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  • Reviewed: 11/17/2010

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Tea and Cancer Prevention: Strengths and Limits of the Evidence

Key Points

  • Tea contains polyphenol compounds, particularly catechins, which are antioxidants and whose biological activities may be relevant to cancer prevention (see Questions 2 and 3).
  • Few clinical trials of tea consumption and cancer prevention have been conducted and their results have been inconclusive (see Question 5).
  • Results of epidemiologic studies examining the association between tea consumption and cancer risk have been inconclusive (see Question 5).
  • Inconsistencies in study findings regarding tea and cancer risk may be due to variability in tea preparation, tea consumption, the bioavailability of tea compounds (the amounts that can be absorbed by the body), lifestyle differences, and individual genetic differences (see Question 5).
  • The National Cancer Institute does not recommend for or against the use of tea to reduce the risk of any type of cancer (see Question 6). 

  1. What is tea?

    Tea is one of the most ancient and popular beverages consumed around the world. Black tea accounts for about 75 percent of the world’s tea consumption (1). In the United States, United Kingdom (UK), and Europe, black tea is the most common tea beverage consumed; green tea is the most popular tea in Japan and China (2). Oolong and white tea are consumed in much lesser amounts around the world (2).

    Tea is made from the leaf of the plant Camellia sinensis. Shortly after harvesting, tea leaves begin to wilt and oxidize. During oxidation, chemicals in the leaves are broken down by enzymes, resulting in darkening of the leaves and the well-recognized aroma of tea. This oxidation process can be stopped by heating, which inactivates the enzymes. The amount of oxidation and other aspects of processing determine a tea’s type. Black tea is produced when tea leaves are wilted, bruised, rolled, and fully oxidized. In contrast, green tea is made from unwilted leaves that are not oxidized. Oolong tea is made from wilted, bruised, and partially oxidized leaves, creating an intermediate kind of tea. White tea is made from young leaves or growth buds that have undergone minimal oxidation. Dry heat or steam can be used to stop the oxidation process, and then the leaves are dried to prepare them for sale.

    Tea is brewed from dried leaves and buds (either in tea bags or loose), prepared from dry instant tea mixes, or sold as ready-to-drink iced teas. So-called herbal teas are not really teas but infusions of boiled water with dried fruits, herbs, and/or flowers. 

  2. What are the ingredients of tea?

    Tea is composed of polyphenols, alkaloids (caffeine, theophylline, and theobromine), amino acids, carbohydrates, proteins, chlorophyll, volatile organic compounds (chemicals that readily produce vapors and contribute to the odor of tea), fluoride, aluminum, minerals, and trace elements (3). The polyphenols, a large group of plant chemicals that includes the catechins (4), are thought to be responsible for the health benefits that have traditionally been attributed to tea, especially green tea. The most active and abundant catechin in green tea is epigallocatechin-3-gallate (EGCG). The active catechins and their respective concentrations in green tea infusions are listed in the table below.

    Catechin Concentrations of Green Tea Infusions
    Catechin in Green Tea InfusionCatechin Concentration
    (mg/L)*
    Catechin Concentration
    (mg/8 fl oz)*
    Epigallocatechin-3-gallate (EGCG)117–44225–106
    Epigallocatechin (EGC)203–47149–113
    Epicatechin-3-gallate (ECG)17–1504–36
    Epicatechin (EC)25–816–19
         *mg = milligram; L = liter; fl oz = fluid ounce. See reference 5.

    Black tea contains much lower concentrations of these catechins than green tea (6). The extended oxidation of black tea increases the concentrations of thearubigins and theaflavins, two types of complex polyphenols (2). Oolong tea contains a mixture of simple polyphenols, such as catechins, and complex polyphenols (2). White and green tea contain similar amounts of EGCG but different amounts of other polyphenols (7).

