There's yet another reason to pass on the meat and potatoes and instead fill your plate with fruit, vegetables, and whole grains. New research from the Preventive Medicine Research Institute in Sausalito, California, finds that a very-low-fat vegan diet is packed with protective nutrients that may help ward off prostate cancer, as well as other diseases.

Ninety-three men with early-stage prostate cancer took part in the one-year study. The men were randomly assigned to eat either a vegan diet in which only 10 percent of their calories came from fat, or to continue eating their regular diet.

The vegan diet focused on whole-grains, fruits, and vegetables, while avoiding oils, margarines, high-fat foods such as nuts and chocolate, and processed foods. Although meats and refined foods have become staples of the modern Western diet, the vegan plan followed in this study is actually more of "a traditional diet in terms of how our ancestors ate," says study author Gerdi Weidner, PhD, Vice President and Director of Research at the Institute. Study co- author Dean Ornish, MD, founder and president of the Institute, is a big proponent of the very-low-fat diet for disease prevention, and has written several books on the subject.

Prostate cancer patients who followed the diet also ate fortified soy protein powder and tomato-based vegetable juice, which contain phytochemicals believed to slow prostate cancer growth. As part of the lifestyle intervention, the men also exercised and participated in stress management and social group support programs. Meanwhile, the control group continued their regular diet and lifestyle program under their doctor's care.

The group that followed the very-low-fat vegan diet decreased their consumption of substances thought to increase the risk of disease, including saturated fat, which has been linked to a higher risk of prostate, breast, and colon cancers. At the same time, they ate more of several nutrients thought to protect against disease, including:

· Fiber (lowers risk of heart disease, type 2 diabetes, colorectal cancer, and death in general)
· Vegetable protein (may protect against cancers of the breast, colon, and prostate)
· Vitamin E (may reduce the risk of prostate and other cancers)
· Folate (protects the heart, and may help prevent prostate and other cancers)
· Selenium (lowers the risk and slows progression of prostate cancer)

The study didn't investigate whether these nutrients actually slowed prostate cancer progression or increased participants' survival, but "the entire program was found to be beneficial for the patients," Dr. Weidner says. An earlier study by the same researchers did find an improvement in prostate- specific antigen (PSA) levels (a marker of prostate cancer progression) in men who followed a vegan diet and incorporated other lifestyle techniques.

Based on the results of this and other research, it appears that eating a very-low-fat vegan diet can provide some protection against not only prostate cancer, but other types of diseases as well, according to Dr. Weidner.

For those interested in following a program like this, please discuss with your doctor.

Sources:
Dewell A, Weidner G, Sumner MD, Chi CS, Ornish D. A very-low-fat vegan diet increases intake of protective dietary factors and decreases intake of pathogenic dietary factors. J Am Diet Assoc. 2008;108:347-356.

Ornish D, Weidner G, Fair WR, Marlin R, Pettengill EB, Raisin CJ, et al. Intensive lifestyle changes may affect the progression of prostate cancer. J Urol. 2005;174:1065-1070.

The magnolia tree is not just beautiful-it's also the source of a potentially potent cancer-fighting drug. Researchers at the University of Pittsburgh have discovered that honokiol, a substance extracted from the root and stem bark of one species of magnolia tree, may help treat-or even prevent-prostate cancer.

Honokiol has been an important component of traditional Japanese and Chinese medicine because of its anti-inflammatory, anti-bacterial, and anti-allergic properties. A few studies have found that honokiol also can interfere with several processes that help cancer cells multiply and spread.

A recent study in the journal Clinical Cancer Research looked at the effects of honokiol on different types of prostate cancer cells. Two types of cell-PC-3 and C4- 2-do not depend on male hormones (androgens) to grow. Another type of prostate cancer cell-LNCaP- does respond to androgens.

In one part of the study, researchers gave male nude mice 1, 2, or 3 milligrams of honokiol three times a week by mouth. Giving the drug this way has an advantage over injections, according to lead author Shivendra Singh, MD, PhD, Director for Basic Research and professor of Pharmacology and Urology at the University of Pittsburgh. "Orally active agents are highly desirable since they do not require supervised administration," says Dr. Singh.

The researchers then implanted PC-3 prostate cancer tumor cells into the mice, and began to measure tumor growth. In mice given the 2-milligram dose of honokiol, the tumors were significantly smaller than tumors in mice that had not received the drug.

