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REVIEW ARTICLE
Year : 2014  |  Volume : 4  |  Issue : 1  |  Page : 4-10

Carcinogens and cancer preventors in diet


1 Department of Oral Medicine, Diagnosis and Radiology, CSMSS Dental College and Hospital, Aurangabad, Maharashtra, India
2 Department of Conservative Dentistry and Endodontics, MGM Dental College and Hospital, Navi Mumbai, Maharashtra, India

Date of Submission28-Feb-2013
Date of Acceptance04-Jul-2013
Date of Web Publication8-Jan-2014

Correspondence Address:
Neha Khambete
C/o, khambete hospital, ward no. 1, opp. Railway goods yard, shrirampur - 413 709, maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2231-0738.124609

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   Abstract 

Cancer is a major burden on the health-care system world-wide not only in the developed countries, but also in the developing countries. Several lines of evidence indicate that diet and nutrition can contribute to human cancer risk. Diet is an important factor in determining cancer incidence in many countries and regions. Diet components relevant to cancer development can be divided into macro-and micro-components. Diet can have both positive and negative effects on carcinogenesis. Several substances in diet such as heterocyclic amines, polycyclic aromatic hydrocarbons, N-nitroso compounds and alcohols have been associated with increased risk of cancer, whereas certain compounds such as phytochemicals and probiotics have cancer preventing properties. This paper aims to review the carcinogenic and cancer preventive properties of dietary substances and their possible mechanisms of action.

Keywords: Cancer, carcinogenesis, diet, nutrition


How to cite this article:
Khambete N, Kumar R. Carcinogens and cancer preventors in diet. Int J Nutr Pharmacol Neurol Dis 2014;4:4-10

How to cite this URL:
Khambete N, Kumar R. Carcinogens and cancer preventors in diet. Int J Nutr Pharmacol Neurol Dis [serial online] 2014 [cited 2018 Jan 24];4:4-10. Available from: http://www.ijnpnd.com/text.asp?2014/4/1/4/124609


   Introduction Top


Cancer is a major burden of disease world-wide not only in developed countries, but also in developing countries. [1] It is known that about 5-10% of all cancers are caused by genetic defects while the rest of 90-95% are caused by environmental factor and life-style, including diet (30-35%), tobacco smoking (25-30%) and alcohol (4-6%). [2] Several lines of evidence indicate that diet and nutrition can contribute to human cancer risk. Foods and dietary behaviors are thought to increase cancer risk, which is due in part to the consumption of food mutagens. These mutagens contribute to cancer along the route of exposure (oral cavity, esophagus, gastrointestinal tract) and in organs that are distant to the route of exposure (e.g., liver). [3] Advances in analytic technology, especially the Ames test have disclosed that in experimental systems an astonishing variety of compounds occurring naturally in the diet are carcinogenic or mutagenic. Ames concluded, "Nature is not benign; no human diet can be entirely free from mutagens and carcinogens." [4]

From the mechanistic view, nutritional factors are classified into genotoxic and non-genotoxic agents. Genotoxic agent begins their action at the deoxyribonucleic acid (DNA) level, causing DNA damage through several mechanisms. Non-genotoxic agents are less defined in their modes of action, but they are presumed to indirectly affect the cell through tumor promoters. These agents are generally macro components, e.g., high fat. [5]

On the other hand, it is also well-recognized that diet and nutrition contain components that can reduce the risk of cancer; thus, nutritionally related cancer ultimately develops from an imbalance of carcinogenesis and anti-carcinogenesis process. [3]


   Mechanisms of Diet Induced Carcinogenesis Top


In general, cancer development has been considered to consist three major steps namely initiation, promotion and progression. Initiation, which is an irreversible process, starts when normal cells are exposed to carcinogenic substances and their DNA undergo damage that remain unrepaired or misread. In chemical carcinogenesis, initiation involves the uptake of a given carcinogen, which is subsequently distributed to organs for metabolism.