    Although iced and ready-to-drink teas are becoming popular worldwide, they may not have the same polyphenol content as an equal volume of brewed tea (8). The polyphenol concentration of any particular tea beverage depends on the type of tea, the amount used, the brew time, and the temperature (3). The highest polyphenol concentration is found in brewed hot tea, less in instant preparations, and lower amounts in iced and ready-to-drink teas (3). As the percentage of tea solids (i.e., dried tea leaves and buds) decreases, so does the polyphenol content (9). Ready-to-drink teas frequently have lower levels of tea solids and lower polyphenol contents because their base ingredient may not be brewed tea (10). The addition of other liquids, such as juice, will further dilute the tea solids (9). Decaffeination reduces the catechin content of teas (11).

    Dietary supplements containing green tea extracts are also available (1). In a U.S. study that evaluated 19 different green tea supplements for tea catechin and caffeine content, the product labels varied in their presentation of catechin and caffeine information, and some values reported on product labels were inconsistent with analyzed values (1). 

  3. How might tea help prevent cancer?

    Among their many biological activities, the predominant polyphenols in green tea―EGCG, EGC, ECG, and EC―and the theaflavins and thearubigins in black teas have antioxidant activity (12). These chemicals, especially EGCG and ECG, have substantial free radical scavenging activity and may protect cells from DNA damage caused by reactive oxygen species (12). Tea polyphenols have also been shown to inhibit tumor cell proliferation and induce apoptosis in laboratory and animal studies (1, 13). In other laboratory and animal studies, tea catechins have been shown to inhibit angiogenesis and tumor cell invasiveness (14). In addition, tea polyphenols may protect against damage caused by ultraviolet (UV) B radiation (13, 15), and they may modulate immune system function (16). Furthermore, green teas have been shown to activate detoxification enzymes, such as glutathione S-transferase and quinone reductase, that may help protect against tumor development (16). Although many of the potential beneficial effects of tea have been attributed to the strong antioxidant activity of tea polyphenols, the precise mechanism by which tea might help prevent cancer has not been established (13). 

  4. Are there safety considerations regarding tea consumption?

    Tea as a food item is generally recognized as safe by the U.S. Food and Drug Administration. Safety studies have looked at the consumption of up to 1200 mg of EGCG in supplement form in healthy adults over 1- to 4-week time periods (17, 18). The adverse effects reported in these studies included excess intestinal gas, nausea, heartburn, stomach ache, abdominal pain, dizziness, headache, and muscle pain (17, 18). In a Japanese study, children aged 6 to 16 years consumed a green tea beverage containing 576 mg catechins (experimental group) or 75 mg catechins (control group) for 24 weeks with no adverse effects (19). The safety of higher doses of catechins in children is not known.

    As with other caffeinated beverages, such as coffee and colas, the caffeine contained in many tea products could potentially cause adverse effects, including tachycardia, palpitations, insomnia, restlessness, nervousness, tremors, headache, abdominal pain, nausea, vomiting, diarrhea, and diuresis (20). However, there is little evidence of health risks for adults consuming moderate amounts of caffeine (about 300 to 400 mg per day). A review by Health Canada concluded that moderate caffeine intakes of up to 400 mg per day (equivalent to 6 mg per kilogram [kg] body weight) were not associated with adverse effects in healthy adults (21). The amount of caffeine present in tea varies by the type of tea; the caffeine content is higher in black teas, ranging from 64 to 112 mg per 8 fl oz serving, followed by oolong tea, which contains about 29 to 53 mg per 8 fl oz serving (4). Green and white teas contain slightly less caffeine, ranging from 24 to 39 mg per 8 fl oz serving and 32 to 37 mg per 8 fl oz serving, respectively (22). Decaffeinated teas contain less than 12 mg caffeine per 8 fl oz serving (22). Research on the effects of caffeine in children is limited (20). In general, caffeine doses of less than 3.0 mg per kg body weight have not resulted in adverse effects in children (20). Higher doses have resulted in some behavioral effects, such as increased nervousness or anxiety and sleep disturbances (21).