Treatment with honokiol halted prostate cancer cell growth in several ways: it decreased cell reproduction, led to a form of programmed cell death called apoptosis, and blocked the formation of blood vessels that feed tumors, according to the researchers. What's more, mice treated with honokiol didn't show any side effects.

The authors also looked at the effects of honokiol on PC-3 and C4-2 cells in the laboratory. They found that the drug inhibited growth and apoptosis in these types of prostate cancer cells, as well.

This was the first study to show the effects of oral honokiol on PC-3 prostate cancer cells, and the first to show that this treatment increases cell death and decreases cell reproduction in prostate cancer cells, regardless of whether they are androgen responsive. The results indicate that honokiol has great promise as a prostate cancer therapy, Dr. Singh says.

The authors refer to honokiol as a "promiscuous" drug because it has so many different biological effects. It also appears to be effective for lung cancer, colorectal cancer, and other types of cancers.

More research is needed to confirm honokiol's effects on prostate cancer and other types of cancer cells. "We are thinking about doing a combination study with other bioactive compounds," Dr. Singh says. "Ultimately, we want to conduct a human study."

Source:
Hahm ER, Arlotti JA, Marynowski SW, Singh SV. Honokiol, a constituent of oriental medicinal herb Magnolia officinalis, inhibits growth of PC-3 xenografts in vivo in association with apoptosis induction. Clin Cancer Res. 2008;14:1248-1257.

Flavopiridol-an extract of a medicinal plant from India-appears to offer real potential for hard-to-treat rhabdoid tumors. For the first time, researchers have shown that this experimental drug can halt the growth of rhabdoid cancer cells, both in a laboratory dish, and in mice.

Rhabdoid tumor is a very rare-and highly aggressive-cancer of the kidney, brain, central nervous system, and soft tissues that occurs in very young children. Because rhabdoid tumors are so hard to treat, only 15 percent of children with this cancer will survive two years. Chemotherapy and other conventional treatments aren't very effective on rhabdoid tumors, for several reasons.

"One reason is that the current treatment regimen of rhabdoid tumors is not based on the biology of the tumor and is not based on the understanding of what is required for the survival of these tumors," explains lead study author Ganjam V. Kalpana, PhD, professor in the Department of Molecular Genetics at Albert Einstein College of Medicine in New York. "Another possibility is that the unique genetics and pathobiology [disease process] of these tumors makes them naturally resistant to even the most aggressive chemotherapy regimen."

Yet another reason rhabdoid tumors have been hard to treat is that until recently, doctors believed that they were just another form of a rare kidney cancer called Wilms' tumor. Researchers now understand that rhabdoid tumors are a unique form of cancer, and they have a better understanding of how these tumors form.

Dr. Kalpana and her colleagues have discovered that the development and survival of rhabdoid tumors hinges on a protein called cyclin D1, which is involved in regulating the cell cycle. This protein, when left unchecked, enables the uncontrolled cell growth that causes cancerous tumors to form. In fact, researchers have found that cyclin D1 tends to be overproduced in certain types of tumors.

Based on their understanding of how rhabdoid tumors form, Dr. Kalpana and her colleagues have been trying to develop more targeted therapies for this cancer. They chose flavopiridol because it targets cyclin D1, the suppression of which has been found in earlier studies by Dr. Kalpana's group to reduce the survival of rhabdoid tumors. They tested flavopiridol on rhabdoid tumor cells in the laboratory, and in mice implanted with rhabdoid tumors.

After five days of treatment, flavopiridol killed 95 to 100 percent of the rhabdoid cells. In the mice, treatment with 7.5 mg/kg of flavopiridol five days a week for two weeks significantly inhibited tumor growth compared to the control mice. Most of the tumors either partially or completely stopped growing, according to Dr. Kalpana.

How might flavopiridol work against rhabdoid tumors? The researchers believe that it stops the cancer cell cycle and triggers a process of natural cell death called apoptosis. The effects of flavopiridol on tumors correspond to a decrease in cyclin D1.

Despite flavopiridol's promise, there are concerns about its potential toxicity. A few of the mice died during the study, although the researchers aren't sure whether this was due to the drug or to the tumor. Previous studies have suggested that flavopiridol might be safe enough to use in children and could be administered in doses that are effective against rhabdoid tumors.

