This webpage explains some important experiments in nutrition and cancer.
     We hope that people who read these materials will have a better chance to save their lives.
     Please read these pages carefully and think about them. You may wish to use this very valuable dietary approach to cancer.

     Strong evidence suggests that people who eat five or more servings of fruits and vegetables a day can cut their risk of cancer from 20% to 50% when compared to those who consume one serving or less. The chemical composition of fruits and vegetables is complex, which makes it difficult to determine which compound or combination of compounds may provide protection against cancer. Eating a wide variety of plant-based foods is the best way to get the necessary components.

Garlic

     Garlic is promoted for use as a preventive measure against the formation of cancer. Although several compounds in garlic may have anti-cancer properties, the diallyl sulfide compounds are said to play a major role. These compounds are reported to prevent cancer by decreasing the activation of carcinogens within the body, reducing the production of carcinogens, and increasing the body's ability to repair damaged DNA. There have been claims that garlic has certain immune boosting properties that may help the body fight off diseases, such as colds or the flu, as well as reduce cancer cell growth. These claims are currently under investigation.
    Several studies from around the world have found that people who consumed higher levels of garlic had a lower risk of certain types of cancers. In particular, human studies have suggested that garlic may play a protective role in stomach, prostate, and colorectal cancers, skin cancer, esophageal cancer.
Garlic (administered intralesionally to mice) was significantly more effective than BCG (bacille Calmette-Guerin), a weakened form of the tuberculosis bacilli, in treating bladder cancer (Lau et al. 1986).
     According to data released at the First World Congress on the Health Significance of Garlic and Garlic Constituents, garlic extract reduced the incidence of breast cancer (in mice) by 70-90% (Langer 1991).
Diallyl disulfide, a sulfur compound, induced apoptosis in noncell lung cancer cells (Hong et al.2000); Diallyl sulfide, a component of garlic oil, inhibited hepatocarcinogenicity following carcinogenic exposure (Hayes et al. 1987); S-allyl cysteine (a derivative of aged garlic extract) inhibited human neuroblastoma cell growth in vitro (Welch et al. 1992); allixin, one of the compounds of aged garlic extract, inhibited the development of skin cancer (Nishino et al. 1990). Diallyl sulfide was highly inhibitory during the initiation phase of esophageal cancer (Wargovich et al. 1992; Leigh, http://www.herb.org/greenpapers/garlic.htm).
S-allyl cysteine (SAC) inhibited proliferation and cell growth of nine human and murine melanoma cell lines, producing positive end results without side effects (Takeyama et al. 1993). Of equal importance, garlic modulated major cell differentiation markers of melanoma. As the cell shows distinguishable characteristics (differentiation), it eventually loses its uncontrollable propensity to divide and replicate.
Researchers from the University of Texas M.D. Anderson Cancer Center (Houston) found that S-allyl cysteine and diallyl sulfide reduced colonic damage and the incidence and frequency of colon tumors if administered 3 hours prior to each carcinogenic injection. S-allyl cysteine inhibited colonic damage by 36% and diallyl sulfide by 47% (Sumiyoshi et al. 1990). Michael Wargovish, M.D. (Houston), claims that diallyl sulfide is one of the most active chemopreventive agents known.
Garlic stimulates proliferation of lymphocytes, those cells comprising 25% of total white blood cells that carry out the principal responsibilities of the immune system (Colic et al. 2000).
Garlic quickens macrophage phagocytosis, a process by which microorganisms and cellular debris are engulfed and destroyed (Lau et al. 1991a,b).
Fraction 4 (F4), a protein isolated from aged garlic extract, enhanced the cytotoxicity of human lymphocytes. Although F4 alone increased cytotoxicity, the effect was amplified when F4 was combined with suboptimal doses of interleukin-2. Data collected from UCLA School of Medicine indicate that F4 is an efficient immune potentiator and may be used for immune therapy (Morioka et al. 1993).
Garlic is on the Commission E (Germany's regulatory agency for herbs) list of approved herbs, and they suggest a dosage of fresh garlic equal to 4 gm/day, or about one large clove per day.
Consumption of large amounts of garlic may lead to irritation of the gastrointestinal tract, causing stomach pain, gas, and vomiting. One study suggests that the use of garlic may increase the risk of bleeding due to its anti-blood clotting properties. It should not be used by people who are undergoing surgery, especially if given blood thinners or if postoperative bleeding is of concern. People on blood thinner medication, such as warfarin, should consult with their doctor before taking garlic supplements.

References
Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum lipoproteins and cholesterol metabolism: a randomized controlled trial. JAMA. 1998;279:1900-1902.
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin, Tx: American Botanical Council; 1998.
Hasler CM. Functional foods: their role in disease prevention and health promotion. Food Technol. 1998;52:57-62.
Levi F, Pasche C, La Vecchia C, Lucchini F, Franceschi S. Food groups and colorectal cancer risk. Br J Cancer 1999;79:1283-1287.
Miller LG. Herbal medicinals: selected clinical considerations focusing on known or potential drug-herb interactions. Arch Intern Med. 1998;158:2200-2211.
Milner JA. Garlic: its anticarcinogenic and antitumor properties. Nutr. Rev. 1996;54:S82-S86.
Riggs DR, DeHaven JI, Lamm DL. Allium sativum (garlic) treatment for murine transitional cell carcinoma. Cancer. 1997;79:1987-1994.
Sundaram SG, Milner JA. Diallyl disulfide induces apoptosis of human colon tumor cells. Carcinogenesis. 1996;17:669-673. Steinmetz KA, Kushi LH, Bostick RM, Folsom AR, Potter JD. Vegetables, fruit, and colon cancer in the Iowa Women's Health Study. Am J Epidemiol. 1994;139:1-15.
You WC, Blot WJ, Chang YS, et al. Allium vegetables and reduced risk of stomach cancer. J Natl Cancer Inst. 1989;81:162-164.

