Cancer Adjuvant Therapy Protocol

Two of the most advanced agents currently in large chemoprevention, intervention trials, or epidemiological studies are all trans retinoic acid (ATRA) and 13-cis-retinoic acid (13-cis-RA).

Note: Retinoic acid is biologically active in two forms: all trans retinoic acid and 9-cis-retinoic acid. Vitamin A and 13-cis-RA are converted to these biologically active forms.

In a Mexican study, physicians treated 32 women with previously untreated cervical carcinoma (ages 14-60) for at least 2 months using oral 13-cis-RA (1 mg per kg body weight a day) and alpha-interferon subcutaneously (6 million units daily): 16 of the women (50%) had major reactions, including four complete clinical responses. Remission occurred in 15 of the patients within 2 months and in one patient within 1 month; toxicity to treatment was described as manageable (Espinoza et al. 1994). The positive results were replicated in other studies using a similar model (Hansgen et al. 1998, 1999).

A study at the University of California investigated the role of 13-cis-RA on the human prostate cancer cell line LNCaP. Researchers found that 13-cis-RA significantly inhibited PSA secretion and tumorigenicity (the ability to form new tumors). It was also noted that tumors that appeared (having escaped 13-cis-RA inhibition) were smaller compared to tumors in nontreated animals (Dahiya et al. 1994). During the course of 13-cis-RA therapy, prostate cancer cells became more differentiated, that is, they looked (microscopically) more like normal prostate cells.

Johns Hopkins Oncology Center evaluated a combination of phenylbutyrate and 13-cis-RA as a differentiation and antiangiogenesis strategy against prostate cancer. (Phenylbutyrate, considered nontoxic, is used to arrest tumor growth and induce differentiation of premalignant and malignant cells.) Tissue examination of tumors showed decreased cell proliferation and increased apoptosis, as well as reduced microvessel density in animals treated with13-cis-RA and phenylbutyrate; the growth of the tumor was inhibited by 82-92%. In contrast, researchers reported 13-cis-RA and phenylbutyrate (when used singularly) suboptimal in terms of clinical benefit (Pili et al. 2001).

A pilot study conducted at M.D. Anderson Cancer Center found ATRA ineffective as a long-term treatment for chronic myelogenous leukemia (CML). Only four of 13 subjects showed a transient, nonsustaining indication of an antileukemic effect (Cortes et al. 1997). However, researchers at the Leukemia Research Fund Centre for Adult Leukemia (London) found combinations of therapeutic agents that included ATRA promising in the treatment of CML. An encouraging combination included alpha-interferon plus ATRA, each agent reducing proliferation 50-60% (Marley et al. 2002).

Cisplatin (a popular chemotherapeutic agent) shares a similar chemotherapeutic profile with ATRA (the ability to induce cytotoxicity through apoptosis). Researchers at the University of California concluded that a combination of ATRA and cisplatin induced apoptosis in significantly more cancer cells (particularly in ovarian and head and neck carcinomas) than either drug alone (Aebi et al. 1997). Lastly, research from Italy showed that a combination of ATRA and IL-2 showed therapeutic value in treating resistant metastatic osteosarcoma (a malignant tumor of the bone) (Todesco et al. 2000).

For decades, researchers have searched for ways to minimize the devastation visited upon the heart during Adriamycin therapy. Adriamycin, though relatively effective, wields a damaging blow to the heart muscle. Several animal studies, including one reported in the Journal of Nutrition, indicated that supplemental vitamin A reduced Adriamycin-induced inflammation and preserved tissue. Vitamin A appears not only to counter Adriamycin damage, but also to increase survival of test animals (Tesoriere et al. 1994). Vitamin A extends similar protection to patients using cisplatin (a drug often used for bladder and ovarian cancer, as well as small cell carcinoma).

Radiation-induced lung injury frequently limits the total dose of thoracic radiotherapy that can be delivered to a patient undergoing treatment, restricting its purposed effectiveness. Several animal studies suggest that supplemental vitamin A may reduce lung inflammation after thoracic radiation and modify radiotherapeutic damage to the lungs (Redlich et al. 1998).