Dr. Kalpana plans to conduct human clinical trials of flavopiridol in the near future. Considering the lack of treatment options for rhabdoid tumors today, she is hopeful that her research will lead to more effective biological therapies for this serious childhood cancer.

Source:
Smith ME, Cimica V, Chinni S, Challagulla K, Mani S, Kalpana GV. Rhabdoid tumor growth is inhibited by flavopiridol. Clinical Cancer Research; 2008;14:523- 532.

This article on Vitamin C and cancer was first published by CancerWire in November 2006. It has been one of the most popular and we reprint it here for those who may have missed it.

Vitamin C whether intravenous or oral is one of the most prevalent types of alternative and complimentary cancer therapies. Yet, this nutrient is still considered "controversial" by mainstream oncology. Since two time Nobel Prize winner (in chemistry and peace) Dr. Linus Pauling advocated its use in cancer starting in the late 1970's, evidence to its efficacy has been quietly and steadily mounting. In this edition of CancerWire we will review the history of this nutrient in cancer, the controversy, and discuss current findings.

Almost all animals and plants synthesize their own vitamin C except humans and a small number of other animals, including, apes, guinea pigs, the red-vented bulbul, a fruit-eating bat and a species of trout. Pure L- ascorbic acid (vitamin C) was first prepared in 1928 by Albert Szent-Gyorgyi and in 1932 it was shown that this substance was vitamin C. In 1954 and 1959 Dr. W. J. McCormick, a Canadian physician, hypothesized that cancer is a collagen disease, secondary to a vitamin C deficiency. His theory was based on the fact that collagen is the "mortar" that binds cells together and if cells stick together, tumors would have a more difficult time breaking away and metastasizing. This concept was expanded upon when, in 1966, Dr. Ewan Cameron wrote a book entitled "Hyaluronidase and Cancer." In it he pointed out that the ground substance or "intercellular cement" that binds cells of normal tissues contains various molecules that strengthen it including glycosaminoglycans and fibrils of collagen. Dr. Cameron discussed how tumors can produce enzymes that breakdown these molecules (i.e. hyaluronidase and collagenase).

Linus Pauling, Ph.D. (chemistry) had been interested in vitamin C for many years and had written previously how people required large amounts of vitamin C (1). Working with Dr. Cameron, Dr. Pauling pointed out that vitamin C could: A) stimulate normal cells to produce increased amounts of a hyaluronidase inhibitor and; B) increase the number of collagen fibrils made (2). Based on these theories, Drs. Pauling and Cameron embarked on a number of studies to test the efficacy of vitamin C in cancer patients.

Early Pauling and Cameron Studies

In 1976, Drs. Pauling and Cameron reported the survival times of 100 terminal cancer patients who were given supplemental ascorbate (10 grams/daily intravenously) and those of a control group of 1,000 patients of similar status treated by the same clinicians in the same hospital (Vale of Leven Hospital in Scotland) who had been managed identically except for the ascorbate. The 1,000 controls were matched by sex, age, primary tumor type, and clinical status. By August 10, 1976 all 1,000 of the controls had died while 18 of the 100 ascorbate-treated patients were still living. As of September 15, 1979, five ascorbate treated patients were still alive and "living normal lives." The 100 acorbate-treated patients lived, on the average, 300 days longer than their matched controls with better quality of life (measured from the time all patients were considered "untreatable").

A second study was performed in 1978 with 100 new ascorbate-treated patients and 1,000 matched controls (about half of the controls were in the original set) (3). This analysis broke out the improved survival times by cancer type. As presented in the graph below, for each type of cancer there was an improvement in survival. (In fact, with the exception of rectum and ovary cancer, the other cancers actually had longer survival in the ascorbate group than indicated in the graph because survivors were still alive when this data was collected and published.)

Mayo Clinic Studies

Pauling's and Cameron's studies were not considered the gold standard in clinical studies. The gold standard was and remains the randomized, prospective, double-blind study in which half the patients are randomized to one arm of a study, half to another arm and neither the patient nor the doctor knows who is getting what.

