have had only local spread within the probable compass of the operation, there being no mention of distal metastases, for example to the liver.

We are told that she followed Dr Kelley’s nutritional regime for five years, and remains well ten years later.   It is interesting that any “nutritional regimen” would work in such a patient, especially a regimen that these stories imply has to be applied with considerable rigor, as maintaining good nutrition is a great problem after gastric resections.


There are grounds for believing this was a relatively well-differentiated gastric cancer variant, and that it was cured by surgery.

Patient 48: Testicular cancer

This patient is described by Gonzalez as “a 33-yer-old man form California who has survived six years since his diagnosis of metastatic testicular cancer.”

In mid-June 1981 Patent 48 was investigated for a recent enlargement of L testis.   The hospital notes refer to a CT scan (report not included), which is said to have shown a  “5 cm X 5 cm X 2 cm mass of nodes in the retroperitoneal region. HcG and alpha-fetoprotein were both within normal limits.

 The left testis was removed June 23 1981 and found to be a “malignant teratoma intermediate.” The tumor was not large; it was fully contained within a 5 X 4.5 X 4.5 cm testis, and there was no involvement of tunica albuginea, rete testis, epididymis or spermatic cord.

Because of the abdominal mass the patient was advised chemotherapy for three months, with a possible retroperitoneal lymph node dissection to follow.

The patient instead chose to pursue the Kelley regime and “within weeks noted an improvement in general health.”   Seven months later on 12th February 1982 he returned to his oncologist.   A CT scan now showed no sign of the mass noted at the previous examination.   The oncologist stated “we will obtain patient’s prior CT scan and review both together”  but there is no record of what was found, unfortunately.

Six years later the patient remains well.


On the face of it a remarkable case, although a review of the radiology could influence that opinion.

Abeloff’s Clinical Oncology states: “In patients with nonseminomatous GCT [germ cell tumors], abdominopelvic CT understaging (false negatives) occurs in as high as 50% of patients, whereas overstaging (false positives) occurs in approximately 10% of patients.”   That 10 percent would presumably arise from the difficulty of defining the parameters of normality in a node; i.e., what size, shape, etc., should be regarded as normal.  A 5 cm single node would presumably not be likely to be a false positive, but a 5 cm “mass of nodes” is referred to in this case, and might qualify.   Certainly, the oncologist who saw this patient refers to “bulky intra-abdominal disease”, but apparently without at that time being in possession of the actual films.

The lack of a biopsy is also always a problem when remission is being claimed.   Such cancers are also known to undergo “spontaneous” remission on occasions but one is reluctant to invoke that explanation either, without much more thorough acquaintance with the case and the way the disease evolved.

Patient 49: Testicular cancer

Patient 49 is described as a “36-year-old man from Louisiana alive eight years since his diagnosis of metastatic testicular cancer.”

This man noted an enlargement of his left testicle in early 1979.   Orchidectomy was carried out on April 4th 1979.  Histology:  high grade “embryonal cell carcinoma showing lymphatic and blood vessel permeation.”

Lymphangiogram was normal but the patient was nevertheless advised to undergo retroperitoneal lymph node dissection, which was performed April 21 1979.  He was found to have numerous large lymph nodes including one intimately attached to the renal vein.   Poorly differentiated embryonal cancer was confirmed involving six lymph nodes.   A further nineteen lymph nodes were recovered and about 12 of those were thought to be firmer than usual and possibly containing metastases.

According to Gonzalez, the patient’s x-rays also showed “possible metastatic disease” in the left lung and hip but this is not documented anywhere.   Bony metastases are not common with this type of cancer and it is unlikely that abdominal nodal dissection would have been advised if more distant spread was known.   In fact, the patient’s surgeon is stated to have recommended retroperitoneal lymph node dissection “to determine conclusively the extent of disease” (that would determine whether the patient was advised chemotherapy or not).

He was advised chemotherapy on the basis of the nodal involvement, but opted for Dr Kelley’s treatment instead.   He remained well eight years later.  Gonzalez allows that he has no evidence of regression of metastatic disease.


It is probable that the surgery cured this man.   Stage ll non-seminomatous tumors are regarded as highly curable, although bulky intra-abdominal disease does reduce the chances of cure so that chemotherapy would normally also be advised as insurance.   This study * gives an idea of the outcomes normally expected:

*Stephenson AJ., Bosl GJ, Motzer RJ, et al. Nonrandomized comparison of primary chemotherapy and retroperitoneal lymph node dissection for clinical Stage II A and II B nonseminomatous germ cell testicular cancer. .J Clin Oncol  2007; 25(35):5597-602St

Patient 50: Uterine cancer

This patient is described as “a 72-year-old woman from Washington state alive nearly 18 years since diagnosis of uterine cancer.”