    Aluminum, a neurotoxic element, is found in varying quantities in tea plants. Studies have found concentrations of aluminum (which is naturally taken up from soil) in infusions of green and black teas that range from 14 to 27 micrograms per liter (μg/L) to 431 to 2239 μg/L (4). The variations in aluminum content may be due to different soil conditions, different harvesting periods, and water quality (4). Aluminum can accumulate in the body and cause osteomalacia and neurodegenerative disorders, especially in individuals with renal failure (4). However, it is not clear how much of the aluminum in tea is bioavailable, and there is no evidence of any aluminum toxicity associated with drinking tea (4).

    Black and green tea may inhibit iron bioavailability from the diet (4). This effect may be important for individuals who suffer from iron-deficiency anemia (4). The authors of a systematic review of 35 studies on the effect of black tea drinking on iron status in the UK concluded that, although tea drinking limited the absorption of non-heme iron from the diet, there was insufficient evidence to conclude that this would have an effect on blood measures (i.e., hemoglobin and ferritin concentrations) of overall iron status in adults (23). However, among preschool children, statistically significant relationships were observed between tea drinking and poor iron status (23). The interaction between tea and iron can be mitigated by consuming, at the same meal, foods that enhance iron absorption, such as those that contain vitamin C (e.g., lemons), and animal foods that are sources of heme iron (e.g., red meat) (4). Consuming tea between meals appears to have a minimal effect on iron absorption (4). 

  5. What evidence from human studies links tea to cancer prevention?

    Tea has long been regarded as an aid to good health, and many believe it can help reduce the risk of cancer. Most studies of tea and cancer prevention have focused on green tea (13). Although tea and/or tea polyphenols have been found in animal studies to inhibit tumorigenesis at different organ sites, including the skin, lung, oral cavity, esophagus, stomach, small intestine, colon, liver, pancreas, and mammary gland (24), the results of human studies—both epidemiologic and clinical studies—have been inconclusive.

    Epidemiologic Studies

    More than 50 epidemiologic studies of the association between tea consumption and cancer risk have been published since 2006. The results of these studies have often been inconsistent, but some have linked tea consumption to reduced risks of cancers of the colon, breast, ovary, prostate, and lung (6, 2557). The inconsistent results may be due to variables such as differences in tea preparation and consumption, the types of tea studied (green, black, or both), the methods of tea production, the bioavailability of tea compounds, genetic variation in how people respond to tea consumption, the concomitant use of tobacco and alcohol, and other lifestyle factors that may influence a person’s risk of developing cancer, such as physical activity or weight status.

    Clinical Trials

    Several clinical trials have investigated the role of tea and tea polyphenols in cancer prevention (5866). However, few trials have examined the effects of tea or tea polyphenols on cancer incidence or mortality.

    Two randomized trials evaluated the effects of tea extracts on premalignant oral lesions (58, 59). One of the trials was a double-blind interventional trial involving 59 people with leukoplakia, which is a putative precursor lesion for oral cancer (58). The trial’s participants were randomly assigned to receive either 3 grams of a mixed tea product, given both orally and topically, or a placebo. After 6 months, 38 percent of the participants in the treatment group had partial regression of their oral lesions compared with 10 percent of the participants in the placebo group. In addition, fewer participants in the treatment group than in the placebo group had an increase in lesion size (3 percent in the treatment group versus 7 percent in the placebo group). Furthermore, mucosal cell proliferation decreased in the treatment group, suggesting a possible protective effect of tea on the development of oral cancer. In contrast, in the second trial, 39 people with high-risk premalignant oral lesions were randomly assigned to receive one of three doses of a green tea extract—500 mg per square meter of body surface area (mg/m2), 750 mg/m2, or 1000 mg/m2—or a placebo three times daily for 12 weeks (59). At the end of the trial, no differences in lesion responses or histology were found between the groups.