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Tomatoes

People who have diets rich in tomatoes, which contain lycopene, appear to have a lower risk of certain types of cancer, of the prostate, lung, and stomach.
These scientists believe lycopene to be a powerful antioxidant, a compound that blocks the action of activated oxygen molecules, known as free radicals, that can damage cells. The antioxidant activity of lycopene is at least twice as great as beta carotene, another carotenoid that is also thought to be an effective cancer-preventing nutrient . Lycopene is considered one of the more effective antioxidants because it is not converted to vitamin A when ingested . Conversion to vitamin A weakens the antioxidant properties of carotenoids like beta carotene.
Dietary lycopene comes primarily from tomatoes, although apricots, guava, watermelon, papaya, and pink grapefruit are also significant sources. Tomatoes are the best source of lycopene. Initial studies have suggested that cooked tomatoes (ie, tomato sauce or paste) are a better source of available lycopene than raw tomato juice because the heating action allows the body to quickly absorb the lycopene. Lycopene can also be taken in the form of soft-gel capsule supplements.
In recent years, the role of the diet in preventing the occurrence of cancer has been a popular and important area of research. The examination of the role of other carotenoids, specifically beta carotene, in preventing cancer began in the 1920s. However, interest in lycopene did not really begin until the late 1980s when it was found that the antioxidant activity of lycopene was twice that of beta carotene. By the late 1990s, over 70 studies have looked for a link between diets high in tomatoes (as a source of lycopene) and a lower risk of cancer.
Studies suggest that diets rich in tomato intake may account for a reduction in the risk of several different types of cancer. The strongest evidence is for a protective effect against cancers of the lung, stomach, and prostate gland. There may also be a protective benefit against cancers of the cervix, breast, oral cavity, pancreas, colorectum, and esophagus.
Population studies from many countries have shown that the risk of developing some cancers are lower in people who either have diets high in tomato products or have higher levels of lycopene in their blood. A population-based case-control study recently found that lycopene from tomato-based foods was associated with a small reduction in risk for prostate cancer. However, a direct relationship has not yet been proven. Other compounds in tomatoes or those diets high in tomato products, either acting alone or with lycopene, may be responsible for the protective effects currently associated with lycopene.
Since interest in lycopene is relatively recent, there have only been a few experimental studies on the role of lycopene in preventing or treating cancer. One animal study found that lycopene treatment reduced the growth of brain tumors. Another animal study showed that chronic intake of lycopene considerably suppressed breast tumor growth. Lycopene has also been shown to interfere with the growth of many different human cancer cell lines in the laboratory, especially those that grow in response to insulin-like growth factor I. Animal and laboratory studies may show a certain substance holds promise as a beneficial treatment, but further studies are necessary to determine if the results apply to humans.
Results of a small clinical study presented at the 1999 annual meeting of the American Association for Cancer Research suggested that lycopene supplements may benefit those with prostate cancer. Among 15 men who had taken two capsules of lycopene every day for about three weeks before surgery, five had smaller, less advanced lesions and the cancer was less likely to have spread beyond the prostate than the men who received a placebo (inactive substance). Lycopene reduces prostate specific antigen (PSA), a measure of prostate cancer activity. In the study, which was presented at the annual meeting of the American Chemical Society (August, 2001), 32 mostly African American patients who had been diagnosed with prostate cancer and were awaiting radical prostatectomy were put on diets that included enough tomato sauce to provide 30 mg/day of lycopene for three weeks.
Mean serum PSA concentrations fell by 17.5%, while a measure of oxidative status fell by 21.3%. DNA damage in the cancer cells fell by 40% after three weeks. Most important, high concentration of lycopene in prostate tissues resulted in a nearly three-fold increase in programmed cell damage among cancer cells.
Lycopene obtained from eating fruits and vegetables has no known side effects and is thought to be safe for humans.
Until more definitive data are available, current recommendations should emphasize the benefits of diets rich in a variety of fruits and vegetables, with some importance placed on tomatoes and tomato-based products (two half-cup servings of tomato sauce per week).

References
American Cancer Society. Chemical in tomatoes may slow prostate cancer growth. News Today. American Cancer Society Web site. Available at: http://www.cancer.org. Accessed December 10, 1999.
Clinton SK. Lycopene: chemistry, biology, and implications for human health and disease. Nutr Rev. 1998;56:35-51.
Gann PH, Ma J, Giovannuci E, et al. Lower prostate risk in men with elevated plasma lycopene levels: results of a prospective study. Cancer Res. 1999;59:1225-1230.
Gerster H. The potential role of lycopene for human health. J Am Coll Nutr. 1997;16:109-126.
Franceschi S, Bidoli E, La Vecchia C, et al. Tomatoes and risk of digestive-tract cancers. Int J Cancer. 1994;59:181-184. Giovannucci E. Tomatoes, tomato-based products, lycopene, and cancer: review of the epidemiologic literature. J Natl Cancer Inst. 1999;91:317-331.
Giovannucci E, Clinton SK. Tomatoes, lycopene, and prostate cancer. Proc Soc Exp Biol Med. 1998;218:129-139.
Kim DJ, Takasuka N, Kim JM, et al. Chemoprevention by lycopene of mouse lung neoplasia after combined initiation treatment with DEN, MNU and DMH. Cancer Lett. 1997;120:15-22.
Michaud DS, Feskanich D, Rimm EB, et al. Intake of specific carotenoids and risk of lung cancer in 2 prospective US cohorts. Am J Clin Nutr. 2000;72:990-997.
Nagasawa H, Mitamura T, Sakamoto S, Yamamoto K. Effects of lycopene on spontaneous mammary tumour development in SHN virgin mice. Anticancer Res. 1995;15:1173-1178.
Norrish AE, Jackson RT, Sharpe SJ, Skeaff CM. Prostate cancer and dietary carotenoids. Am J Epidemiol. 2000;151:119-123.
Okajima E, Tsutsumi M, Ozono S. Inhibitory effect of tomato juice on rat urinary bladder carcinogenesis after N-butyl-N-(4-hydroxybutyl)nitrosamine initiation. Jpn J Cancer Res. 1998;89:22-26.
Paiva SA, Russell RM. Beta-carotene and other carotenoids as antioxidants. J Am Coll Nutr. 1999;18:426-433.
Porrini M, Riso P. Lymphocyte lycopene concentration and DNA protection from oxidative damage is increased in women after a short period of tomato consumption. J Nutr. 2000;130:189-192.
Rao AV, Agarwal S. Bioavailability and in vivo antioxidant properties of lycopene from tomato products and their possible role in the prevention of cancer. Nutr Cancer. 1998;31:199-203.

