Analysis

Autogenous Vaccine: A Defense Against the Bacterial Organism that Causes Cancer

In 1947, Virginia Livingston Wheeler proposed that human cancer was caused by an infectious organism, which she observed while she was working with scleroderma patients. She noticed that their skin lesions resembled those of a sarcoma, and since she believed scleroderma was caused by bacteria,1 she extended that idea to the cause of cancer. The microscopic “organisms” she observed in extracts of the tumors had no cell walls so she called them L-cells (free of cell walls). She observed a variety of different forms that she claimed represented different forms (pleomorphic) of the same bacterium.2 She named the organism Progenitor cryptocides (PC).3 Wheeler postulated that PC was ubiquitous but harmless in normal humans and animals.4

Between 1949 and 1953, Wheeler’s co workers S. A. Jackson and I. C. Diller reported they successfully cultured PC from tumor tissue extracts and characterized it as an acid-fast organism in the order Actinomycetales.5 Because these “bodies” were seen in tumor tissues, Wheeler opined that the cancer-causing filterable DNA and RNA viruses were really PC without cell walls.4

In 1970 Wheeler summarized her hypothesis of the cause of cancer:

One specific type of highly pleomorphic microorganism has been isolated consistently by us from human malignancies of every obtainable variety for the past 20 years. This microbe has been reported in some or many of its various guises since the beginning of the 19th century and it has been periodically rediscovered, renamed, reinterpreted or re-misinterpreted. But the organism remained an unclassified mystery, due in part to its remarkable pleomorphism which in its various phases may resemble viruses, micrococci, diphtheroids, bacilli and fungi.6

Over the years, Wheeler modified her ideas about the cause of cancer. She added that it was a degenerative disease resulting from a weakened immune system that allowed the PC to grow unchecked. Based on this concept, she postulated that a vaccine prepared against PC from the cancer patient (an “autogenous vaccine”) would inactivate the PC and effectively treat the cancer. Regarding the use of this vaccine she wrote, “We use the autogenous vaccines in the treatment of many of our patients, whether they have cancer or not. In our field of medicine which is allergy and immunology as well as internal medicine we do not represent to the cancer patient that the use of the autogenous vaccine is for the treatment of cancer. Rather, that it is a treatment for the underlying cause of the cancer, the failure of their immune competence.”* Wheeler’s autogenous vaccine therapy was a major part of the treatment program offered in the clinic she opened in San Diego, California, in 1969.7

Wheeler was aware of Beard’s “trophoblastic” theory of cancer formation,8 The theory that cancer was caused by the malfunctioning of embryonic cells originated with John Beard (1902), a Scottish embryologist9 who postulated that a distinct embryonic cell, the trophoblast, was responsible for “eroding” a site in the uterus in which the developing fetus could grow. These trophoblasts had destructive potential and therefore needed to be destroyed as soon as they served their purpose. This destruction, he said, was accomplished by fetal pancreatic enzymes. If the trophoblasts escaped destruction, he said, they proliferated and caused malignant chorio-epithelioma in the uterine tissues.

Wheeler believed that chorionic gonadotrophin (hCG), produced in the cells of the placenta of a pregnant female, is also found in cancers of embryonic ectodermal (trophoblastic) tissues.9 Thus, she expected it might be found in the blood of cancer patients. She also knew that antibiotics from organisms in the order Actinomycetales (i.e., actinomycin) inhibited endocrine hormone activity.10 She had concluded that PC organisms were seen in extracts from human cancers, so she examined PC culture fluids for the presence of hCG. In 1974 Wheeler reported that PC organisms in culture were producing hCG. With this finding she composed the hypothesis for PC as the cause of cancer.

Wheeler also believed there was a relationship between diet, PC, and cancer,4 and concluded that the source of the PC was food. Ingested PC then took up residence within the cells of the intestinal tract, lost their cell walls, and proliferated. Under these conditions they were able to share their nucelic acids with those in the human cells they inhabited and gained the ability to produce hCG. The excess hCG they produced suppressed the lymphoid tissues in immune system and prevented them from producing anticancer antibodies. The result, she said, was a cancer.

Wheeler believed that PC was a microscopic plant, and concluded that substances that regulate plant growth would inhibit the growth of PC. Abscisic acid is a plant hormone and an analog of retinoic acid. In a paper on the role of nutrition in the immunotherapy of cancer,4 Wheeler states, “A number of years ago I discovered that abscisic acid has a neutralizing action on PC by diminishing the CG they produce in vitro.” She gave no reference in support of this claim.