Vitamin A (in dosages of 25,000 IU a day) offers significant protection against radiation-induced tissue damage. Various cancer patients use more than 100,000 IU of a water-soluble vitamin A liquid a day, a dosage that must be physician supervised. Do not supplement with vitamin A if the cancer involves the thyroid gland or if the liver is damaged. Both professionals and patients should consult Appendix A to read about avoiding vitamin A toxicity. Good food sources of vitamin A include liver and fish liver oils and green and yellow fruits and vegetables such as apricots, asparagus, broccoli, cantaloupe, carrots, collards, papayas, peaches, pumpkins, spinach, and sweet potatoes. High-potency water-soluble vitamin A is available as a dietary supplement.

Vitamin C (ascorbic acid)--has a chemotherapeutic effect on many cancers, promotes collagen production, sequestering the tumor, and reduces the toxicity of conventional therapies
Linus Pauling, winner of the Nobel Prize for Chemistry in 1954 and the Nobel Prize for Peace in 1963, believed strongly that vitamin C could play an important role in cancer treatment. More recently, various scientists have defied the possibility, suggesting health hazards with megadose levels of ascorbic acid. Abram Hoffer, M.D. and Ph.D., (a Canadian psychiatrist who has infinitely contributed to the integrated cancer movement), once commented: "Accusations will come and go, but the benefits of vitamin C will endure."

About 30 years ago, Dr. Pauling suggested to Ewan Cameron, a Scottish surgeon, that he administer 10 grams of vitamin C a day to patients with advanced cancer for whom conventional treatments had ceased to be of benefit (Cameron et al. 1993). Over an 8-year period, 500 patients with varying stages and types of cancer were treated with vitamin C therapy. The initial observation showed those receiving 10 grams of vitamin C a day improved their state of well-being, as measured by increased appetite and mental alertness, as well as a decreased need for pain-killing drugs. A retrospective analysis of the study showed that those using vitamin C lived considerably longer than those not supplemented.

Fortunately, a new breed of vitamin C proponents are emerging, apparently as convinced of the merits of vitamin C as the ascorbic acid pioneers. Various clinics are using injectable vitamin C and showing results. Dr. Hugh Riordan, recognized as the world authority on this procedure, practices from Wichita, KS, at the Center for the Improvement of Human Functioning International. Dr. Riordan's vitamin C story began in 1984 when he treated his first cancer patient, a 70-year-old renal cell carcinoma patient with metastasis to the lung and liver, using injectable vitamin C. (Renal cell carcinoma is deadly, having only a 5% response rate.)

The initial treatment began with 15 grams of vitamin C administered intravenously 2 times a week; showing excellent tolerance, the vitamin C dosage was increased to 30 grams twice weekly. Within 6 weeks, the patient showed a favorable response to treatment and at the 12-week interval was pronounced tumor-free. The patient lived 14 additional years and died of congestive heart failure with no evidence of tumors.

In 1989, the Wichita Center formed a research group, referred to as the RECNAC Team. A philanthropist funded their research, giving instructions to isolate the cancer mechanism and to find a nontoxic treatment to end the scourge. A team of 13 physicians and scientists joined forces in an effort to fulfill the donor's commission.

In light of the favorable initial response to IV vitamin C, the first agent the group investigated was ascorbic acid. The group found vitamin C preferentially toxic to tumor cells, that is, it kills tumor cells long before it kills normal cells. Researchers at the NIH had reached similar conclusions and in 1969 prophesied that vitamin C would become the chemotherapeutic agent of the future.

The biochemical nature of vitamin C is fascinating in regard to cancer. In low doses, vitamin C assumes the nature of an antioxidant; in high dosages, vitamin C changes roles and becomes a prooxidant, inducing peroxide production. Tumor cells have a relative catalase deficiency, an enzyme necessary to detoxify hydrogen peroxide to water and oxygen. A 10- to 100-fold difference in catalase concentrations exists between tumor cells and normal cells. Without the protection of catalase, peroxide accumulates in cancerous cells, along with aldehydes (toxic byproducts of the reaction), causing death to malignant cells. On the other hand, normal, healthy tissues have the protection of the detoxification enzyme and are spared destruction by peroxide and aldehyde. Comment: Vitamin C, a virtually nontoxic nutrient (Bowie et al. 2000), could cause a transient diarrhea if not absorbed properly.