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Broccolli

 

Recent investigations have shown that the frequent consumption of cruciferous vegetables is associated with a decreased risk for cancer. A recent population-based study found that high levels of the carotenoid lutein (obtained from vegetables such as broccoli, spinach, and lettuce) were associated with fewer cancers of the colon. An epidemiologic study published in 1999 in the Journal of the National Cancer Institute revealed that eating cruciferous vegetables seemed to reduce bladder cancer risk, while other vegetables and fruits did not appear to have the same benefit. Some studies have shown that eating broccoli lowers the risk of prostate cancer.
Researchers at Johns Hopkins University have suggested that sulforaphane, which is present in the broccoli sprouts before the vegetable matures, may be the primary cancer-prevention agent. A study showed that cancer development was reduced by 60% to 80% in laboratory animals that were fed sulforaphane. The compound is thought to prompt the body into manufacturing an enzyme that prevents tumor formation.
The effects of broccoli on the growth of specific cancers have also been studied. For example, scientists at the University of California at Berkeley found that a chemical component of broccoli, indole-3-carbinol (I3C), inhibited the growth of cultured breast cancer cells in a laboratory study.
In yet another study conducted jointly with US and Chinese researchers, it was found that chemicals present in broccoli, cabbage, and other cruciferous vegetables may protect against lung cancer. Researchers studied more than 18,000 men. They recorded 259 cases of lung cancer during the study's follow-up period. The researchers found that the men with detectable amounts of isothiocyanate from broccoli in their bodies had a 36% lower risk of developing lung cancer over a 10-year period.
Scientists caution that as promising as broccoli may be as an excellent food for preventing cancer, the results of studies cannot be considered in isolation. The anticancer effects of any single food cannot be completely understood without evaluating it as part of a bigger dietary picture. It is still unclear whether it is the lutein, sulforaphane, indole-3-carbinol, isothiocyanate or other compounds that, working together and in the right quantities, protect individuals against cancer development. Studies have shown as little as 150 grams of broccoli a day could have a significant effect on a person's risk of contracting cancer. Researchers found that men who ate two or more half-cup servings of broccoli per week had a 44 percent lower incidence of bladder cancer compared to men who ate less than one serving per week. Some researchers suggest that small amounts of broccoli sprouts may protect against the risk of cancer as effectively as much larger amounts of the mature vegetable.
Broccoli can be eaten raw, boiled, or steamed, but retains the most nutrients when eaten raw. Cooking reduces some of the benefits of broccoli because the heating process seems to destroy some beneficial anticarcinogenic compounds. When the vegetable is cut up or chewed, this substances are released that turns their into products researchers believe can fight cancer two ways — by detoxifying carcinogens and by suppressing the growth of existing cancerous tumors.
Broccoli is safe to eat. Since it is a food high in fiber, eating large amounts of it may cause gas. High fiber foods should be reduced or avoided in people with diarrhea and some other colon problems.

References
Cao G, Booth SL, Sadowski JA, Prior RL. Increases in human plasma antioxidant capacity after consumption of controlled diets high in fruit and vegetables. Am J Clin Nutr. 1998;68:1081-1087.
Cover CM, Hsieh SJ, Tran SH, et al. Indole-3-carbinol inhibits the expression of cyclin-dependent kinase-6 and induces a G1cell cycle arrest of human breast cancer cells independent of estrogen receptor signaling. J Biol Chem. 1998;273:3838-3847.
Fahey JW, Zhang Y, Talalay P. Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proc Natl Acad Sci U S A.1997;94:10367-10372.
Gamet-Payrastre L, Li P, Lumeau S, et al. Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells. Cancer Res. 2000;60:1426-1433.
Hasler CM. Functional foods: their role in disease prevention and health promotion. Quackwatch Web site. Available at: http://www.quackwatch.com. Accessed May 8, 2000.
Michaud DS, Spiegelman D, Clinton SK, Rimm EB, Willett WC, Giovannucci EL. Fruit and vegetable intake and incidence of bladder cancer in a male prospective cohort. J Natl Cancer Inst. 1999;91:605-613.
Nestle M. Broccoli sprouts in cancer prevention. Nutr Rev. 1998;56:127-130.
Shapiro TA, Fahey JW, Wade KL, Stephenson KK, Talalay P. Human metabolism and excretion of cancer chemoprotective glucosinolates and isothiocyanates of cruciferous vegetables. Cancer Epidemiol Biomarkers Prev. 1998;7:1091-1100.
Slattery ML, Benson J, Curtin K, Ma KN, Schaeffer D, Potter JD. Carotenoids and colon cancer. Am J Clin Nutr. 2000;71:575-582.
Zhang Y, Kensler TW, Cho CG, Posner GH, Talalay P. Anticarcinogenic activities of sulforaphane and structurally related synthetic norbornyl isothiocyanates. Proc Natl Acad Sci U S A. 1994;91:3147-3150.
S. J London, J-M.Yuan, F-L. Chung, Y-T. Gao, G.A. Coetzee, R. K Ross, M. C. Yu Isothiocyanates, glutathione S-transferase M1 and T1 polymorphisms, and lung-cancer risk: a prospective study of men in Shanghai, China The Lancet 356: 724-729 (2000).