    Two other randomized trials examined the effects of tea on urine levels of 8-hydroxydeoxyguanosine (8-OHdG), a biomarker of oxidative DNA damage that may be a predictor of increased cancer risk. Urinary 8-OHdG levels are higher in individuals with lung cancer than in control subjects, and human breast, lung, liver, kidney, brain, stomach, and ovarian tumor tissue has a higher content of 8-OHdG than adjacent nontumor tissue (60). In one trial, 133 adult heavy smokers were randomly assigned to drink 4 cups of one of the following beverages each day for 4 months: decaffeinated green tea, decaffeinated black tea, or water (60). Among those who drank green tea, there was a statistically significant 31 percent decrease in urinary levels of 8-OHdG; in the black tea group, there was no change in urinary 8-OHdG levels (60). In the second trial, 124 individuals at increased risk of liver cancer due to hepatitis B virus infection and aflatoxin exposure took a placebo or 500 mg or 1000 mg of a green tea polyphenol supplement daily (61). The two supplement doses were reported to be equivalent to 2 or 4 cups, respectively, of green tea infusions. No other tea or tea products were consumed. Compared with those in the placebo group, individuals who took the green tea supplement at either dose for 3 months had substantially lower urinary 8-OHdG levels (61). Although these trials indicate that green tea polyphenols from tea or supplements can reduce urinary 8-OHdG levels, it is unclear if reduced 8-OHdG levels are associated with reduced cancer risk.

    Additional trials have investigated whether green tea catechins or green tea extracts alter prostate cancer risk. In a double-blind, placebo-controlled study, 60 men took 200 mg of green tea catechin or a placebo three times daily for 1 year (62). These men had high-grade prostatic intraepithelial neoplasia, which is thought to be a precursor of prostate cancer. After 1 year, fewer prostate cancers were detected in the green tea catechin group (1 cancer in 30 men) compared with the placebo group (9 cancers in 30 men) (62). Two other clinical trials, both uncontrolled studies, investigated the use of green tea extracts to reduce prostate-specific antigen levels in men with prostate cancer and found no evidence of such a reduction (63, 64).

    Another trial examined the effect of tea polyphenols on serum pepsinogen levels in 163 individuals with high serum pepsinogen levels (65). Serum pepsinogen is a biomarker of gastric atrophy and an indicator of increased risk for stomach cancer. The participants in this trial were given either one or six 100-mg capsules of tea polyphenols daily for 1 year. Each capsule was the equivalent of about 1.7 cups of tea. After 1 year, no decrease in serum pepsinogen levels was observed in either treatment group (65).

    In yet another trial, a possible role for green tea supplements in treating precancerous lesions of the esophagus was investigated (66). In the trial, 200 Chinese participants with such lesions were treated with 5 mg of a decaffeinated green tea extract daily or a placebo. After 12 months, lesion histopathology was scored as improved, unchanged, or deteriorated. The trial found no difference between the treatment and placebo groups with regard to changes in the esophageal lesions or in abnormal cell proliferation (66). 

  6. Does the National Cancer Institute (NCI) recommend the use of tea to prevent cancer?

    NCI is a research institution. It develops evidence-based research results for others to interpret. In general, therefore, NCI does not make recommendations about specific medical or dietary interventions.

    Moreover, as noted above (see Question 5), the evidence regarding the potential benefits of tea consumption in relation to cancer is inconclusive at present.