Other advantages of vitamin C, apart from its chemotherapy-like effectiveness, are its wide window of safety compared to standard chemotherapeutics and its ability to preserve immune function. Many patients succumb, not because of the cancer, but rather from an infection, a postchemotherapeutic response, resulting from a battered immune system. Vitamin C appears to allow a totally different profile to emerge; the immune system is protected and pathogenic organisms are less likely to attack.

Vitamin C is preferentially toxic to many types of cancer cells, including 20 different melanoma lines. Ovarian cell lines are more susceptible to vitamin C-induced toxicity than pancreatic cells, replicating the end results observed when administering standard chemotherapeutics to pancreatic patients. Breast cancer appears to be one of the most responsive cancers to IV vitamin C.

As research continued, it was found that much higher concentrations of vitamin C were required to kill cancer cells than originally thought, about 600 mg/dL. Also, as the density of the cells increased, the efficacy of vitamin C decreased. These discoveries were relevant, for the RECNAC team found it extremely difficult to reach vitamin C concentrations greater than 200 mg/dL even when administered intravenously (Riordan et al. 2000). The team began looking for ways to increase the sensitivity of tumor cells to vitamin C.

Dr. Riordan discovered that alpha-lipoic acid (a water- and lipid-soluble antioxidant that recycles vitamin C for continued service) enhanced the toxic effect of ascorbic acid. Lipoic acid decreased the dose of vitamin C required to kill tumor cells from 700 to 120 mg/dL (Riordan et al. 2000). The kill mentality of vitamin C is further enhanced by 1000 mcg of vitamin B12, which forms cobalt ascorbate (a benevolent but toxic-to-cancer-cells agent). Vitamin K, selenium, quercetin, niacinamide, biotin, and grape seed extract are also regarded as potentiation factors.

The goal is to achieve and maintain (for a period of time) 400 mg/dL of vitamin C in the plasma; at this concentration, every cancer cell line tested is sensitive to vitamin C. After reaching an ascorbic acid peak (as occurs during infusion), the level returns to near baseline levels 24 hours after the IV.

Another perk regarding vitamin C is its ability to increase collagen production, the glue that holds the body together. Vitamin C is required for the hydrox-ylation of proline, which in turn is required for collagen production. Much of Cameron/Pauling's research centered upon vitamin C's ability to inhibit enzymes that degrade or break down the extracellular matrix. The RECNAC team affirmed their work but added that vitamin C dramatically increased the collagen within tumor cells, an act that tended to immobilize the cells, gluing the cell in place. Without mobility, metastasis is blocked.

The RECNAC team found it difficult to produce enough vitamin C-induced cytotoxicity to kill out prostate cancer (PC3 cancer cell line). Up to 900 mg/dL resulted in only 50% cytotoxicity. But other mechanisms, including collagen synthesis, render vitamin C valuable to prostate cancer patients. According to Neil Riordan (son of Dr. Hugh Riordan), "We have prostate cancer patients (17 years out) with rock-hard prostate cancer that has never metastasized who receive periodic infusions of vitamin C." Vitamin C seems to increase collagen production so effectively that cancer cells are locked, or glued, in place, not able to migrate to other tissues.

Because vitamin C (supported by lipoic acid) appears to have come of age as a cancer therapy, it is strongly advised that patients contact a physician trained in administering infusions and monitoring progress. By giving vitamin C intravenously, doctors can achieve a blood saturation that far eclipses that attained by administering vitamin C orally (200% versus 2%). A high dose is critical to achieve a chemotherapeutic kill.

A Hickman line allows large doses of vitamin C to be self-administered at home on a daily to weekly basis over a period of months, stepping down or up in frequency according to response. Otherwise the treatment can be administered as an outpatient. Dr. Riordan says that contraindications to vitamin C therapy are few but include individuals with kidney failure and on dialysis, as well as those with hemochromatosis. Also, physicians should screen for a red blood cell glucose-6 phosphate dehydrogenase deficiency, a rare condition whose presence can lead to a hemolytic crisis involving red blood cell breakdown.