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If you are a woman, you should be concerned about breast cancer. If you are a man, you should be concerned about prostate cancer. And if you are concerned about either breast cancer or prostate cancer, you should know that eating cruciferous vegetables, such as broccoli and cabbage, is really good for you. Eating half of a head of cabbage each day or extremely large amounts of other cruciferous vegetables is what it would take to get the kind of health risk reduction you're looking for-and that is neither practical nor palatable.
The indole group of sulfur compounds binds to chemical carcinogens and activates enzymes that in turn detoxify those chemical carcinogens. Indole-3-carbinol (I3C is a phytonutrient that occurs naturally in certain cruciferous vegetables), appearing to affect estrogen metabolism in ways that might help prevent breast cancer, and indole-3-carbinol may also be critical in preventing or retarding prostate cancer. I3C is the specific phytonutrient that has been shown to act as a catalyst to pull estradiol down a benign pathway to 2-hydroxyestrone. After isolating I3C, scientists have been able to prepare nutraceuticals of I3C at the proper physiologic dose to help prevent both breast cancer in women and prostate cancer in men. Every non-pregnant woman3 and every man should consider taking pharmacy grade I3C as part of his or her daily nutraceutical regimen for disease prevention.
In 1991 researchers at the Institute for Hormone Research in New York City proved that I3C significantly reduced the incidence and, in fact, the number of tumors in female mice prone to developing breast cancer. In human studies, levels of "strong" estrogen declined and levels of "weak" estrogen increased and most important, there was a marked decrease in the level of the estrogen metabolite associated with breast and endometrial cancer (16-alpha-hydroxyestrone). Furthermore, I3C fits into the aryl hydrocarbon (Ah) receptor but according to researchers at Texas A&M, unlike the toxic chemical dioxin, that also activates the Ah receptor, I3C not only positively affects estrogen metabolism but I3C also can keep dioxin out of the cells. Studies, such as in 1998 from the University of California at Berkeley have shown that indole-3-carbinol was 30 percent more effective than tamoxifen in inhibiting the growth of estrogen receptor — positive breast cancer cells. A summary of recent studies shows that this vegetable extract:
- Increases the conversion of estradiol to “weaker” (2OHE) estrogen, which has been shown to reduce breast cancer incidence.
-Works in estrogen receptor negative breast cancer cells.
- Stops human cancer cells from growing (54-61%) and provokes the cells to self-destruct (apoptosis).
- Inhibits MCF7 human breast cancer cells better than tamoxifen under laboratory conditions.
- Protects against the environmental toxin, dioxin.
- Restores p21 tumor suppressor gene.
- Provides antioxidant protection.
But if I3C alters estrogen metabolism, how can it be effective in preventing or even retarding prostate cancer? When the cancer cell is stopped at the checkpoint, the body has more of a chance to destroy it before it can grow. Furthermore, because it is the balance of hormone cells in prostate cancer that is important, rather than the level of any particular hormone, how is it possible for I3C to be effective against prostate cancer? The answer is that its effectiveness against prostate cancer comes from the other anticancer properties that I3C contains. Indole-3-carbinol has been shown to force cancer cells to stop at "checkpoints," like a normal, healthy cell does before replicating. It also has the potential to help restore communication to the sex hormones through the Ah receptor discussed above. In prostate cancer, sex hormone cells cannot communicate normally, telling other cells to do things like grow. It appears that I3C is one of a few substances that have the ability to restore communications.
An extract from cabbage may reverse precancerous changes of the cervix (CIN), according to a trial published in the August, 2000 edition of Gynecologic Oncology.
These results add to those of earlier trials in which I3C supplementation has shown promise as a potential preventive agent against breast cancer and recurrent respiratory papillomatosis (a benign lung condition which, like most cases of CIN, is caused by the human papilloma virus, or HPV). I3C has previously demonstrated protective effects against cervical cancer in test tube studies.
Men who consume a lot of cruciferous vegetables — specifically, broccoli and cabbage — may reduce their risk of bladder cancer. The higher the intake of cruciferous vegetables, the lower the bladder cancer risk. Of all the vegetables, only broccoli and cabbage intake seemed to have an impact on bladder cancer risk. Because the rate of bladder cancer in men is three to four times higher than in women, the researchers note that the findings may not apply to women.
In China (Department of Epidemiology, Harbin Medical College, Heilongjiang), consumption of cabbage was found to protect against brain tumor development.
Thus it would be wise to take heed of what your grandmother used to tell you: "Eat your vegetables. They're good for you."

References
American Institute for Cancer Research, September 25, 2000.
Cohen, J. H., et al. "Fruit and vegetable intakes and prostate cancer risk," Journal of the National Cancer Institute, (2000).Vol. 92 pp. 61-8.
Cover, Carolyn M., Bjeldanes, Firestone et al. Journal of Biological Chemist February 13, 1998.
Journal of the British Academy of Anti-Aging Medicine, August 2000, p.33.
Journal of Cellular Biochemisty Supplements 28/29:111-6. Strang Cancer Prevention Center, New York, NY.
Bell MC, Crowley-Nowick P, Bradlow HL, et al. Placebo-controlled trial on indole-3-carbinol in the treatment of CIN. Gynecologic Oncol 2000;78:123–9.
Wong GY, Bradlow L, Sepkovic D, et al. Dose-ranging study of indole-3-carbinol for breast cancer prevention. J Cell Biochem Suppl 1997;28–9:111–6.
Rosen CA, Woodson GE, Thompson JW, et al. Preliminary results of the use of indole-3-carbinol for recurrent respiratory papillomatosis. Otolaryngol Head Neck Surg 1998;118:810–5.
Yuan F, Chen DZ, Liu K, et al. Anti-estrogenic activities of indole-3-carbinol in cervical cells: implication for prevention of cervical cancer. Anticancer Res 1999;19:1673–80.
Jinfu Hu, Carlo La Vecchia, et al. Diet and brain cancer in adults: A case-control study in Northeast China International Journal of Cancer. 81(1):20-3, 1999 Mar 31.

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Honey

Caffeic Acid Phenethyl Ester (CAPE) is a phenolic antioxidant derived from honey bee propolis. Most people think of honey as something to put in tea, but test tube studies suggest that CAPE has antioxidant, anti-inflammatory, and anticancer properties. One of the most significant medical journal articles described how the caffeic acids in propolis and honey might prevent colon cancer, which kills some 60,000 Americans each year. Chinthalapally V. Rao, Ph.D., of the American health Foundation, Valhalla, N.Y., reported in Cancer Research (Sept.15,1993; 53:1482-88) that these caffeic acids prevented the formation of precancerous tissue in rats after they were exposed to cancer-causing chemicals.
Several components isolated from propolis have been shown to have anticancer activity. This study (Anticancer Res 2001 May-Jun;21(3B):1665-71 Luo J, Soh JW, Xing WQ, Mao Y, Matsuno T, Weinstein IB.) demonstrates that the compound PM-3 (3-[2-dimethyl-8-(3-methyl-2-butenyl)benzopyran]-6-propenoic acid) isolated from Brazilian propolis markedly inhibits the growth of MCF-7 human breast cancer cells. This effect was associated with inhibition of cell cycle progression and induction of apoptosis. Treatment of MCF-7 cells with PM-3 arrested cells in the G1 phase and resulted in a decrease in the protein levels of cyclin D1 and cyclin E. PM-3 also inhibited the expression of cyclin D1 at the transcriptional level when examined in cyclin D1 promoter luciferase assays. Induction of apoptosis by PM-3 occurred within 48 hours after treatment of MCF-7 cells. The MCF-7 treated cells also displayed a decrease in the level of the estrogen receptor (ER) protein and inhibition of estrogen response element (ERE) promoter activity. Therefore, PM-3 merits further investigation with respect to breast cancer chemoprevention or therapy.
Preliminary research suggests that the sweet spread may keep tumors from recurring after a certain type of colon-cancer surgery. In experiments with mice, Turkish researchers found that honey seemed to block tumors from taking hold in the animals. The investigators made incisions in the animals' necks and injected them with tumor cells. Half of the mice had honey smeared in the incisions before and after the tumor-cell injections. Only 8 of the 30 developed tumors, compared with all of the honey-less mice.
Recent studies by Gribel and Pashinskii indicated that honey possessed moderate antitumor and pronounced antimetastatic effects in five different strains of rat and mouse tumors. Furthermore, honey potentiated the antitumor activity of chemotherapeutic drugs such as 5-fluorouracil and cyclophosphamide.
-- Gribel, N.V., and Pashinskii, V.G.
Antitumor properties of honey. Vopr. Onkol., 36:704-709, 1990.
C.V. Rao at the American Health Foundation in Valhalla, New York found caffeic acids in propolis are inhibitors of colon cancers in animals. Other research shows hive products have the ability to prevent and halt the spread of malignant diseases. Earlier research by M.T. Huang also published in Cancer Research found caffeic acids effective in inhibiting skin cancer tumors in mice.
-- American Bee Journal, June 1994
Again, without actual human studies, these results suggest the need for future research but do not prove propolis effective for any particular condition.