Selected References 

  1. Seeram NP, Henning SM, Niu Y, et al. Catechin and caffeine content of green tea dietary supplements and correlation with antioxidant capacity. Journal of Agricultural and Food Chemistry 2006; 54(5):1599–1603. [PubMed Abstract] 

  2. Mukhtar H, Ahmad N. Tea polyphenols: Prevention of cancer and optimizing health. American Journal of Clinical Nutrition 2000; 71(6 Suppl):1698S–1702S. [PubMed Abstract] 

  3. Cabrera C, Giménez R, López MC. Determination of tea components with antioxidant activity. Journal of Agricultural and Food Chemistry 2003; 51(15):4427–4435. [PubMed Abstract] 

  4. Cabrera C, Artacho R, Giménez R. Beneficial effects of green tea―a review. Journal of the American College of Nutrition 2006; 25(2):79–99. [PubMed Abstract] 

  5. Reto M, Figueira ME, Filipe HM, Almeida CM. Chemical composition of green tea (Camellia sinensis) infusions commercialized in Portugal. Plant Foods for Human Nutrition 2007; 62(4):139–144. [PubMed Abstract] 

  6. Wu AH, Yu MC. Tea, hormone-related cancers and endogenous hormone levels. Molecular Nutrition and Food Research 2006; 50(2):160–169. [PubMed Abstract] 

  7. Santana-Rios G, Orner GA, Xu M, Izquierdo-Pulido M, Dashwood RH. Inhibition by white tea of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-induced colonic aberrant crypts in the F344 rat. Nutrition and Cancer 2001; 41(1 and 2):98–103. [PubMed Abstract] 

  8. Chen ZY, Zhu QY, Tsang D, Huang Y. Degradation of green tea catechins in tea drinks. Journal of Agricultural and Food Chemistry 2001; 49(1):477–482. [PubMed Abstract] 

  9. Peterson J, Dwyer J, Jacques P, et al. Tea variety and brewing techniques influence flavonoid content of black tea. Journal of Food Composition and Analysis 2004; 17(3–4):397–405. [Journal Abstract] 

  10. Arts ICW, van de Putte B, Hollman PCH. Catechin contents of foods commonly consumed in the Netherlands. 2. Tea, wine, fruit juices, and chocolate milk. Journal of Agricultural and Food Chemistry 2000; 48(5):1752–1757. [PubMed Abstract] 

  11. Henning SM, Fajardo-Lira C, Lee HW, et al. Catechin content of 18 teas and a green tea extract supplement correlates with the antioxidant capacity. Nutrition and Cancer 2003; 45(2):226–235. [PubMed Abstract] 

  12. Henning SM, Niu Y, Lee NH, et al. Bioavailability and antioxidant activity of tea flavanols after consumption of green tea, black tea, or a green tea extract supplement. American Journal of Clinical Nutrition 2004; 80(6):1558–1564. [PubMed Abstract] 

  13. Lambert JD, Yang CS. Mechanisms of cancer prevention by tea constituents. Journal of Nutrition 2003; 133(10):3262S–3267S. [PubMed Abstract] 

  14. Zaveri NT. Green tea and its polyphenolic catechins: Medicinal uses in cancer and noncancer applications. Life Sciences 2006; 78(18):2073–2080. [PubMed Abstract] 

  15. Elmets CA, Singh D, Tubesing K, et al. Cutaneous photoprotection from ultraviolet injury by green tea polyphenols. Journal of the American Academy of Dermatology 2001; 44(3):425–432. [PubMed Abstract] 

  16. Steele VE, Kelloff GJ, Balentine D, et al. Comparative chemopreventive mechanisms of green tea, black tea and selected polyphenol extracts measured by in vitro bioassays. Carcinogenesis 2000; 21(1):63–67. [PubMed Abstract] 

  17. Chow HH, Hakim IA, Vining DR, et al. Effects of dosing condition on the oral bioavailability of green tea catechins after single-dose administration of polyphenon E in healthy individuals. Clinical Cancer Research 2005; 11(12):4627–4633. [PubMed Abstract] 

  18. Chow HS, Cai Y, Hakim IA, et al. Pharmacokinetics and safety of green tea polyphenols after multiple-dose administration of epigallocatechin gallate and polyphenon E in healthy individuals. Clinical Cancer Research 2003; 9(9):3312–3319. [PubMed Abstract] 