Large IV doses of vitamin C should be reached gradually to establish tolerance. Begin with 15 grams for one or two sessions and then advance to 50 grams and, if necessary, to 100 grams. The exact dose is determined by the individual's plasma saturation immediately after an infusion. Never stop the therapy abruptly because a rebound effect could result in scurvy. Patients should allow weeks or even months weaning off the treatment, with oral vitamin C therapy used on the days between infusions.

The Center for the Improvement of Human Functioning has completed a 10-year research project using high dose IV vitamin C. Dr. Riordan's patented method recently underwent Phase I clinical trials at the University of Nebraska Medical School Hospital, establishing the nontoxicity of treatment. Dr. Riordan is now proceeding with a Phase II clinical trial, under the auspices of the National Institutes of Health, using therapeutic doses of vitamin C on renal adenoma patients. While a number of orthomolecular physicians are using IV vitamin C therapy, it is recommended that Dr. Riordan's protocol become the backbone of the therapy. Instructions are available to physicians upon request from the center.

Center for the Improvement of Human Functioning
3100 North Hillside Avenue
Wichita, KS 67219
(316) 682-3100

Other chemotherapeutic credits awarded to vitamin C:
Vitamin C prolongs the lives of test animals undergoing conventional treatment by protecting normal cells against chemotherapy-induced toxicity; in tandem, vitamin C increases the cytotoxicity targeted at the cancer (Antunes et al. 1998; Giri et al. 1998). Dr. Kedar N. Prasad (University of Colorado) determined that when 5-FU was administered in union with vitamin C, the kill rate was boosted from 38-95.5%. X-ray therapy, according to Dr. Prasad, decreased cancer growth 72%, but adding vitamin C to the regime decreased cancer growth 98.2%. Dr. Prasad, agreeing with most 21st century scientists, endorses a full spectrum antioxidant rather than emphasizing isolated nutrients (Prasad et al. 1999; Moss 2000).

Infection arising from the ulcer-causing bacterium Heliobacter pylori increases the risk of developing stomach cancer (Uemura et al. 2001), as well as pancreatic cancer (Stolzenberg-Solomon et al. 2001). High doses of vitamin C inhibit the growth of H. pylori, both in vitro and in vivo (Zhang et al. 1997). A study showed vitamin C levels to be consistently low in individuals with the H. pylori infection (The Analyst 2002).
Researchers from Cornell and Seoul National universities found that vitamin C inhibited the cancer-causing effects of hydrogen peroxide on gap junction. Gap junction refers to small channels that allow communication between cells, a process referred to as gap junction intercellular communication (GJIC). If hydrogen peroxide is not blocked, GJIC falters, encouraging the carcinogenic process, specifically abnormal cell growth. Note: It was determined from the study that quercetin was even more protective than vitamin C (Lee 2002).
The NCI recently reported that frequent intake of vitamin C from food and supplement sources was associated with a protective effect against multiple myeloma, particularly among Caucasians. African Americans benefited less from ascorbic acid intake (Brown et al. 2001).
NF-kB is a central mediator of altered gene expression during inflammation and is implicated in a number of pathologies, including cancer. Irish researchers showed that vitamin C inhibited the activation of NF-kB by multiple stimuli, including IL-1 and TNF-alpha (Bowie et al. 2000).
It should be reemphasized that oral vitamin C does not bestow equal benefits compared to IV vitamin C. If a patient with a hard tumor elects to use oral vitamin C, ascorbic acid buffered with sodium may produce better results. If the cancer is bloodborne (leukemia, lymphoma, or myeloma), ascorbic acid crystals buffered with calcium appears to offer greater advantage. Recall that the majority of the patients enrolled in the Cameron/Pauling vitamin C cancer study used from 6-12 grams a day. Food sources of vitamin C are berries, citrus fruits, papayas, and pineapple, as well as tomatoes, broccoli, Brussels sprouts, dandelion and mustard greens, peas, sweet peppers, and spinach.