In 1980 Wheeler published a physicians’ handbook.7,8 In it she summarized her rationale for the cause of cancer and presented a protocol for an outpatient treatment of the diagnosed colon cancer patient:

  1. Clinical laboratory tests: SMA-30, X-rays, ultrasound, darkfield microscopic exam of blood, and PPD testing after injection of BCG.
  2. Procedures: Collection of urine sample for culture of PC to be used in autogenous vaccine preparation.
  3. Treatments: Whole blood transfusion, coffee enemas 2x/day, high colonics 2x/week.
  4. Injections: Vitamin B-12, gamma globulin, BCG, and a “purified antigen” that is made from L-form PC that produce CG. Vaccine organisms are prepared from the patient’s urine and the vaccine is administered intravenously.
  5. Infusions: Vitamin C (titrated upward from 15 g per day as tolerated by the patient), Vitamin B-6 (300 mg), Calcium gluconate if bone metastases are present, Compazine if there is persistent nausea from the vitamin C.
  6. Administer as needed: Antibiotics, abscisic acid, mineral supplements, digestive enzymes.
  7. Diet: Eliminate all PC-infected foods; “hormone stimulators” such as milk products, sugar, white flour, processed foods, irritants, carcinogens (tobacco, coffee, alcohol, and hair dyes); avoid all narcotics, sedatives, steroids, chemotherapeutic agents, and radiation; eat only fresh fruits, vegatables, vegatable juices containing liver or spleen powder, nuts and grains with added lamb and fish, vitamins, minerals, and “food supplements.”
  8. Recommended: Mental and spiritual programming.

CRITIQUE

Wheeler promoted the idea that stimulation of the patient’s immune system by immunotherapy was the means of controlling cancer, which she believed was a degenerative disease. She based this conclusion on her idea that the normal human immune system carries out a constant surveillance for newly emerging cancer cells and that when it recognizes them, it has the functional ability (immune competence) to destroy them. Wheeler claimed her treatment regimen increased immune competence so the body could heal itself.

Immune survaillance over cancer

In 1959 Lewis Thomas11 raised the question of whether cellular immunity might be the mechanism by which the human body protects itself from cancer. By 1976 the experimental evidence casting doubt on this hypothesis was overwhelming. In 1986, a recapitulation of all the literature on the subject of immune surveillance over cancer was published by Stutman.12 Scientific data from experimental, clinical, and animal testing of the proposed mechanisms clearly demonstrated that the normal human immune system could be made to notice the presence of tumor cells only after it had been artificially manipulated, in vitro. Stutman concluded, “The existing generalizations about the existence of an anticancer immune surveillance system are completely unwarranted.”

Immune competence

There are about 33 different effector cells that are part of the normal human immune system.13 Immune competency therefore reflects the corelationship between all these cells and requires a normal response of each when the entire system is stimulated. The measure of immune incompetence implies, at the very least, a determination of the kind and number of immune cells that are present and functioning normally. Immune competency is a measure of the performance of the number and function of the T and B lymphocytes, the complement system, the types of circulating antibodies and the activity of phagocytic macrophages.14 None of the publications from the Wheeler clinic describes the determination of a patient’s immune competence.

The claim that cancer results from immune incompetence

To validate her claim that cancer results from immune incompentence, Wheeler would have to show (l) that immune incompetence exists and (2) that correction of the determined incompetence would result in a cure.

Immune stimulation results when antigen molecules contact specific receptors of functionally competent target cells in lymphoid tissues. But if, for example, the stimulator used is a T-cell-specific antigen and the patient is one whose T-cell population has been greatly depleted by disease or by previous therapy, there is no target cell for the antigen to contact and there is no stimulation. What is needed in such a case is restoration of deficient immune system cells, not its stimulation.

Since most of the patients who attend Wheeler’s clinic would have been treated with chemotherapy and/or radiation, and would have advanced disease, the possibility exists that they would be lymphoid-tissue depleted. Therefore, before treatment could begin, the degree of immune incompetence would have to be determined. If the treatment plan called for use of an adjuvant such as BCG, it should be tested to confirm that it can enhance or restore the effectiveness of immune potentiators to be used.

Adjuvants14 are substances that augment weak immune responses to antigens. That is, they may increase contact between the antigen and receptors on antigensensitive cells, increase the pool of antigen-sensitive cells, increase the proliferation of antigen-sensitive cells, or increase antibody production. Therefore, to be effective, an adjuvant such as BCG must be shown to elicit the response required for the immunologic needs of each patient.