To test whether ascorbate was effective, Dr. Charles Moertel and his colleagues at the Mayo Clinic conducted two randomized placebo controlled studies (published in 1979 and 1985) of patients each with advanced cancer (4). Patients randomized to the treatment group were given 10 grams of oral ascorbate, and neither study showed significant benefit. (In the first study, median survival was improved two weeks with the ascorbate group.) Because Moertel's studies were taken as definitive, ascorbate treatment was considered useless. There were however, at least three significant differences between the Mayo Clinic's "definitive" studies and those of Drs. Pauling and Cameron.

Difference #1

The overwhelming majority (52 of 60 or 87%) of the patients in the first Mayo study had received chemotherapy before the study began. In contrast, only 4% of the patients in Pauling and Cameron study had received chemo. Pauling wrote, "It is known that cytotoxic chemotherapy damages the immune system and might prevent the vitamin C from being effective, inasmuch as it functions mainly by potentiating this system.(5)"

This is a valid critique. A Pubmed search for vitamin C reveals a large number of peer reviewed medical and scientific journal articles that demonstrate that vitamin C scavenges free radicals when it acts as an antioxidant (6), helps neutralize carcinogenic chemicals such as nitrosamine and nitrites (7), enhances lymphocyte function and mobilization of phagocytes (8), improves natural killer cell activities (9), modulates cell growth and differentiation (10), and enhances IgA, IgG and IgM antibody levels (11). Several of these mechanisms are directly related to the body's immune system and to cancer resistance. Cytotoxic (cell-killing) chemotherapy is notorious for seriously compromising the patient's immune system by killing the cells that mediate immunity. (In the 1985 Mayo clinic study, this difference was removed as none of the Mayo patients were administered prior chemotherapy.)

Difference #2

A commentary published by doctors from the National Institute of Health (NIH) in 2000 pointed out that there was a second significant difference in study design that may have accounted for the different results in the Mayo Clinic studies (12). The authors explained that intravenous (IV) administration (used by Pauling and Cameron) was superior to oral administration (used by Moertel) in respect to bioavailability of the vitamin. The NIH authors said, "Clinical data show that when ascorbate is given orally, fasting plasma concentrations are tightly controlled at <100 µM. As doses exceed 200 mg, absorption decreases, urine excretion increases, and ascorbate bioavailability is reduced. In contrast, when 1.25 grams of ascorbate are administered intravenously, concentrations as high as 1 mM (1,000 µM) are achieved...It is now clear that intravenous administration of ascorbate can yield very high plasma levels, while oral treatment does not." The NIH authors concluded that, "Moertel's results were not comparable to those of Cameron, as ascorbate was given orally and not intravenously. In retrospect, the route of administration may have been key.(13)" This observation was repeated in another peer reviewed paper published in 2004 which stated "Because efficacy of vitamin C treatment cannot be judged from clinical trials that use only oral dosing, the role of vitamin C in cancer treatment should be reevaluated. (14)" Vitamin C pharmacokinetics: implications for oral and intravenous use.

Difference #3

And yet a third difference with the Mayo Clinic study was that vitamin C administration was discontinued immediately after a patient could no longer take oral medications or there was progression of the disease. Apparently, in the Pauling and Cameron studies the IV doses continued regardless of the patient's changing status. Vitamin C was provided during the life of the patient. However, in Moertel's studies, because it was administered orally, vitamin C was discontinued in a large number of patients whenever there was a sign of worsening. According to writer Ralph Moss, "Because of the odd departure from Cameron's protocol, patients in the treatment arm of the experiment (in Moertel's second study) received vitamin C for a median time of only 10 weeks. None of the Mayo patients died while receiving it. Their deaths occurred after the vitamin had been taken away from them.(15)"

Obviously if the Mayo Clinic studies were designed to test the outcomes of Drs. Pauling and Cameron then they should have replicated their methodology of administration (as long as it was scientifically reliable and clinically appropriate). Why didn't Moertel's group administer the vitamin intravenously throughout the life of the patient? We don't know. Any one of these discrepancies should have been sufficient for a complete reevaluation, but as is so often the case, the cancer establishment had successfully "proved" that a mere vitamin was of no value in cancer and the case was closed. Or was it?

In the intervening 20 years since Moertel's last study two trends have continued: 1) patients are being administered IV vitamin C in various cancer clinics around the world and many are showing benefit; 2) the overall plausibility of ascorbic acid administered intravenously as a cancer therapy is being better understood by recent insights into clinical pharmacokinetics and its in vitro cancer-specific cytotoxicity.