Vitamin D--promotes differentiation, inhibits angiogenesis, regulates cell division
According to Bill Sardi, journalist and consumer advocate, the news media occasionally reports a cancer cluster occurring among workers in a specific building. Often the individuals work out of dark basement offices or sealed sterile rooms where they must wear space-like protective clothing. Indoor environmental screening seldom identifies a cause contributory to the cancers. Rather, a growing body of evidence suggests the cancers may be attributable to a missing protective factor, the sunshine vitamin, vitamin D (Sardi 2000).

Current recommendations to avoid natural sunrays to thwart the possibility of a deadly melanoma may be allowing other endangerments. For more than 50 years, medical literature has affirmed that regular sun exposure is associated with a substantial decrease in death rates from certain types of cancers (NSN 2000). It is estimated that moderate sunning without sunscreen--enough to avail oneself of vitamin D production but not enough to damage the skin--could prevent 30,000 cancer deaths in the United States each year (Ainsleigh 1993). The most damaging of the sun's rays occur between the hours of 10 a.m. and 3 p.m. and are thus the hours demanding the greatest watchfulness.

Cancer Research reported that evidence points to a prostate, breast, and colon cancer belt in the United States, which lies in northern latitudes under more cloud cover than other regions (Studzinski et al. 1995). The logic propelling this theory hearkens back to the fact that certain regions in the United States, such as the San Joaquin Valley cities and Tucson, AZ; Phoenix, AZ; Albuquerque, NM; El Paso, TX; Miami, FL; Jacksonville, FL; Tampa, FL; and Orlando, FL; have a lower incidence of breast and bowel cancers. Conversely, New York; Chicago; Boston; Philadelphia; New Haven, CT; Pittsburgh; and Cleveland, OH; have the highest rates of breast and intestinal cancer of the 29 major cites in the United States. Researchers have connected the dots and found that greater hours of year-round sunlight correlate to a lower rate of breast and intestinal cancer.

Vitamin D is formed in the skin of animals and humans by the action of shortwave UV light, the so-called fast-tanning sunrays. Precursors of vitamin D in the skin are converted into cholecalciferol, a weak form of vitamin D3, which is then transported to the liver and kidneys where enzymes convert it to 1,25-dihydroxycholecalciferol, the more potent form of vitamin D3 (Sardi 2000). Although vitamin D exists in two molecular forms, vitamin D3 (cholecalciferol) found in animal skin and vitamin D2 (ergocalciferol) found in yeast, vitamin D3 is believed to exhibit more potent cancer-inhibiting properties and is therefore the preferred form to use.

Dark-skinned people require more sun exposure to produce vitamin D because the thickness of the skin layer (the stratum corneum) affects the absorption of UV radiation. Black human skin is thicker than white skin and thus transmits only about 40% of the UV rays needed for vitamin D production. Darkly pigmented individuals who live in sunny equatorial climates experience a higher mortality rate from breast and prostate cancer when they move to geographic areas that are deprived of sunlight exposure in winter months (AngwaFo1998; Sardi 2000).

Women with breast cancer are twice as likely to have a fault in the gene required to utilize vitamin D, according to Joseph Mercola, D.O. New research from London suggests that women with polymorphisms (genetic variations) of the vitamin D receptor gene may be less able to benefit from the nutrient. The study added to the increasing evidence that vitamin D receptor gene polymorphisms play a role in the disease process (Bretherton-Watt et al. 2001). Identifying the at-risk groups (through the assessment of genetic variations in the vitamin D receptor) appears to be a forthcoming tool for planning intervention strategies.

Researchers reported that human leukemia cells (cultured in the presence of vitamin D) exhibited a reduced rate of tumor growth when injected into mice. Cells grown in vitamin D3 failed to form detectable tumors in 11 of 12 inoculated mice (Wang et al. 1997). Dutch researchers explained the anticarcinogenic profile of vitamin D, saying it confronts multiple stages of cancer development, including apoptosis, differentiation, angiogenesis, and metastasis, as well as regulating the cell growth cycle (van den Bemd et al. 2002).