Metabolic activation leads to reactive (electrophilic) species, which can bind to DNA rather than excretory carrier molecules. The binding can then cause coding errors at the time of replication leading to mutation. The somatic mutation in a damaged cell can then be reproduced during mitosis to produce clones of mutated cells [Figure 1]. The next stage in the carcinogenesis process, which is promotion, is the expansion of the damaged cells to form an actively proliferating multi-cellular premalignant tumor cell population. The last stage known as progression is the irreversible process, which produces new clone of tumor cells with increased proliferative capacity, invasiveness and metastasis.
Figure 1: Mechanism of dietary carcinogenesis

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Food mutagens absorbed orally pass through the liver and are distributed in the body. Those carcinogenic compounds are classified as direct act directly on DNA, but most require enzymatic conversion and are thus labeled as indirect or pro-carcinogens. Metabolic activation of procarcinogen is controlled by phase I reactions while phase II reactions protect the body through the transformation of activated compounds into inert products, which are easily eliminated from the body. Metabolic activation occurs predominantly in the liver at the endoplasmic reticulum where the cytochrome P450 (important enzyme in phase I reactions) is more abundant. The results are powerful electrophilic product capable of establishing interaction to the nucleophilic component (DNA, ribonucleic acid (RNA and proteins), alter the structural integrity and forming covalent bounding, called as adduct. If the adduct being produced by metabolic activation is not able to be repaired by DNA repair before the replication process, then a mutation in proto-oncogene and tumor suppressor gene will occur which is a very important step in carcinogenesis initiation.

On the contrary, non-genotoxic carcinogens do not need metabolic activation, do not react directly with DNA and do not raise adducts; they act as promoters and modulate cell growth and cell death and are potential to have the effect of genotoxic carcinogens. [3]


   Dietary Carcinogens and Their Sources Top


Microcomponents

Aflatoxin B1


Aflatoxin is a kind of mycotoxins produced by the mold Aspergillus flavus, which can be found in legumes, corns, soybeans, rice, milk and cheese. In animal models, AFB1 had been proved to induce liver cancer. Although, AFB1 synergies hepatitis B and C infections in the causation of liver cancer both laboratory and epidemiological data have established the role of aflatoxin in liver carcinogenesis. [6] It has been shown that AFB1 exposure occurs through the consumption of mold-contaminated groundnuts, grains and animal feed, which can be transmitted transplacentally and to newborns through breast-feeding. [4],[5],[7]

Fumonisins

Fumonisin was discovered in South Africa in 1988. Fumonisins are a family of toxic and carcinogenic mycotoxin produced by Fusarium verticillioides (formerly Fusarium moniliforme), a common fungal contaminant of maize. Some studies have associated consumption of maize contaminated with fumonisins to human esophageal carcinoma in some parts of South Africa and China. [8]

Ochratoxins

Ochratoxin A (OTA) is a mycotoxin produced as secondary metabolite by species of Aspergillus and Penicillium. It is found as contaminant in human foods, including various cereals, coffee, cocoa, wines and dried fruits. Depending on the dose, OTA may be carcinogenic, genotoxic, immunotoxic or teratogenic. International Agency for Research on Cancer (IARC) has classified it in group 2B as possibly carcinogenic to humans. The kidney has been shown to be a target organ. [9],[10]

Polycyclic aromatic hydrocarbons

PAH are compounds formed during incomplete combustion of organic matter. Many PAH have been established experimentally as carcinogens. [3] Cigarette smoking has also been shown to contribute to PAH burden in man. PAH compounds are formed during incomplete combustion of organic matter. Smoked foods, e.g. ham, sausages and fish may contain PAH, resulting from incomplete combustion in food processing. Benzo (a) pyrene represents the best characterized PAH compound obtained from the diet. In several animal species, administration of benzo (a) pyrene by different routes has been shown to result in the production of tumors. Benzo (a) pyrene adducts have been linked to cancer risk in the lung and they are also associated with site-specific hot spot mutations in the p53 tumor-suppressor gene. [3]