  19. Matsuyama T, Tanaka Y, Kamimaki I, Nagao T, Tokimitsu I. Catechin safely improved higher levels of fatness, blood pressure, and cholesterol in children. Obesity 2008; 16(6):1338–1348. [PubMed Abstract] 

  20. Higdon JV, Frei B. Coffee and health: A review of recent human research. Critical Reviews in Food Science and Nutrition 2006; 46(2):101–123. [PubMed Abstract] 

  21. Nawrot P, Jordan S, Eastwood J, et al. Effects of caffeine on human health. Food Additives and Contaminants 2003; 20(1):1–30. [PubMed Abstract] 

  22. Chin JM, Merves ML, Goldberger BA, Sampson-Cone A, Cone EJ. Caffeine content of brewed teas. Journal of Analytical Toxicology 2008; 32(8):702–704. [PubMed Abstract] 

  23. Nelson M, Poulter J. Impact of tea drinking on iron status in the UK: A review. Journal of Human Nutrition and Dietetics 2004; 17(1):43–54. [PubMed Abstract] 

  24. Yang CS, Maliakal P, Meng X. Inhibition of carcinogenesis by tea. Annual Review of Pharmacology and Toxicology 2002; 42:25–54. [PubMed Abstract] 

  25. August DA, Landau J, Caputo D, et al. Ingestion of green tea rapidly decreases prostaglandin E2 levels in rectal mucosa in humans. Cancer Epidemiology, Biomarkers and Prevention 1999; 8(8):709–713. [PubMed Abstract] 

  26. Sun CL, Yuan JM, Koh WP, Lee HP, Yu MC. Green tea and black tea consumption in relation to colorectal cancer risk: The Singapore Chinese Health Study. Carcinogenesis 2007; 28(10):2143–2148. [PubMed Abstract] 

  27. Yang G, Shu XO, Li H, et al. Prospective cohort study of green tea consumption and colorectal cancer risk in women. Cancer Epidemiology, Biomarkers and Prevention 2007; 16(6):1219–1223. [PubMed Abstract] 

  28. Yuan JM, Gao YT, Yang CS, Yu MC. Urinary biomarkers of tea polyphenols and risk of colorectal cancer in the Shanghai Cohort Study. International Journal of Cancer 2006; 120(6):1344–1350. [PubMed Abstract] 

  29. Simons CC, Leurs Lj, Weijenberg MP, et al. Fluid intake and colorectal cancer risk in the Netherlands Cohort Study. Nutrition and Cancer 2010; 62(3):307–321. [PubMed Abstract] 

  30. Zhang X, Albanes D, Beeson LW, et al. Risk of colon cancer and coffee, tea, and sugar-sweetened soft drink intake: Pooled analysis of prospective cohort studies. Journal of the National Cancer Institute 2010; 102(11):771–783. [PubMed Abstract] 

  31. Ganmaa D, Willett WC, Li TY, et al. Coffee, tea, caffeine and risk of breast cancer: A 22-year follow-up. International Journal of Cancer 2008; 122(9):2071–2076. [PubMed Abstract] 

  32. Inoue M, Robien K, Wang R, et al. Green tea intake, MTHFR/TYMS genotype and breast cancer risk: The Singapore Chinese Health Study. Carcinogenesis 2008; 29(10):1967–1972. [PubMed Abstract] 

  33. Zhang M, Holman CD, Huang J-P, Xie X. Green tea and the prevention of breast cancer: A case-control study in Southeast China. Carcinogenesis 2007; 28(5):1074–1078. [PubMed Abstract] 

  34. Zhang M, Huang J, Xie X, Holman CD. Dietary intakes of mushrooms and green tea combine to reduce the risk of breast cancer in Chinese women. International Journal of Cancer 2009; 124(6):1404–1408. [PubMed Abstract] 