Finally, clinical laboratory data from each treated patient must demonstrate a direct relationship between the treatment and the improving clinical picture.

Wheeler offers no evidence that her patients are immune incompetent, that her treatment restores function to immune systems, or that there is an improvement in immune function that correlates with the clinical improvement.

The claim that cancer is caused by progenitor cryptocides, a pleomorphic, acid-fast organism of the order Actinomycetales

The idea that cancer is caused by a microorganism did not originate with Wheeler. In fact, she is one in a long line of people who believed it. The presence of a microbe in cancer tissue was first reported by Scottish pathologist William Russell in 1890.15 In the 50 years that followed, numerous individuals expressed the belief that cancer resulted from an infection with specific microbial organisms.16–22 The last in this line was T. J. Glover.23–25 He claimed to isolate a filterable, pleomorphic “cancer microbe” from blood of a cancer patient; that it could be changed to spore forming bacilli if allowed to dry for several months; that if the organism was first grown on a “special culture media” it caused malignant tumors when injected into animals; and that “terminal” patients improved when he treated them with an “anticancer serum” he produced in horses using cultures of the “cancer microbe.”

Before a bacterial cause for disease is proved, experimental data must fulfill Koch’s postulates.26 These postulates provide the means for specifying a pathogenic organism’s action. The organism must be shown to be present in all cases of the disease, pure cultures of the organism must produce the disease when they are inoculated into experimental animals, and after producing the disease, the organisms must be reisolated from diseased tissues and recultured.

None of the theories proposed between 1890 and 1970 on bacterial cause of human cancer was ever tested using the criteria of Koch’s postulates. No one has ever shown that a vaccine made against them prevented or cured cancer. However, given the discovery of the cancercausing viruses,27 the possibility that some bacteria might be the cause of cancer was not a matter of indifference to cancer researchers, despite extensive negative investigations into the ubiquitous organism Mycoplasma.28 Therefore it was not unexpected that cancer researchers at the National Cancer Institute (NCI) would recognize Virginia Livingston Wheeler’s theme or that they would try to verify her claims.29 NCI investigators asked the following questions about Wheeler’s claims: (l) Has the identity of the organism called PC been independently confirmed? (2) Have Koch’s postulates with PC organisms been confirmed? (3) Have clinical trials been carried out using her treatment regimen?29

In regard to the precise classification of Wheeler’s observed organism, three microbiology experts from the National Institutes of Health (NIH) found that the absence of acceptable classification procedures made it impossible for them to identify her “cancer organism.”29 Cohen and Strampp30 could not identify the organisms in the sample of PC that Wheeler gave them. Acevedo found that the PC Wheeler provided him was Staphylococcus epidermidis—a common skin bacterium.31

Given no specific identification evidence to support her claim, it is apparent that the organisms Wheeler claimed are PC could belong to any one of many different bacterial species. With no data demonstrating that PC fulfilled Koch’s postulates, there is no reason to believe that Wheeler’s organisms are in any way related to human cancers.

Claim that PC produce human chorionic gonadotrophin

Beginning in 19482 Wheeler reported seeing enormous numbers of microbial particles when she viewed the blood of a cancer patient by darkfield microscopy. She concluded that these organisms were the cause of the cancer. In 1970,6 based on her acceptance of John Beard’s “trophoblast” theory of cancer9 and on the presence of hCG in the serum of some cancer patients, she tested PC culture fluids for hCG and found what she thought was hCG. This finding was an important discovery and its implications drew the attention of many investigators. Among these was Dr. Hernan Acevedo. Acevedo was interested in the significance of the hCG in the culture fluid of the bacteria from cancer patients. By 1985, using modern methods of identification and verification, Acevedo31 and Domingue32 showed that the CG-producing bacteria isolated from cancer patients by Wheeler was not the unique bacterium Progenitor cryptocides, as she had claimed.5,6 Neither was the synthesis of the CG-like material by diverse bacterial strains a unique phenomenon. They also showed that not every cancer-associated bacterium had the ability to synthesize this protein and that all bacteria that expressed CG-like material did not indicate the presence of active cancer. In fact, the membranes of over 300 species of gram-negative organisms as well as those of many mammalian cells contain this immunologically and biolgically crossreactive hCG as an integral part of their structure but as yet its biological role in bacteria is unknown.33