Since vitamin D can cause calcium to be released from bones (a condition referred to as hypercalcemia), large doses of vitamin D cannot be used in patients whose medical history or genetics puts them at increased risk. Because of the value gained from vitamin D, researchers are continuously searching for ways to administer the vitamin without risking toxicity. An interesting combination has emerged: vitamin D3 and vanadium (a metallic element). Using this combination, vitamin D retains its anticancer activity and vanadium addresses the problem of hypercalcemia (Basak et al. 2000).

To test the efficacy of the combination, rats were supplemented with vanadium or vitamin D3 or both vanadium and D3 4 weeks prior to induced liver cancer and continued thereafter until the 20th week. After 20 weeks of supplementation, the vitamin D3-vanadium combination had significantly reduced the number and size of abnormal hepatic nodules. The combination also showed an additive effect, reducing the number and size of hyperplastic nodes from 83.3% to 37.5%. In addition, vanadium proved effective, blocking the entry of calcium into cells.

Researchers at Johns Hopkins University have developed a modified form of vitamin D (referred to as a deltanoid) and determined that it delays the onset and reduces the number of skin cancers in laboratory mice. The research team microscopically altered the structure of vitamin D, producing a potentially effective cancer therapeutic. The vitamin D analog retained its anticancer profile but diminished the threat of hypercalcemia. The most effective of the four analogs tested was a doubly modified hybrid compound containing fluorine (Posner 2000).

During the study, mice were painted with a chemical substance, inducing cancerous tumors; concurrently the animals were given the deltanoid. After 20 weeks, the fluorine-containing analog had reduced the incidence of tumors more than 25%, while the actual number fell 63% (BBC News 2000). Deltanoids are in the early stages of development and, unfortunately, it may take 10 years before they become available. In the interim, Dr. Gary Posner (Johns Hopkins University) presented the findings before the American Chemical Society, saying the development of a drug with the possibility of preventing cancer represents a historic milestone. It is possible that deltanoids could lessen the need for hormone treatments or aggressive chemotherapy. Patients could theoretically stay on the treatment for the remainder of their life to keep the cancer from advancing.

Recent studies indicate that moderate or severe hypovitaminosis D was present in 66% of patients taking daily vitamin D in amounts less than the recommended dosage for their age; 37% of patients taking vitamin D daily were still found deficient. A landmark paper in the American Journal of Clinical Nutrition showed that adults may need (at a minimum) 5 times the 200-IU RDA, or 1000 IU a day, to protect against cancer (Vieth 1999). Therapeutic dosages of vitamin D typically range from 800-4000 IU a day. Monthly kidney function blood tests (creatine, BUN, etc.) should be done if daily vitamin D intake exceeds 1400 IU. These tests are included in most standard blood chemistry tests that cancer patients take regularly to guard against anemia and overt immunosuppression.

Food sources of vitamin D include egg yolks, organ meats, fortified dairy products, butter, cod liver oil, and cold-water fish, such as salmon, herring, and mackerel. Vitamin D enhancers are vitamins A and C, calcium, magnesium, phosphorus, and choline. Antagonists are mineral oil, phenobarbital, and laxatives.

Vitamin E--is an antioxidant that can protect smokers, reduces radiation damage, potentiates chemotherapy, and inhibits many types of cancers
Researchers are examining the inhibitory role of vitamin E in the growth of a number of human tumor cells, as well as its defensive functions in overcoming treatment-induced toxicity. The impact of vitamin E (perhaps acting through its antioxidant strengths) is significant, as evidenced by the following studies:

After examining 29,000 male smokers in Finland, researchers found that high blood levels of alpha-tocopherol reduced the incidence of lung cancer about 19%. The relationship appears stronger among younger persons and among those with less cumulative smoke exposure. These findings suggest that high levels of alpha-tocopherol, if present during the early critical stages of tumorigenesis, may inhibit lung cancer development (Woodson et al. 1999).
A combination of vitamin E and pentoxifylline (PTX), a drug that inhibits abnormal platelet aggregation, allowing more blood to reach irradiated areas, resulted in a 50% regression of superficial radiation-induced fibrosis (the proliferation of fibrous connective tissue) in half of the patients studied (Gottlober et al. 1996; Delanian 1998). A suggested dosage is 800 mg a day of PTX and 1000 IU per day of vitamin E.
The first report of an antimelanoma effect obtained from vitamin E succinate in vivo came recently from the Southern Illinois University School of Medicine (Malafa et al. 2002).
Gamma-tocopherol inhibits COX-2 activity, demonstrating anti-inflammatory properties (Jiang et al. 2001; LE 2002).
The use of vitamin E, in combination with vitamins A and C, led to a fourfold reduction in p53 mutations (Brotzman et al. 1999). This is an extremely important finding because p53 mutations indicate a more malignant, aggressive form of cancer.
Prasad evaluated (1) vitamin E's ability to reduce cancer growth, (2) the ability of chemotherapeutic agents to inhibit cancer, and (3) the reduction in tumor growth using a combination of vitamin E and chemotherapeutic agents. The following chart illustrates Dr. Prasad's findings (Prasad et al. 1999; Moss 2000).
The American Journal of Epidemiology reported that men with a high intake of vitamin E are 65% less likely to develop colorectal adenomas (precursors to colon cancer) compared to men with low vitamin E intake (Tseng et al. 1996).
A Finnish study demonstrated lower morbidity and mortality from prostate cancer in men taking 50 mg of synthetic alpha-tocopherol daily. Subsequent testing determined gamma-tocopherol to be superior, however, to alpha-tocopherol in terms of cell inhibition (Moyad et al. 1999). Johns Hopkins School of Hygiene and Public Health showed that men in the highest fifth of the distribution for gamma-tocopherol had a fivefold reduction in the risk of developing prostate cancer compared to those in the lowest fifth. In addition, statistically significant protection from high levels of selenium and alpha-tocopherol occurred only when gamma-tocopherol concentrations were also high (Helzlsourer et al. 2000).
Researchers from the University of Rochester (reporting in the May 28, 2002 issue of the Proceedings of the National Academy of Sciences) identified vitamin E's mode of efficacy in regard to prostate protection. Vitamin E interferes with two proteins (the receptor for testosterone and prostate-specific antigen [PSA]). The fewer androgen receptors there are on a prostate cancer cell, the less capable the remaining receptors are of turning on genes that stimulate prostate cancer growth and progression. PSA serves as a good marker molecule for androgen receptor activity (Mercola 2002b).
Washington State University announced that toco-trienols, quite similar to a tocopherol (but for the addition of an unsaturated tail in its chemical structure), accumulate in adipose tissues, including mammary glands. If a cell becomes diseased, the tocotrienol is prepared for action, ready to inhibit growth and regulate aberrant cellular activity at its onset. Curiously, the more cancerous the cell, the more susceptible it is to tocotrienols. Paul Sylvester (assistant professor of zoology) commented before the National Institutes of Health that scientists have been focusing upon the wrong form of vitamin E (the tocopherols), which show little protection against breast cancer. Tocotrienols appear to inhibit proliferation of human breast cancer cells by as much as 50% (Nesaretnam et al. 1998; Timon Press Release). Results suggest that tocotrienols are effective inhibitors of both estrogen receptor-negative and -positive cells and that combinations with tamoxifen should be considered as a possible improvement in breast cancer therapy. This strategy could significantly reduce the amount of tamoxifen required to impact the cancer (Guthrie et al. 1997).
Cortisol (associated with poorer survival) and IL-6 (a negative marker for various cancers) were significantly lower in 24 laboratory animals that received alpha-tocopherol before a cortisol-IL-6 challenge (Webel et al. 1998).
Vitamin E ...................Chemotherapeutic Agent ..........Combination with Vitamin E
47% growth inhibition ..............Bleomycin, 46% .........tumor reduction 71% reduction
...............................5-FU, 37% tumor reduction .........85% reduction
.............................Adriamycin, 58% tumor reduction ...88% reduction
..............................Cisplatin, 57% tumor reduction ......82% reduction

A suggested vitamin E dosage is from 400-2000 IU a day of alpha-tocopherol in union with gamma E tocopherol. (For optimal results, use 80% alpha-tocopherol and 20% gamma-tocopherol.) Recall that tocotrienols have emerged as a star player in both breast cancer prevention and management. A tocotrienol dosage is 240 mg each day. Good food sources of vitamin E are cold-pressed vegetable oils, wheat germ, eggs, dark green vegetables, nuts, brown rice, and butter.