  35. Shrubsole MJ, Lu W, Chen Z, et al. Drinking green tea modestly reduces breast cancer risk. Journal of Nutrition 2009; 139(2):310–316. [PubMed Abstract] 

  36. Kumar N, Titus-Ernstoff L, Newcomb P, et al. Tea consumption and risk of breast cancer. Cancer Epidemiology, Biomarkers and Prevention 2009; 18(1):341–345. [PubMed Abstract] 

  37. Ogunleye AA, Xue F, Michels KB. Green tea consumption and breast cancer risk or recurrence: A meta-analysis. Breast Cancer Research and Treatment 2010; 119(2):477–484. [PubMed Abstract] 

  38. Larsson SC, Bergkvist L, Wolk A. Coffee and black tea consumption and risk of breast cancer by estrogen and progesterone receptor status in a Swedish cohort. Cancer Causes and Control 2009; 20(10):2039–2044. [PubMed Abstract] 

  39. Luo J, Gao Y-T, Chow WH, et al. Urinary polyphenols and breast cancer risk: Results from the Shanghai Women’s Health Study. Breast Cancer Research and Treatment 2010; 120(3):693–702. [PubMed Abstract] 

  40. Bhoo Pathy N, Peeters P, van Gils C, et al. Coffee and tea intake and risk of breast cancer. Breast Cancer Research and Treatment 2010; 121(2):461–467. [PubMed Abstract] 

  41. Dai Q, Shu XO, Li H, et al. Is green tea drinking associated with a later onset of breast cancer? Annals of Epidemiology 2010; 20(1):74–81. [PubMed Abstract] 

  42. Iwasaki M, Inoue M, Sasazuki S, et al. Plasma tea polyphenol levels and subsequent risk of breast cancer among Japanese women: A nested case-control study. Breast Cancer Research and Treatment 2010; Epub ahead of print May 4, 2010. [PubMed Abstract] 

  43. Gates MA, Tworoger SS, Hecht JL, et al. A prospective study of dietary flavonoid intake and incidence of epithelial ovarian cancer. International Journal of Cancer 2007; 121(10):2225–2232. [PubMed Abstract] 

  44. Silvera SA, Jain M, Howe GR, Miller AB, Rohan TE. Intake of coffee and tea and risk of ovarian cancer: A prospective cohort study. Nutrition and Cancer 2007; 58(1):22–27. [PubMed Abstract] 

  45. Steevens J, Schouten LJ, Verhage BA, Goldbohm RA, van den Brandt PA. Tea and coffee drinking and ovarian cancer risk: Results from the Netherlands Cohort Study and a meta-analysis. British Journal of Cancer 2007; 97(9):1291–1294. [PubMed Abstract] 

  46. Baker JA, Boakye K, McCann SE, et al. Consumption of black tea or coffee and risk of ovarian cancer. International Journal of Gynecological Cancer 2007; 17(1):50–54. [PubMed Abstract] 

  47. Song YJ, Kristal AR, Wicklund KG, Cushing-Haugen KL, Rossing MA. Coffee, tea, colas, and risk of epithelial ovarian cancer. Cancer Epidemiology, Biomarkers and Prevention 2008; 17(3):712–716. [PubMed Abstract] 

  48. Zhou B, Yang L, Wang L, et al. The association of tea consumption with ovarian cancer risk: A metaanalysis. American Journal of Obstetrics and Gynecology 2007; 197(6):594.e1–e6. [PubMed Abstract] 

  49. Wang L, Lee IM, Zhang SM, et al. Dietary intake of selected flavonols, flavones, and flavonoid-rich foods and risk of cancer in middle-aged and older women. American Journal of Clinical Nutrition 2009; 89(3):905–912. [PubMed Abstract] 

  50. Nagle CM, Olsen CM, Bain CJ, et al. Tea consumption and risk of ovarian cancer. Cancer Causes and Control 2010; 21(9):1485–1491. [PubMed Abstract] 