References
Pascual C, Gonzalez R, Torricella RG. Scavenging action of propolis extract against oxygen radicals. J Ethnopharmacol. 1994;41:9–13.
Volpert R, Elstner EF. Interactions of different extracts of propolis with leukocytes and leukocytic enzymes. Arzneimittelforschung. 1996;46:47–51.
Khayyal MT, el-Ghazaly MA, el-Khatib AS. Mechanisms involved in the antiinflammatory effect of propolis extract. Drugs Exp Clin Res. 1993;19:197–203.
Strehl E, Volpert R, Elstner EF. Biochemical activities of propolis-extracts. III. Inhibition of dihydrofolate reductase. Z Naturforsch [C]. 1994;49:39–43.
Frenkel K, Wei H, Bhimani R, et al. Inhibition of tumor promoter-mediated processes in mouse skin and bovine lens by caffeic acid phenethyl ester. Cancer Res. 1993;53:1255–1261.
Hladon B, Bylka W, Ellnain-Wojtaszek M, et al. In vivo studies on the cytostatic activity of propolis extracts. Arzneimittelforschung. 1980;30:1847–1848.
Scheller S, Krol W, Swiacik J, et al. Antitumoral property of ethanolic extract of propolis in mice-bearing Ehrlich carcinoma, as compared to bleomycin. Z Naturforsch [C]. 1989;44:1063–1065.

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Green tea

Green tea is widely consumed in Japan, China, and other Asian nations and is becoming more popular in Western nations. Some reports indicate green tea may have the ability to help prevent certain cancers from developing, including prostate, stomach, and esophageal cancers. Surveys conducted in Japan show that people who consumed green tea had much lower incidence of stomach, liver, pancreatic, breast, lung, esophageal and skin cancers.
Green tea may prevent cancer in the following ways:
- Neutralizing cancer-causing agents
- Protecting cells against mutation from cancercausing agents
- Protecting against free radical damage
- Protecting against cellular damage from ionizing radiation
Green tea contains chemicals known as polyphenols, which have antioxidant properties. An antioxidant is a compound that blocks the action of activated oxygen molecules, known as free radicals, that can damage cells. One major element in green tea is epigallocatechin-3-gallate (EGCG), a compound that is believed to block production of an enzyme required for cancer cell growth. EGCG may work by suppressing the formation of blood vessels, a process called angiogenesis, thereby cutting off the supply of blood to cancer cells.
Three cups a day or more is the amount typically taken for cancer prevention and treatment. Green tea is usually brewed using 1 to 2 teaspoons of the dried tea in a cup of boiling water, or is steeped for 3 to 15 minutes. Green tea extracts are also available in capsule form. Three capsules of green tea extract a day are recommended by proponents, but this dosage and its effects remain uncertain.
Researchers from the Shanghai Cancer Institute and the NCI conducted a large population study in 1994 comparing green tea drinkers to non-green tea drinkers. They found that green tea drinking was associated with 60% fewer cancers of the esophagus for people who did not smoke.
"Our research shows that green tea leaves are rich in this anti-cancer compound, with concentrations high enough to induce anti-cancer effects in the body," says Dorothy Morre, professor of foods and nutrition in Purdue's School of Consumer and Family Sciences (38th annual meeting of the American Society for Cell Biology in San Francisco). The Morres found that EGCg inhibits the growth of, and kills, cancerous human mammary cells in culture, but does not kill cultured, non-cancerous human mammary cells.
Green tea is generally considered safe. Asians have consumed this tea for thousands of years with few dangerous side effects. However, some people may develop allergic reactions and should stop drinking it. Drinking large amounts of tea may cause nutritional and other problems because of the caffeine content and the strong binding activities of the polyphenols. Because caffeine acts as a stimulant, people with irregular heartbeats or who have anxiety attacks should not drink more than 2 cups a day. Women who are pregnant or breast-feeding should not drink green tea in large amounts.

References
Bushman JL. Green tea and cancer in humans: a review of the literature. Nutr Cancer. 1998;31:151-159.
Gao YT, McLaughlin JK, Blot WJ, Ji BT, Dai Q, Fraumeni JF Jr. Reduced risk of esophageal cancer associated with green tea consumption. J Natl Cancer Inst. 1994;86:855-858.
Ji BT, Chow WH, Hsing AW, et al. Green tea consumption and the risk of pancreatic and colorectal cancers. Int J Cancer. 1997;70:255-258.
Lyn-Cook BD, Rogers T, Yan Y, Blann EB, Kadlubar FF, Hammons GJ. Chemopreventive effects of tea extracts and various components on human pancreatic and prostate tumor cells in vitro. Nutr Cancer. 1999;35:80-86.
Mayo Clinic. Prostate cancer and green tea. Mayo Clinic Health Oasis Web site. Available at: http://www.may-ohealth.org/mayo/9901/htm/tea.htm. Accessed May 8, 2000.
Medical Economics. PDR for Herbal Medicines. Montvale, NJ:Medical Economics Company; 1998.
Steele VE, Kelloff GJ, Balentine D. Comparative chemopreventive mechanisms of green tea, black tea and selected polyphenol extracts measured by in vitro bioassays. Carcinogenesis. 2000;21:63-67.
University of Texas Center for Alternative Medicine Research in Cancer. Green tea summary. University of Texas-Houston Health Science Center Web site. Available at: http://www.sph.uth.tmc.edu/utcam/summary/greentea.htm. Accessed May 8, 2000.
Yang CS. Tea and health. Nutrition. 1999;15:946-949.