Vitamin K--is a growth regulator, promotes apoptosis, and decreases proinflammatory cytokines
Scientists at the University of Pittsburgh Cancer Institute (UPCI) have discovered a novel form of vitamin K that appears extremely promising in the treatment of primary liver cancer, a type notoriously resistant to chemotherapy. The research in the Journal of Biological Chemistry described an innovative approach to treat (and possibly prevent) cancer by triggering apoptosis (Ni 1998).

The UPCI team found that a vitamin K analog, Compound 5 (CPD5), causes an imbalance in the normal activity of enzymes that controls the addition or removal of small molecules (phosphate groups) from proteins inside cells. Specifically, CPD5 blocks the activity of enzymes (protein-L-Tyrosine phosphatases) that normally remove phosphate groups from selected proteins inside liver cancer cells. CPD5, however, does not interfere with another group of enzymes called protein L-Tyrosine-kinases, which add phosphate groups to the same proteins. The result is an excess of L-Tyrosine-phosphorylated proteins, which triggers a variety of activities within cells, including the shutting down and subsequent death of the cell.

Dr. Brian Carr, professor of surgery at the Thomas E. Starzl Transplantation Institute and director of the Liver Cancer Center at UPCI, believes it may be possible to remove some individuals from liver transplant waiting lists if CPD5 is as effective in humans as it is experimentally. However, the vitamin K compound is not limited to killing liver cancer; in tissue culture the compound was also effective against melanoma and breast cancers. Although the new vitamin K is not in clinical testing at this time, clients and physicians may contact the UPCI's Cancer Information and Referral Service at (800)237-4PCI (4724) or (412) 624-1115 for periodic updates regarding the treatment. Inquirers can also visit the university's website at http://www.cml.upmc.edu.

Researchers reporting in the journal Cytokine found vitamin K compounds potently inhibited IL-6 production by lipopolysaccharide-stimulated fibroblasts, which are recognized as rich sources of cytokines (Reddi et al. 1995). This finding has significant anticancer implications because overexpression of IL-6 is intricately involved in the inflammatory process, bone resorption, the activation of telomerase, and cancer proliferation. A suggested vitamin K dosage is 10 mg a day. Interesting research relating to the use of vitamin K concurrent with anticoagulant therapy (not usually a recommended practice) appears in the protocol Cardiovascular Disease: Comprehensive Analysis in the section dedicated to vitamin K.

OTHER FACTORS AFFECTING PATIENT OUTCOME

What Should Cancer Patients Eat?
For a cancer patient who appreciates the importance of a properly planned diet, the task is daunting. The diversity of the population minimizes the likelihood of a universal diet; nonetheless, most diets are hyped as being nutritionally correct for everyone. This section of the material explores dietary variables, conceding that many generalities exist, that is, eat organic when available and eat on schedule to avoid blood glucose swings. Select foods characterized by color and texture. Avoid synthetic and refined foods: white flour products and sugar as well as trans fats (those fats altered by overheating, hydrogenation, and refining). Avoiding well done meats and exposure to hetero-cyclic amines (formed during high temperature cooking) eliminates another significant cancer source (Zheng et al. 1998).

Tumors are primarily obligate glucose metabolizers, meaning they require sugar for survival. Even though the brain normally uses high amounts of glucose, hepatomas (a tumor of the liver) and fibrosarcomas (a sarcoma that contains fibrous connective tissue) consume roughly as much glucose as the brain. Evidence suggests that various types of cancer have even greater sugar requirements, with some consuming nearly twice as much glucose as the brain.

Some Americans continuously satisfy cancer's appetite, ingesting as much as 295 pounds of sugar a year. Epidemiological studies showed that the risk of biliary tract cancer (in older women) more than doubled when their diet was structured around sugar-laden choices. It is common for breast cancer patients to confess having an insatiable craving for sugar.

Cancer Adjuvant Therapy Pg (1) (2) (3) (4) (5) (6) (7)

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