Heterocyclic amines

HCA are the carcinogenic chemicals formed within muscle meats during most types of high temperature cooking, through a pyrolysis process from amino acids, proteins and creatines. In rats and mice HCA target the liver, lung, urinary bladder, small and large intestines, forestomach, skin, oral cavity, mammary glands, clitoral gland and prostate in the ventral lobe. [7] One of the most common is the 2-amino-1-methyl-6-phenylimidazole [4,5-b] pyridine (PhIP). PhIP induces tumors of the breast, colon and prostate. HCA formation is influenced by four factors: Type of food, cooking method, temperature and time. HCA are found in cooked muscle meats (beef, pork, of fish). Cooking methods, such as frying, broiling and barbecuing produce the largest amounts of HCAs. However, HCAs exposure can be reduced by varying methods of cooking meats, especially by stewing and boiling and having the meats partially cooked by microwave, before frying, broiling or barbecuing. [5]

N-nitrosamines

Both nitrate and nitrite are capable to form nitrosamines, a large group of compounds with common carcinogenic mechanism. Humans are exposed to N-nitroso compounds in diet from a variety of cured meats and fish products. Sodium nitrite has been used as food addictive for preservation and as coloring substance in meat. N-nitrosamines may also be derived from nicotine of tobacco smoking. Cancer of the lung, liver, kidney, mammary gland, stomach, pancreas, bladder or esophagus has been observed and these sites are also considered to be the targeted organs. [11],[12],[13]

Alcohol

Epidemiological data have identified chronic alcohol consumption as a significant risk factor for upper alimentary tract cancer, including cancer of the oropharynx, larynx and esophagus and of the liver. The increased risk in the large intestine and in the breast is much smaller. However, although the risk is lower, carcinogenesis can be enhanced with relatively low daily doses of ethanol. The metabolism of ethanol leads to the generation of acetaldehyde and free radicals. Evidence has accumulated that acetaldehyde is predominantly responsible for alcohol associated carcinogenesis. [14]

Macrocomponents

Total calorie intake


Excess calorie intake has been known to contribute to increase the risk of several cancers, e.g.,ss breast, colon and prostate cancer. Digestion, absorption, metabolism and excretion of fat deposits require oxidative metabolism, which create free radicals capable of causing DNA damage. Significant positive associations were found between obesity and higher death rates for the following cancers: Esophagus, colon and rectum, liver, gallbladder, pancreas, kidney, stomach, prostate, breast, uterus, cervix and ovary. [7],[15]

Fatty acids

Animal fat rich in saturated fatty acids and plant-derived oils, such as corn oil, sun-flower seed oil, which are rich in linoleic acid, one of the n-6 polyunsaturated fatty acids (PUFA)/arachydonic acid are suggested to enhance cancer development. Increased levels of linoleic acid in the erythrocytes of premenopausal women are related to increase the risk of breast cancer. In contrast, n-3 PUFA (linolenic acid), which derives from fish oils, especially eicosapentaenoic acid, docosahexaenoic acid and n-9 monounsaturated fatty acids/oleic acid, like olive oils are known to have protective effects against carcinogenesis. [16]


   Mechanism of Action of Anti-Cancer Agents Top


The process of carcinogenesis consists of three major steps: Initiation, where an irreversible change is affected in the cellular genes; promotion, where the initiated cells expand by self-proliferation leading to abnormal growth and further mutations and progression, where the cells detach from the primary tumor and invade other organs and tissues, forming metastatic growths. Angiogenesis plays an important role in the tumor metastasis. Different types of cancer genes - oncogenes and anti-oncogenes (tumor suppressor genes) -are involved in cancer development. Gain of function mutations in the oncogenes, leading to abnormal cell proliferation and loss of function mutations in the anti-oncogenes leading to suppression of cell differentiation and apoptosis are the major events leading to cancer development. [17] There is now considerable evidence that the chemopreventive properties of plant-based food are related to their ability to block the progression of latent microtumors. These properties arise from the high content of phytochemicals, molecules that target several key events in the development of cancer. Intensive research conducted over the last few years has shown that phytochemicals derived from the diet interfere with tumor progression by acting directly on tumor cells as well as by modifying the tumor's microenvironment (stroma) and creating physiologic conditions that are hostile to tumor growth.