Following menopause in 1966 this patient developed per vaginam bleeding, and endometrial biopsy revealed what was described as “Grade lll adenocarcinoma.” (No biopsy report is provided, but the subsequent recurrence of this cancer, which was reported as showing “an identical pattern” to the primary cancer, describes “A malignant glandular pattern with cribriforming consistent with an endometrial origin … As in the previous material, small foci of squamous differentiation are present.”)

She was recommended radiation as initial treatment to be followed by hysterectomy, and received 5120 rads as an intra-uterine implant.   Hysterectomy and bilateral oophorectomy was performed a month later, on December 9th 1969.  No evidence of metastatic disease at operation.

For six years she remained well, then began experiencing gradually worsening fatigue, malaise, depression, and chronic lower abdominal pain.  Multiple medical consultations could find no cause and one doctor told her she had a bad case of nerves.

However In “late fall” 1975 she was admitted for further evaluation of a mass in the left pelvic area, thought most likely to be recurrent uterine cancer.  A chest x-ray also revealed suspicious lesions in both lungs in the form of “several nodules” measuring up to 1.3 cm in diameter and described as “probably representing metastases.”

On November 24 1975 Patient 50 underwent resection of a 5.5 cm X 3 cm X 2 cm pelvic tumor. There was no other intra-abdominal spread.  The histopathology is described above.  A further chest x-ray after surgery is said to have confirmed the lung lesions..

She was discharged from hospital December 1st 1975.   There is no medical documentation provided thereafter, until a doctor’s letter 11 years later, dated November 16th 1984, expressing surprise that a chest x-ray now showed no signs of the lesions thought to have been metastases.

According to Gonzalez’ characteristically dramatic version of events she was advised to undergo “aggressive chemotherapy at once” but the patient would only accept hormonal treatment in the form of 17-alpha-hydroxyprogesterone.

“Subsequently she seemed to worsen despite the hormone therapy, becoming increasingly fatigued and lethargic, and experiencing constant shortness of breath assumed to be due to the metastatic disease in her lungs.  By March 1976 she was largely bedridden, apparently in a near terminal state.”

“By chance, Patient 50 learnt of Dr Kelley and decided to proceed with his therapy. After discontinuing the progesterone, she consulted with Dr Kelley and in early April 1976 began the full nutritional regimen.  Although her physicians objected to such “quackery, ” within a year all her symptoms including her respiratory distress, resolved. “

She is said to have been in good health over 11 years later.  In November 1984 she requested a chest x-ray from her doctor.  It showed that the previous presumed metastatic lesions were no longer visible, and gave rise to the letter described above.


A remarkable thing about this case is that it took six years for this lady’s recurrent uterine tumor to declare itself.  This suggests a very slowly growing cancer. Such slow-growing tumors have long been recognized to be more responsive to progestogens*.

This case hangs mainly upon the diagnosis of small, unbiopsied pulmonary secondaries and their apparent disappearance.  With better documentation it may well have transpired that the resolution of these lesions occurred while taking the progesterone and before starting the Kelley treatment.  We also have no independent documentation of how long she took progestational agents.

Although long term cure might be expected to be rare from that treatment alone, one study* reports that, with the use of progesterone for advanced uterine cancer “After 13 yr of observation, 13.4% of the women appeared to be potentially ‘cured’…”

Gonzalez makes much of deterioration in her physical state including constant shortness of breath “assumed due to the metastatic disease in the lungs” up until March 1976.    Accepting such an interpretation would require radiological evidence of a parallel progression of the pulmonary disease – evidence which is lacking despite the patient’s apparent continued contact with her doctors.   There are other possible causes of breathlessness post-operatively, and it is also rather unlikely that what appears to have been a very slowly growing kind of cancer until that point would have brought her to such a debilitated state in such a time interval.

This case is considerably undermined by the possibility of a response to the hormonal intervention, and poor documentation of the state of the disease at the point when the Kelley treatment was commenced.

*Riefenstein EC, Jr. The treatment of advanced endometrial cancer with hydroxyprogesterone caproate. Gynecol Oncol 1974;2(2-3):377-414

Also see:   Kennedy BJ, A Progestogen for Treatment of Advanced Endometrial Cancer.  JAMA 1963; 184(10):758-761

and, more recently:

Yang S, Thiel KW, De Geest K, Leslie KK.  Reviving progesterone therapy in the molecular age. Discov Med 2011; 12(64): 205-212