Based on experiments with the rat and mouse tissue before and after an induction malignancy, Slifkin34 concluded that gene coding for the CG-like protein was present in all cells but needed to be turned on by the malignant transformation. As early as 1972 Tsuruhara35 reported that hCG had 16 moles of the sugar sialic acid per mole of protein and that it was this sugar that gave the hormone its ability to exert a biological effect in vivo. Without sialic acid, the CG-like material was instantly cleared from the circulation. Yoshimoto36 found that the CG-like material in normal human liver and colon tissue was not sialylated, in contrast with placental tissue, and while this desialylated CG had no biological activity, it was immunologically reactive. In 1979, Mauro et al.37 found that the CG-like material from Wheeler’s PC contained no sialic acid moiety. Since hCG hormone activity requires sialic acid, the CG-like material from Wheeler’s PC could not perform the physiologic role she ascribed to it.

The ubiquitous nature of CG-like material was proved by the work of Yoshimoto,38 who showed that it was present in all normal tissues tested. But the CG-like material they isolated did not bind to a Con ASepharose column and they found that the sialic acid content of these fractions were l0% or less than the content of sialic acid in placental tissue. They found that when sialic acid was removed from normal placental hCG, it was cleared from the circulation so rapidly that it had no opportunity to exert hormonal activity. They concluded that only placental tissues had the ability to sialylate the CG-like peptide and to convert it to the hormone form. It is of interest that patients whose nontrophoblastic tumors secrete CG-like material show none of the symptoms usually seen in trophoblastic tissue diseases with excess hCG secretion.

The proven role of hCG in pregnancy is the maintenence of the early corpus luteum by ensuring a continued estrogen and progesterone supply and the regulation of testosterone production by fetal testicular tissue.39,40 Although a literature search turned up papers postulating that hCG might suppress certain immune responses,41–43 no reports were found with experimental evidence that hCG inhibited growth of malignant cells.

Claim that abscisic acid, a plant hormone and an analog of retinoic acid, inhibits cancer growth by neutralizing hCG

Because retinoids were known to inhibit tumor cell growth44 and because Wheeler believed that PC was a plant cell, she postulated that the phytohormone abscisic acid, an analog of retinoic acid,45 would inhibit cancer by preventing hCG formation in PC.46 Wheeler’s literature contains no experimental evidence that supports such a conclusion. In one study, comparisons of the biological activity of analogs of retinoic acid, abscisic acid was included.47 As the standard, spontaneously transformed mouse fibroblasts (Balb/3T12-3 cells) were treated with biologically active retinoic acid and the degree of increased adhesion to the culture dish surface was determined. The investigators then compared this cell-to-surface-attachment activity with that obtained using the 15 retinoic acid analogs. Six analogs completely failed to induce adhesion of the transformed fibroblasts and abscisic acid was among them. Since the adhesion assay estimates biolgical activity of retinoids,47 abscisic acid must be considered a vitamin A analog with no biological activity.

SUMMARY AND CONCLUSIONS

The components of the autogenous vaccine treatment of the Virginia Livingston Wheeler Clinic can be summarized as follows: A bacterium she discovered and identified, Progenitor cryptocides (PC), is claimed to cause cancer; a vaccine she makes against the PC organisms from patient urine is said to suppress the cancer-causing activity of the PC; cancer is a disease of immune incompetence and stimulation of the immune system will fight the cancer; a protein made by the PC is the human hormone, chorionic gonadotrophin; when PC secretes chorionic gonadotrophin into the patient it suppresses the “anticancer surveillance function” of the normal immune system; PC cells are plant cells, so the plant hormone abscisic acid, an analog of the anticancer vitamin retinoic acid, suppresses PC growth and hCG production; all processed foods are depleted of nutrients and contain toxins; all poultry contains PC organisms; to lessen the PC burden, an all-natural vegatarian diet supplemented with vitamins and minerals must be adopted; detoxification with coffee enemas cleanses the bowel of toxic waste material.

The rationale for each of these components of the Wheeler treatment for cancer is characterized by the same common flaw: None of them is supported by any reproducible, independently confirmed scientific evidence. In the absence of evidence there is no reason for either the patient or the members of the scientific community to believe the claims.