  51. Kurahashi N, Sasazuki S, Iwasaki M, Inoue M, Tsugane S. Green tea consumption and prostate cancer risk in Japanese men: A prospective study. American Journal of Epidemiology 2008; 167(1):71–77. [PubMed Abstract] 

  52. Jian L, Lee AH, Binns CW. Tea and lycopene protect against prostate cancer. Asian Pacific Journal of Clinical Nutrition 2007; 16(Suppl 1):453–457. [PubMed Abstract] 

  53. Li Q, Kakizaki M, Kuriyama S, et al. Green tea consumption and lung cancer risk: The Ohsaki study. British Journal of Cancer 2008; 99(7):1179–1184. [PubMed Abstract] 

  54. Cui Y, Morgenstern H, Greenland S, et al. Dietary flavonoid intake and lung cancer—a population-based case-control study. Cancer 2008; 112(10):2241–2248. [PubMed Abstract] 

  55. Kubík A, Zatloukal P, Tomášek L, et al. A case-control study of lifestyle and lung cancer associations by histological types. Neoplasma 2008; 55(3):192–199. [PubMed Abstract] 

  56. Kubík A, Zatloukal P, Tomášek L, et al. Interactions between smoking and other exposures associated with lung cancer risk in women: Diet and physical activity. Neoplasma 2007; 54(1):83–88. [PubMed Abstract] 

  57. Tang N, Wu Y, Zhou B, Wang B, Yu R. Green tea, black tea consumption and risk of lung cancer: A meta-analysis. Lung Cancer 2009; 65(3):274–283. [PubMed Abstract] 

  58. Li N, Sun Z, Han C, Chen J. The chemopreventive effects of tea on human oral precancerous mucosa lesions. Proceedings from the Society of Experimental Biology and Medicine 1999; 220(4):218–224. [PubMed Abstract] 

  59. Tsao AS, Liu D, Martin J, et al. Phase II randomized, placebo-controlled trial of green tea extract in patients with high-risk oral premalignant lesions. Cancer Prevention Research 2009; 2(11):931–941. [PubMed Abstract] 

  60. Hakim IA, Harris RB, Brown S, et al. Effect of increased tea consumption on oxidative DNA damage among smokers: A randomized controlled study. Journal of Nutrition 2003; 133(10):3303S–3309S. [PubMed Abstract] 

  61. Luo H, Tang L, Tang M, et al. Phase IIa chemoprevention trial of green tea polyphenols in high-risk individuals of liver cancer: Modulation of urinary excretion of green tea polyphenols and 8-hydroxydeoxyguanosine. Carcinogenesis 2006; 27(2):262–268. [PubMed Abstract] 

  62. Bettuzzi S, Brausi M, Rizzi F, et al. Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: A preliminary report from a one-year proof-of-principle study. Cancer Research 2006; 66(2):1234–1240. [PubMed Abstract] 

  63. Jatoi A, Ellison N, Burch PA, et al. A phase II trial of green tea in the treatment of patients with androgen independent metastatic prostate carcinoma. Cancer 2003; 97(6):1442–1446. [PubMed Abstract] 

  64. Choan E, Segal R, Jonker D, et al. A prospective clinical trial of green tea for hormone refractory prostate cancer: An evaluation of the complementary/alternative therapy approach. Urologic Oncology: Seminars and Original Investigations 2005; 23(2):108–113. [PubMed Abstract] 

  65. Hamajima N, Tajima K, Tominaga S, et al. Tea polyphenol intake and changes in serum pepsinogen levels. Japanese Journal of Cancer Research 1999; 90(2):136–143. [PubMed Abstract] 

  66. Wang LD, Zhou Q, Feng CW, et al. Intervention and follow-up on human esophageal precancerous lesions in Henan, northern China, a high-incidence area for esophageal cancer. Gan To Kagaku Ryoho 2002; 29(Suppl 1):159–172. [PubMed Abstract]


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