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Grape

The compound found in the skins of red grapes (resveratrol) is being studied to see how it affects the development and progression of heart disease and cancer.
Resveratrol is found in 70 different plants, including mulberries and peanuts, but grapes and grape products are the richest source. All wines have some resveratrol, but the highest concentration is in red wine. (Jang M, et al. Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Science 1997;275(5297):218-20.) Resveratrol was discovered after hundreds of tests in search of anti-cancer compounds. The compound has been tested only in cell cultures and laboratory animals. In an 18-week study of mice, doses of resveratrol reduced the number of skin tumors by up to 98 percent compared with skin cancers on control mice.
It occurs in the vines, roots, seeds, and stalks, but its highest concentration is in the skin, which contains 50-100 micrograms (µg) per gram. Resveratrol is a phytoalexin, a class of antibiotic compounds produced as a part of a plant's defense system against disease.
Resveratrol is being studied to see how it affects the initiation, promotion, and progression of cancer. With regard to tumor initiation, it has been shown to act as an antioxidant by inhibiting free radical formation, and as an anti-mutagen in rat models. Resveratrol appears to decrease tumor promotion activity by inhibiting cyclooxygenase-1 (COX-1), an enzyme that converts arachidonic acid to pro-inflammatory substances that stimulate tumor-cell growth. Studies related to progression have found that resveratrol induced human promyelocytic leukemia cell differentiation and inhibited ribonucleotide reductase, an enzyme needed for DNA synthesis in proliferating cells. One appealing characteristic of resveratrol's anti-cancer potential is its minimal toxicity to blood-forming cells. More studies using both cellular and animal models are needed before any such data would be applicable to human use.
The similarity in structure between resveratrol and diethylstilbestrol (a synthetic estrogen) has prompted investigations into resveratrol's potential as a phytoestrogen (a plant compound that produces estrogen-like effects). However, these properties also stimulate the growth of human breast cancer cells. This finding seems contrary to its other anticancer activities, and is a cause for concern.
Fresh, preserved, and dried grapes are used in the form of liquid extracts, tinctures, gargles, enemas, douches, and compresses. Grape skins are used to make wine. Grape seed extract and resveratrol are available in tablets and capsule supplements. The dosages vary depending on the manufacturer. Because there havent been any clinical studies, the optimal therapeutic dosage hasnt been established for resveratrol. Based on animal studies, a reasonable therapeutic dosage of resveratrol might be about 500 mg daily.
The complete grape diet begins with a period of fasting and eating only grapes for 1 or 2 weeks. Then, fresh fruits and sour milk can also be consumed. The next stage of the diet includes raw vegetables, salads, nuts, dairy products, honey, and olive oil. During the final stage of the diet, if a person is doing well, they may be given one cooked meal per day.
An exclusive grape diet is unhealthy and does not supply the body with adequate amounts of protein and important nutrients, such as vitamin B 12. Grape seed extract is believed to be safe, but additional research is needed for confirmation.
The amount of resveratrol in red wine varies greatly, and increased consumption of wine to increase resveratrol intake poses certain health risks. Alcohol is associated with increased risks of cancers of the mouth, esophagus, pharynx, larynx, and liver in both men and women, and of breast cancer in women. Cancer risk also increases with the amount of alcohol consumed. However, the cardiovascularand the anticarcinogenic benefits of moderate drinking may outweigh the risk of cancer in men over age 50 and in women over age 60.

References
American Cancer Society. Unproven methods of cancer management. Grape diet. CA Cancer J Clin. 1974;24:144-146.
Ashley MJ, Ferrence R, Room R, Bondy S, Rehm J, Single E. Moderate drinking and health. Implications of recent evidence. Can Fam Physician. 1997;43:687-694.
Bown D. Encyclopedia of Herbs & Their Uses. New York, NY: DK Publishing Inc; 1995.
Celotti E and others. Resveratrol content of some wines obtained from dried Valpolicella grapes: Recioto and Amarone. Journal of Chromatography A 730(1-2): 47-52, 1996.
Clement MV and others. Chemopreventive agent resveratrol, a natural product derived from grapes, triggers CD95 signaling-dependent apoptosis in human tumor cells. Blood 92:996-1002, 1998.
Fetrow CW, Avila JR. Professional's Handbook of Complementary and Alternative Medicines. Springhouse, Pa: Springhouse Corp; 1999.
Fontecave M and others. Resveratrol, a remarkable inhibitor of ribonucleotide reductase. FEBS Letters 421:277-279, 1998.
Gehm H and others. Resveratrol, a polyphenolic compound found in grapes and wine, is an agonist for the estrogen receptor. Proceedings of the National Academy of Sciences U.S.A. 94:557-562, 1997.
Jang M and others. Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Science 275:218-220, 1997.
Kopp P. Resveratrol, a phytoestrogen found in red wine. A possible explanation for the conundrum of the 'French paradox'? European Journal of Endocrinology 138:619-620, 1998.
McElderry MQB. Grape expectations: the resveratrol story. Quackwatch Web site. Available at: http://www.quack-watch.com. Accessed October 21, 1999.
Mitchell SH, Zhu W, Young CY. Resveratrol inhibits the expression and function of the androgen receptor in LNCaP prostate cancer cells. Cancer Res. 1999;59:5892-5895.
Moss RW. Herbs Against Cancer. New York, NY: Equinox Press; 1998.
Nuttall SL, Kendall MJ, Bombardelli E, Morazzoni P. An evaluation of the antioxidant activity of a standardized grape seed extract, Leucoselect. J Clin Pharm Ther. 1998;23:385-389.
Subbaramaiah K, Michaluart P, Chung WJ, Tanabe T, Telang N, Dannenberg AJ. Resveratrol inhibits cyclooxygenase-2 transcription in human mammary epithelial cells. Ann NY Acad Sci. 1999;889:214-223.