Clinical Examples

A reading of Drs. Cameron and Pauling's book "Cancer and Vitamin C" provides 26 case histories of patients with various cancers who received a benefit from vitamin C including: brain, breast, prostate, bladder, lung, stomach, ovarian cancer, leukemia and mesothelioma. But, since Cameron and Pauling have been considered advocates of vitamin C, here is another source. Three case examples come from a peer reviewed article whose authors come from the National Cancer Institute, the National Institutes of Health, and other universities. In a March 2006 article entitled "Intravenously administered vitamin C as cancer therapy: three cases" the authors examined clinical details of three cases in accordance with National Cancer Institute (NCI) Best Case Series guidelines (16). Tumor pathology was verified by pathologists at the NCI who were unaware of diagnosis or treatment.

Case #1

The first case involved the regression of pulmonary metastatic renal cancer in a patient who had received high-dose intravenous vitamin C therapy and no orthodox cancer therapies. The patient declined conventional cancer treatment and instead chose to receive high-dose vitamin C administered intravenously at a dosage of 65 g twice per week starting in October 1996 and continuing for 10 months. She also used other alternative therapies, including: thymus protein extract, N-acetylcysteine, niacinamide and whole thyroid extract. In June 1997 chest radiography results were normal except for one remaining abnormality in the left lung field, possibly a pulmonary scar. The patient died at the end of 2002 from lung cancer. She was a long-standing cigarette smoker.

Case #2

The second case involved a 49-year-old man with a primary bladder tumor with multiple satellite tumors extending 2-3 cm around it. The following is an excerpt from the article: "The patient declined systemic or intravesical chemotherapy or radiotherapy and instead chose intravenous vitamin C treatment. He received 30 g of vitamin C twice per week for 3 months, followed by 30 g once every 1-2 months for 4 years, interspersed with periods of 1-2 months during which he had more frequent infusions. Histopathologic review at the NIH revealed a grade 3/3 papillary transitional cell carcinoma invading the muscularis propria. Now, 9 years after diagnosis, the patient is in good health with no symptoms of recurrence or metastasis. The patient used the following supplements: botanical extract, chondroitin sulfate, chromium picolinate, flax oil, glucosamine sulfate, á-lipoic acid, Lactobacillus acidophilus and L. rhamnosus and selenium."

Case #3

The third case involved a 66-year-old woman who was diagnosed in January 1995 with a diffuse large B-cell lymphoma. The following is an excerpt from the article: "The patient's oncologist recommended local radiation therapy and chemotherapy. Although she agreed to a 5-week course of local radiation therapy, the patient refused chemotherapy, electing instead to receive vitamin C intravenously. She received 15 g of vitamin C twice per week for about 2 months, 15 g once to twice per week for about 7 months, and then 15 g once every 2-3 months for about 1 year.In late April 1995 a new left cervical lymph node was detected, and histopathologic review identified a biopsy specimen as identical to the original tumor. The patient once again refused chemotherapy and continued her program of intravenous vitamin C injections...Intravenous vitamin C therapy continued through late December 1996, at which time the patient was in normal health and had no clinical sign of lymphoma. The patient remains in normal health 10 years after the diagnosis of diffuse large B-cell lymphoma, never having received chemotherapy. The patient used additional products: â-carotene, bioflavonoids, chondroitin sulfate, coenzyme Q10, dehydroepiandrosterone, a multiple vitamin supplement, N-acetylcysteine, a botanical supplement and bismuth tablets...Patients with untreated stage III diffuse B-cell lymphoma have a dismal prognosis. This case, like the preceding one, is unusual in that the patient refused chemotherapy, which might have produced a long-term remission. It appears, nonetheless, that a cure occurred in connection with intravenous vitamin C infusions."

Although these case histories by themselves are insufficient to prove that vitamin C is an effective treatment for cancer, in the words of the authors, these histories "increase the clinical plausibility of the notion that vitamin C administered intravenously might have effects on cancer under certain circumstances. (17)"

Clinical Pharmacokinetics and In Vitro Cancer- Specific Cytotoxicity

The number of peer reviewed journal articles continues to grow that describe the clinical pharmacokinetics and in vitro cancer-specific cytotoxicity of vitamin C. For example, an article published in the Annals of Internal Medicine set out the pharmacokinetics of intravenous vitamin C (18); another article in the journal Nature discussed how vitamin C preferentially killed melanoma cells (19); and there have been several articles in Anticancer Research(20), and Oncology (21) that described how ascorbate killed various other cancer cell lines in vitro.