Virginia Livingston Wheeler died in her 80s in the early 1990s. This thoroughly researched and reported discussion was constructed after my experience with the Wheeler Clinic through the Cancer Advisory Council of the State of California investigation. The council members and the Food and Drug Section of the Department of Consumer Affairs knew of Wheeler’s clinic and had information on the methods in use there. I had attended Wheeler’s lectures at a Cancer Control Society meeting, and I saw the slides depicting the PC organisms. Some appeared as cocci, some as rods, some staining gram-positive, some negative, and one culture looked like the mold actinomyces. I concluded she was culturing different contaminants, and calling them the same organism in differing forms. Could any educated physician or scientist really make that simple an error? The answer, of course, was yes. Pseudomedicine advocates do so all the time.

Dr. Jerry Lewis and I wrote separate analyses of the problem. We established that her methods were not standard of care, yet the medical board would not proceed with a winnable case without an injured patient. Such patients characteristically remain loyal to errant practitioners. The question of the Wheeler vaccine’s legal status required knowing whether or not the use was a commercial one or whether her methods were a matter only between her and the patient and thus for the medical board alone. We determined that the material was being processed, reinjected, and paid for by the patient. This technicality allowed the state to move in and request the court to have the clinic cease using the material, which the court finally did. Although the court ruling not to use the “vaccine” is still valid, the clinic continues to treat patients—with or without the vaccine.—Ed.


Notes

* Treating cancer with unapproved methods outside of formal research conditions is a felony in California.—Ed.