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Chili pepper

In the countries where diets are traditionally high in capsaicin (the chili pepper substance, the fruits contain 0.1-1.5% capsaicin), the cancer death rates for men and women are significantly lower than they are in countries with less chili pepper consumption (World Health Organization statistics). When capsaicin was administered to rats receiving carcinogenic agents, the incidence of certain tumors was decreased over controls. Capsaicin has been found to preferentially inhibit the growth of cancer cells in laboratory studies. Experiments have shown that capsaicin seems to be able to detoxify a wide range of chemical carcinogens which, if left free to roam the body, could set up mutations that lead to cancers. It also induces apoptosis in various immortalized or malignant cell lines.
Researchers tested the capsaicin on human skin cancer cells to analyze how the cells reacted. They found that the majority of the skin cancer cells exposed to the substances died. The researchers say these substances seem to kill cells by damaging the cell membranes and limiting the amount of oxygen that reaches the cancer cells.
Study authors Numsen Hail Jr. and Reuben Lotan, PhD, of the University of Texas M.D. Anderson Cancer Center in Houston say if more studies confirm these findings, the compounds may eventually be used in skin patches or creams that could treat or prevent skin cancers.
A different human study found that people who ate the most cayenne actually had lower rates of stomach cancer.
A chili pepper tincture can be used in the amount of 0.3–1 ml TID. An infusion can be made by pouring a cup of boiling water onto 1/2–1 tsp of cayenne powder and let set for 10 minutes. A teaspoon of this infusion can be mixed with water and drunk three to four times daily.

References
Buiatti E, Palli D, Decarli A, et al. A case-control study of gastric cancer and diet in Italy. Int J Cancer 1989;44:611–6.
Lopez-Carrillo L, Lopez-Cervantes M, Robles-Diaz G, Ramirez-Espitia A, Mohar-Betancourt A, Meneses-Garcia A, Lopez-Vidal Y, Blair A. Capsaicin consumption, Helicobacter pylori positivity and gastric cancer in Mexico. Int J Cancer. 2003 Aug 20;106(2):277-82.
Macho A, Lucena C, Sancho R, Daddario N, Minassi A, Munoz E, Appendino G.
Non-pungent capsaicinoids from sweet pepper synthesis and evaluation of the chemopreventive and anticancer potential. Eur J Nutr. 2003 Jan;42(1):2-9.
Zhang J, Nagasaki M, Tanaka Y, Morikawa S. Capsaicin inhibits growth of adult T-cell leukemia cells. Leuk Res. 2003 Mar;27(3):275-83.
Surh YJ. Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review. Food Chem Toxicol. 2002 Aug;40(8):1091-7.
Park KK, Chun KS, Yook JI, Surh YJ. Lack of tumor promoting activity of capsaicin, a principal pungent ingredient of red pepper, in mouse skin carcinogenesis. Anticancer Res. 1998 Nov-Dec;18(6A):4201-5.
Surh YJ, Lee E, Lee JM. Chemoprotective properties of some pungent ingredients present in red pepper and ginger. Mutat Res. 1998 Jun 18;402(1-2):259-67.
Surh YJ, Lee SS. Capsaicin in hot chili pepper: carcinogen, co-carcinogen or anticarcinogen? Food Chem Toxicol. 1996 Mar;34(3):313-6.
Lopez-Carrillo L, Hernandez Avila M, Dubrow R. Chili pepper consumption and gastric cancer in Mexico: a case-control study. Am J Epidemiol. 1994 Feb 1;139(3):263-71.
Kang JY, Alexander B, Barker F, Man WK, Williamson RC. The effect of chilli ingestion on gastrointestinal mucosal proliferation and azoxymethane-induced cancer in the rat. J Gastroenterol Hepatol. 1992 Mar-Apr;7(2):194-8.

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Turmeric

Turmeric is a spice grown in India and other tropical regions of Asia. It has a long history of use in herbal remedies, particularly in China, India, and Indonesia. The root of the plant contains the active ingredient, curcumin.
Some researchers believe turmeric may prevent and slow the growth of a number of cancers, particularly tumors of the esophagus, mouth, intestines, stomach, breast and skin.One researcher states that curcumin, inhibited the formation of cancer-causing enzymes in rodents, although this has not been tested in humans. Some researchers have speculated that curcumin, after it enters the body, changes into tetrahydrocurcumin, which may be a potent antioxidant. Curcumin was also shown to increase apoptosis (cell death), it inhibited growth of tumors in the colon.
Turmeric root is on the Commission E (Germany's regulatory agency for herbs) list of approved herbs, and it is available in powdered form in most grocery stores. It can also be made into a tea or purchased as a tincture or tablets. An ointment made from turmeric can be applied to the skin. Although there is no standardized dose for turmeric, some practitioners recommend taking a teaspoon with each meal.
Researchers have studied turmeric extensively to determine if it is an effective antioxidant and anti-inflammatory agent, and whether it holds any promise as a cancer drug. However, all of the evidence so far comes from laboratory or animal studies. Animal and laboratory studies may show a certain substance holds promise as a beneficial treatment, but further studies are necessary to determine if the results apply to humans.
According to a review article published by researchers from the Ohio State University in Columbus, curcumin demonstrated anticancer effects at virtually all stages of tumor development in rodents and showed potential to kill cancer cells and prevent normal cells from becoming cancerous. This was particularly true for cancers of the breast, intestines, colon, stomach, and skin in rodents; however, this was not tested in humans.
A French laboratory study concluded that curcumin appeared to be a potent inhibitor of cancer development. Several additional laboratory studies also concluded that curcumin might prevent and slow the growth of some types of tumor cells. Two animal studies conducted in India found that curcumin slowed the growth and spread of cancer in mice. Controlled clinical trials are needed to determine what, if any, medical benefits turmeric offers to humans.
Another study by a team of researchers at the University of Texas has revealed yet another therapeutic property of curcumin. It is found that curcumin could stop cancer cells with multiple myeloma from replicating and kill off the remaining cancerous cells.
The researchers added curcumin to a sample of human cells with multiple myeloma (MM) and found that it restricted the multiplication of nuclear factor kappa-B (NF-kappaB). The scientists had found NF-kappaB to be present in all MM cells and believe it to be the activator of the cancer. The curcumin seemed to de-activate NF-kappaB and stop further activity.
Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day.
People taking anticoagulant medications, drugs that suppress the immune system, or non-steroidal pain relievers (such as Ibuprofen) should avoid turmeric. Persons with bleeding disorders, obstructions of the bile duct, or a history of ulcers, also should avoid turmeric. Women who are pregnant or breast-feeding should not use this herb.