Vitamin C and Collagen

You may recall that Drs. Cameron and Pauling pointed out that Vitamin C could increase the number of collagen fibrils made. In the last 20 years biochemists have described the molecular basis of scurvy and in doing so have helped us understand how vitamin C and collagen are related. Apparently vitamin C plays a role in collagen metabolism by acting as a cofactor in the enzymatic reactions involved in the hydroxylation of praline and lysine. Without this hydroxylation, proper aligned stable helices of the alpha chains are not formed, so the procollagen that is formed is unstable and degraded (22).

May Prolong Life

Vitamin C has many roles that may be associated with fighting cancer including: acting as an anti-oxidant and scavenging free radicals, supporting the various immune cells, modulating cell growth and differentiation, helping to synthesize carnitine which is essential for the transport of fat to mitochondria, and possibly even strengthening collagen. Perhaps Dr. Pauling and his colleagues were right that vitamin C is a benefit to cancer patients so we will conclude with their words, "Vitamin C is not a miraculous cure for cancer, but...it significantly prolongs the life of the cancer patient...We believe that supplemental ascorbate can be of real help to all cancer patients and of quite dramatic benefit to a fortunate few.(23)"

End Notes

1 See for example: Pauling L., "Evolution and the need for ascorbic acid" Proc Natl Acad Sci 1970 Dec;67 (4):1643-8. Available at: http://www.pubmedcentral.nih.gov/picrender.fcgi? artid=283405&blobtype=pdf And see Pauling L., "The significance of the evidence about ascorbic acid and the common cold" Proc Natl Acad Sci 1971 Nov;68 (11):2678-81 Available at: http://www.pubmedcentral.nih.gov/picrender.fcgi? artid=389499&blobtype=pdf
2 Ewan Cameron and Linus Pauling, "Cancer and Vitamin C" 1979; see also original research - Cameron E, Pauling L. "Supplemental ascorbate in the supportive treatment of cancer: Prolongation of survival times in terminal human cancer" Proc Natl Acad Sci 1976 Oct;73(10):3685-9. Available at: http://www.pubmedcentral.nih.gov/picrender.fcgi? artid=431183&blobtype=pdf
3 Ewan Cameron and Linus Pauling, "Cancer and Vitamin C" 1979; see also original research - Cameron E, Pauling L. "Supplemental ascorbate in the supportive treatment of cancer: reevaluation of prolongation of survival times in terminal human cancer." Proc Natl Acad Sci 1978 Sep;75(9):4538-42. Available at: http://www.pubmedcentral.nih.gov/picrender.fcgi? artid=336151&blobtype=pdf
4 Moertel CG, et al., "Failure of high-dose vitamin C (ascorbic acid) therapy to benefit patients with advanced cancer. A controlled trial" N Engl J Med. 1979 Sep 27;301(13):687-90. Moertel CG, et al., "High- dose vitamin C versus placebo in the treatment of patients with advanced cancer who have had no prior chemotherapy. A randomized double-blind comparison" N Engl J Med. 1985 Jan 17;312(3):137- 41.
5 Ewan Cameron and Linus Pauling, "Cancer and Vitamin C" 1979, pp. 142-3.
6 See for example: Duarte TL, Lunec J. "When is an antioxidant not an antioxidant? A review of novel actions and reactions of vitamin C." Free Radic Res. 2005 Jul;39(7):671-86.
7 See for example: Tannenbaum SR, et al., "Inhibition of nitrosamine formation by ascorbic acid." Am J Clin Nutr. 1991 Jan;53(1 Suppl):247S-250S.
8 See for example: Hernanz A, et al., "Effect of age, culture medium and lymphocyte presence on ascorbate content of peritoneal macrophages from mice and guinea pigs during phagocytosis" Int Arch Allergy Appl Immunol. 1990;91(2):166-70.
9 See for example: Heuser G and Vojdani A.. "Enhancement of natural killer cell activity and T and B cell function by buffered vitamin C in patients exposed to toxic chemicals: the role of protein kinase- C" Immunopharmacol Immunotoxicol. 1997 Aug;19 (3):291-312.
10 See for example: Mitsumoto Y, et al., A long-lasting vitamin C derivative, ascorbic acid 2-phosphate, increases myogenin gene expression and promotes differentiation in L6 muscle cells.Biochem Biophys Res Commun. 1994 Feb 28;199(1):394-402.
11 See for example: Mitsuzumi H, et al., "Requirement of cytokines for augmentation of the antigen-specific antibody responses by ascorbate in cultured murine T- cell-depleted splenocytes." Jpn J Pharmacol. 1998 Oct;78(2):169-79.
12 Padayatty SJ, and Levine M. "Reevaluation of ascorbate in cancer treatment: emerging evidence, open minds and serendipity." J Am Coll Nutr. 2000 Aug;19(4):423-5. Available here: http://www.jacn.org/cgi/reprint/19/4/423
13 Padayatty SJ, and Levine M. "Reevaluation of ascorbate in cancer treatment: emerging evidence, open minds and serendipity." J Am Coll Nutr. 2000 Aug;19(4):423-5. See p. 423. Available here: http://www.jacn.org/cgi/reprint/19/4/423
14 Padayatty SJ,et al., Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med. 2004 Apr 6;140(7):533-7. Available here: http://www.annals.org/cgi/reprint/140/7/533.pdf
15 Ralph W. Moss, The Cancer Industry 1989 p. 224.
16 Padayatty SJ, et al., "Intravenously administered vitamin C as cancer therapy: three cases." CMAJ. 2006 Mar 28;174(7):937-42. Available here: http://www.pubmedcentral.nih.gov/picrender.fcgi? artid=1405876&blobtype=pdf
17 Padayatty SJ, et al., "Intravenously administered vitamin C as cancer therapy: three cases." CMAJ. 2006 Mar 28;174(7):937-42. See p. 940.
18 Padayatty SJ,et al., Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med. 2004 Apr 6;140(7):533-7. Available here: http://www.annals.org/cgi/reprint/140/7/533.pdf
19 Bram S, et al., "Vitamin C preferential toxicity for malignant melanoma cells" Nature 1980;284:629-31.
20 Leung PY, et al., "Cytotoxic effect of ascorbate and its derivatives on cultured malignant and nonmalignant cell lines" Anticancer Res1993;13:475- 80.
21 Benade L, et al., Synergistic killing of Ehrlich ascites carcinoma cells by ascorbate and 3-amino- 1,2,4,-triazole. Oncology 1969;23:33-43.
22 See for example: Davidson, V and Sittman D, The National Medical Series for Independent Study - Biochemistry 3rd Edition 1994, p. 316.
23 Ewan Cameron and Linus Pauling, "Cancer and Vitamin C" 1979 p. 130. SIZE