REFERENCES

  1. Wheeler VL. Etiology of scleroderma—a preliminary clinical report. J Med Soc. NJ. 1947
  2. Wuerthele-Caspe V, Allen RM. Microorganisms associated with neoplasms. NY Microscopical Soc Bull. 1948; 2: 2–31.
  3. Wuerthele-Caspe V, Alexander-Jackson E, Anderson JA, Hillier J, Allen RM, Smith LW. Cultural properties and pathogenicity of certain microorgansism obtained from various proliferative and neoplastic diseases. Am J Med Sci. 1950; 220: 638–646.
  4. Livingston-Wheeler V. Role of nutrition in immunotherapy of cancer. J Int Acad Prev Med. 1979; 5: 54–75.
  5. Wuerthele-Caspe V. Cultural, immunological, biochemical properties of Progenitor Cryptosides. Trans NY Acad Sci. 1974; 2(6): 569–682.
  6. Wuerthele-Caspe V, Alexander Jackson E. A specific type of orgnaism cultivated from malignancy: bacteriology and proposed classification. Ann NY Acad Sci. 1970; 174:(2): 431–1056.
  7. Wheeler VL, Wheeler OW. Microbiology of Cancer: A Physicians Handbook. Livingston Wheeler Clinic; 1980.
  8. Wheeler VL, Wheeler OW, Majnarich JJ. Production of CG in vitro by Progenitor cryptosides, a member of the order Actinomycetales. Cytobiologiische Revue. Nr l/1982. Ott Verlag, CH-3600, Thun 7.
  9. Beard J. The Enzyme Treatment of Cancer. London: Chatto &Windus; 1911.
  10. Wuerthele-Caspe Livingston V. Cancer: A New Breakthrough. Self-published: 1972.
  11. Thomas L. Quoted in: Lawerence HS, ed. Cellular and Humoral Aspects of the Hypersensitive States. New York, NY: Hoeber-Harper; 1959: 529–532.
  12. Stutman O. Spontaneous, viral and chemically induced tumors in the nude mouse. In: Fogh J, Giovanella B, eds. The Nude Mouse in Experimental and Clinical Research. New York, NY: Academic Press; 1978: 411–423.
  13. Keren DF, Warren JS. The immune system and diagnostic immunology. In: Diagnostic Immunology. Baltimore, Md: Williams and Wilkins; 1992.
  14. Goding JW. In: Monoclonal Antibodies: Principles and Practices. New York, NY: Academic Press; 1983: chaps. 2, 3, 8.
  15. Russell W. A lecture. BMJ 1890; 2: 1356–1360.
  16. Leyton AA, Leyton HL. Observations on the etiology of sarcoma in the rat. Lancet. 1916; 1: 513
  17. Young J. An organism from carcinomatous growths. Edinburgh Med J. 1921; 27: 212–221.
  18. Nuzum JL. Production of metastasizing cancer in breasts of dogs and primary epithelioma by repeated injection of micrococcus from human breast cancer. Surg Gyn Obst. 1925; 11: 343–352.
  19. Stern EW, Sturdivant BF, Stern A. Parasites isolated from cancer growths. Proc Natl Acad Sci. 1925; 11: 662–669.
  20. Scott MJ. The parasitic origin of carcinoma. Northwest Med. 1925; 24: 162–166.
  21. Scott MJ. Clinical experiences with cancer antitoxin. J Cancer. 1926; 3: 1–6.
  22. Glover TJ. A study of the Rous sarcoma #1. Can Lancet Pract. 1926; 66: 49.
  23. Glover TJ. The bacteriology of cancer. Can Lancet Pract. 1930; 74: 92–111.
  24. Glover TJ. The production of malignant growth in the G. pig. Pub Health Rep. 1933.
  25. Glover TJ, Engle S. Studies in Malignancy. New York, NY: Murdock Foundation; 1938.
  26. Etiologic proof of infectious agents. In: Zinsser Microbiology. 18th ed. Joklik WK, Willet HP, Amos DB, eds. Norwalk, Conn: Appelton-Century-Crofts; 1984: 4–5.
  27. Tumor viruses. In: Zinsser Microbiology. 18th ed. Joklik, Willet HP, Amos DB, eds. Norwalk, Conn: Appelton-Century-Crofts; 1984: 927–956.
  28. Mycoplasma. In: Zinsser Microbiology. 18th ed. Joklik WK, Willet HP, Amos DB, eds. Norwalk, Conn: AppeltonCentury-Crofts; 1984: 793–798.
  29. Morrison BH III. Report to Congress. 1978.
  30. Cohen H, Strampp A. Bacterial synthesis of a substance similar to hCG. Proc Soc Exp Biol Med. 1976; 152: 408–410.
  31. Acevedo HF, Campbell-Acevedo E, Kloos WE. Expression of human CG-like material in coagulase negative Staphylococcus species. Infect Immun. 1985; 50(3): 860–868.
  32. Domingue GJ. Filterable cell-associated cell wall deficient bacteria in renal disease. In: Domingue GJ, ed. Cell Wall Deficient Bacteria: Basic Principles and Clinical Significance. Reading, Mass: Addison-Wesley; 1982: 121–148.
  33. Markowitz J. Protoplasmic and plasma membrane relationships. Trends Biochem Sci. 1976; 1: 161–163.
  34. Slifkin M, Acevedo HF, Pardo M, Pouchet GR, Rakshan M. Human CG in cancer cells: ultrastructural localization. Proc 3rd Int Symp. 1976; 357.
  35. Tsuruhara T, Dufau ML, Hickman J. Biological activity of desialylated CG. Endocrinolgy. 1972; 91: 296–301.
  36. Yashimoto Y. Human CG-like material in non-endocrine tissues of normal individuals. Science. 1977; 197(64303): 575–577.
  37. Maruo T, Cohen H, Segal SV, Koide SS. Production of CG-like factor by a microorganism. Proc Natl Acad Sci USA. 1979; 76(12): 6622–6626.
  38. Yashimoto Y. Ubiquitous nature of CG-like material. Am J Obst Gyn. 1979; 134(7): 729–733.
  39. Goodman LS, Gilman A, eds. Pharmacological Basis of Therapeutics. 4th ed. New York, NY: Macmillan; 1970: 1524–1529.
  40. Bahl OP. Human chorionic gonadotrophin: purification and physiochemical properties: the nature of the carbohydrate units. J Biol Chem. 1969; 244: 567–583.
  41. Lange PH. Suppression of antitumor lymphocyte mediated cytotoxicity by hCG. J Urol. 1976; 115: 95–98.
  42. Kellen JA, Kolin A, Acevedo HF. Effects of antibodies to CG in malignant growth. I. Rat 3230 AC mammary adenocarcinoma. Cancer. 1982; 49(11): 2300–2304
  43. O’Dell WD, Griffin J. Pulsatile secretion of hCG in normal adults. N Eng J Med. 1987; 317(27): 1688–1701
  44. Ziegler RG. A review of epidemiolgic evidence that carotenoids reduce the risk of cancer. J Nutr. 1989; 119: 116–122.
  45. Livingston-Wheeler VC. Role of nutrition in the immunotherapy of cancer. J Int Acad Prev Med. 1979; 5(2): 54–71.
  46. Wuerthele-Caspe Livingston V. Abscisic Acid: Tablets and Process. U.S. Patent #3958025. May 1976.
  47. Adamo S, Deluca LM, Akalovsky I, Bhat P. Retinoid-induced adhesion in cultured transformed mouse fibroblasts. J Natl Cancer Inst. 1979; 62: 1473–1478.