References
Aggarwal BB, Kumar A, Bharti AC. Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res. 2003 Jan-Feb;23(1A):363-98.
Afaq F, Adhami VM, Ahmad N, et al. Botanical antioxidants for chemoprevention of photocarcinogenesis. Front Biosci. 2002;7:d784-92.
Arbiser JL, Klauber N, Rohan R, et al. Curcumin is an in vivo inhibitor of angiogenesis. Mol Med. 1998;4:376-383.
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin, Tx: American Botanical Council; 1998.
Bown D. Encyclopedia of Herbs & Their Uses. New York, NY: DK Publishing Inc; 1995.
Cheng AL, Hsu CH, Lin JK, et al. Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or pre-malignant lesions. Anticancer Res. 2001;21:2895-2900.
Dorai T, Gehani N, Katz A. Therapeutic potential of curcumin in human prostate cancer. Curcumin inhibits tyrosine kinase activity of epidermal growth factor receptor and depletes the protein. Mol Urol. 2000;4:1-6.
Deshpande SS, Ingle AD, Maru GB. Chemopreventive efficacy of curcumin-free aqueous turmeric extract in 7,12-dimethylbenz(a)anthracene-induced rat mammary tumorigenesis. Cancer Lett. 1998;123:35-40.
Leu TH, Maa MC. The molecular mechanisms for the antitumorigenic effect of curcumin. Curr Med Chem Anti-Canc Agents. 2002 May;2(3):357-70.
Li JK, Lin-Shia SY. Mechanisms of cancer chemoprevention by curcumin. Proc Natl Sci Counc Repub China B. 2001;25:59-66.
Deshpande SS, Ingle AD, Maru GB. Inhibitory effects of curcumin-free aqueous turmeric extract on benzo[a]pyrene-induced forestomach papillomas in mice. Cancer Lett. 1997; 118:79-85.
Ireson CR, Jones DJ, Orr S, et al. Metabolism of the cancer chemopreventive agent curcumin in human and rat intestine. Cancer Epidemiol Biomarkers Prev. 2002;11:105-111.
Hastak K, Lubri N, Jakhi SD, More C, John A, Ghaisas SD, Bhide SV. Effect of turmeric oil and turmeric oleoresin on cytogenetic damage in patients suffering from oral submucous fibrosis. Cancer Lett. 1997:116:265-269.
Fetrow CW, Avila JR. Professional's Handbook of Complementary and Alternative Medicines. Springhouse, Pa: Springhouse Corp; 1999.
Krishnaswamy K, Goud VK, Sesikeran B, et al. Retardation of experimental tumorigenesis and reduction in DNA adducts by turmeric and curcumin. Nutr Cancer. 1998;30:163-166.
Medical Economics. PDR for Herbal Medicines. Montvale, NJ: Medical Economics Company; 1998:786-787.
Nagabhushan M, Bhide SV. Curcumin as an inhibitor of cancer. J Am Coll Nutr. 1992;11:192-198.
Simon A, Allais DP, Duroux JL, et al. Inhibitory effect of curcuminoids on MCF-7 cell proliferation and structure-activity relationships. Cancer Lett. 1998;129:111-116.
Surh YJ. Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review. Food Chem Toxicol. 2002 Aug;40(8):1091-7.
Stoner GD, Mukhtar H. Polyphenols as cancer chemopreventive agents. J Cell Biochem. 1995;22:169-180.

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Ginger

Some research findings show that ginger (more exactly, [6]-gingerol, a pungent ingredient present in ginger) can be taken to relieve nausea in cancer patients who are receiving chemotherapy. Some proponents have claimed ginger is able to prevent tumors from developing.
Recent preliminary results in animals showing some effect in slowing or preventing tumor growth are not well understood but warrant further investigation.
Cisplatin is one of the chemotherapy drugs associated with nausea, vomiting, and delayed emptying of the stomach. Researchers from India found that extracts from ginger helped to speed up this process in dogs and rats that were given cisplatin chemotherapy.
Ginger root (fresh or dried) is used in cooking and preparing herbal remedies and soft drinks. A broad range of daily doses of ginger are reported, from 250 mg to 1 g. For nausea, the usual dose is 250 mg-1 g of powdered ginger taken with a liquid several times per day.
People with cancer should consult their physician before taking ginger because it has the potential to interfere with blood clotting and prolong bleeding time. Published studies are in disagreement about the likelihood of this side effect. The risk of serious bleeding may be increased if the person is also taking medication that can lower platelet (blood cells that help the blood to clot) counts or an anticoagulant (a drug that interferes with blood clotting such as warfarin). In rare cases, some people have experienced an allergic reaction to ginger and occasional mild upset stomach.

References
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin, Tx: American Botanical Council; 1998.
Fetrow CW, Avila JR. Professional's Handbook of Complementary and Alternative Medicines. Springhouse, Pa: Springhouse Corp; 1999.
Janssen PL, Meyboom S, van Staveren WA, de Vegt F, Katan MB. Consumption of ginger (Zingiber officinale roscoe) does not affect ex vivo platelet thromboxane production in humans. Eur J Clin Nutr. 1996;50:772-774.
Lumb AB. Effect of dried ginger on human platelet function. Thromb Haemost. 1994;71:110-111.
Medical Economics. PDR for Herbal Medicines. Montvale, NJ: Medical Economics Company; 1998.
Miller LG. Herbal medicinals: selected clinical considerations focusing on known or potential drug-herb interactions. Arch Intern Med. 1998;158:2200-2211.
O'Hara MA, Kiefer D, Farrell K, Kemper K. A review of 12 commonly used medicinal herbs. Arch Fam Med. 1998;7:523-536.
Pharmacopeial Forum. USP urges further study of ginger; creates NF monograph. US Pharmacopeia Web site. Available at: http://www.usp.org. Accessed May 8, 2000.
Sharma SS, Gupta YK. Reversal of cisplatin-induced delay in gastric emptying in rats by ginger (Zingiber officinale). J Ethnopharmacol. 1998;62:49-55.
Surh YJ. Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review. Food Chem Toxicol. 2002 Aug;40(8):1091-7.
Spaulding-Albright N. A review of some herbal and related products commonly used in cancer patients. J Am Diet Assoc. 1997 Oct; 97(10 Suppl 2): S208-15.

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