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Mesothelioma Research Foundation of America - The mission of the Mesothelioma Research Foundation of America is to fund research that will lead to the quickest cure for mesothelioma. Mesothelioma, a cancer of the lining of the lungs caused by asbestos exposure, has very few treatment options at this time. Since the year 2001, the foundation has funded the opening of the Mesothelioma Laboratory under the supervision of Dr. Parkash Gill at the USC/Norris who is currently investigating Veglin, an anti-angiogenesis agent. A Phase I study of Veglin has demonstrated some success in patients suffering from lymphoma, sarcoma, and colon and lung cancers. Phase II studies are on-going with the hope they will demonstrate continued clinical efficacy in mesothelioma and other cancers. For more information about the Phase II study of Veglin you may contact Dr. Gill through the mesothelioma Research Foundation of America. 1-800-909-Meso (6376) http://www.mesorfa.org

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Haelan Products offers Haelan 951, an international award-winning, super nutritious, fermented soybean protein beverage. Clinical research and numerous reports from doctors and cancer patients have demonstrated that Haelan 951 helps protect cancer patients from the toxic side-effects of chemotherapy and radiation treatments. In addition, one study found that the soy isoflavone genistein (which is found in Haelan 951) produced greater apoptosis with both chemotherapy and radiation treatments. Apoptosis means "programmed cell death" and it is a goal of most orthodox cancer therapies. Because Haelan 951 is a nutritional supplement, not a cancer treatment, it was used in this study to offset the toxicity of the treatments, not as a cancer therapy. http://www.haelan9 51.com