Direct inhibitory actions on tumor cells

Reduction of damage to DNA


Phytochemicals elicit their anti-cancer effects by modulating the enzymatic systems responsible for neutralizing these carcinogens, either by reducing their carcinogenic potential or by increasing their excretion. [18],[19],[20]

Cytotoxicity against tumor cells

Several phytochemicals also inhibit tumor growth by directly inducing cancer cell death by apoptosis. Overall, the cytotoxic properties of diet-derived phytochemicals contribute to the chemo preventive effects associated with intake of plant-derived foods and could play an essential role in preventing the growth of cells that have already acquired an initiated phenotype (precancerous cells). [21],[22],[23]

Anti-proliferative activity

Recent researches have shown that various phytochemicals reduce the tumor cell proliferation by causing cell cycle arrest and inducing apoptosis. Their actions are exerted at various stages of cell cycle. Certain phytochemicals act at mitochondrial and nuclear level to inhibit cell division. [24]

Effects on tumor microenvironment

Antiangiogenic properties


Angiogenesis is the process by which tumor cells stimulate the formation of new blood vessel networks that sustain the development of cancer by providing oxygen and nutrients to tumor cells. Work has shown that several phytochemicals possess strong antiangiogenic activity and that this effect likely plays a significant role in their chemopreventive properties. [22],[25]

Anti-inflammatory effects

It is becoming increasingly clear that inflammatory stimuli participate in the progression of several cancers, including those of the colorectum, breast and lung. In addition to the important role of dietary PUFAs, there is also growing evidence that several phytochemicals from dietary sources reduce inflammatory processes and that this anti-inflammatory effect contributes to their anti-cancer properties. [26],[27]

Several classifications of the mechanisms of anti-cancer agents have been proposed by a number of investigators. Wattenberg (1985) subdivided anticarcinogens into two major categories; blocking agents and suppressing agents on the basis by which they exert a protective effect at specific stages of multi-step carcinogenesis. Blocking agents are substances that can inhibit initiation either by inhibiting the formation of carcinogens from pre-cursor molecules or reactive intermediates from the parent carcinogens or by preventing the ultimate electrophilic species from interacting with macromolecules such as DNA, RNA and proteins. Suppressing gents act at the promotion or the progression stage by preventing the malignant expression of initiated cells. [28]

Phytochemicals

Phytochemicals are naturally occurring, biologically active chemical compounds in plants. The prefix "phyto" is from a Greek word meaning plant. In plants, phytochemicals act as a natural defense system for host plants and provide color, aroma and flavor. More than 4000 of these compounds have been discovered to date. Phytochemicals are rich sources of vitamins and antioxidants, which are thought to have anti-cancer properties. They are divided into flavonoids, carotenoids, indoles, isothiocyanates, polyphenols, capsaicin, phytoestrogens, phytosterols, protease inhibitors, saponins, sufides, tannins and terpenes. [16],[28],[29],[30],[31],[32]

The anti-cancer activity of phytochemicals is summarized in [Table 1].
Table 1: Anticancer activity of phytochemicals

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Clinical trials

Breast cancer prevention


The investigation of bioactive food components for breast cancer prevention is based on population and case-control studies. For example, some studies suggested that a diet characterized by a high intake of vegetables, including cruciferous vegetables (e.g., broccoli, cauliflower, cabbage and kale), is associated with a decreased risk of breast cancer. Epidemiologic and animal data suggest that isoflavones are associated with the prevention of cancer. Trials of retinoids have been equivocal and current phase I and II trials are being conducted to determine their usefulness as chemopreventive agents for various cancers, including breast cancer. A nested case-control study investigated the association between serum and plasma concentration of retinol, retinyl palmitate, α-and β carotene, β-cryptoxanthin, lutein, lycopene and α-and α-tocopherol and subsequent development of breast cancer. The results showed about a 50% reduction in breast cancer risk in women with high levels of β-carotene, lycopene and total carotene compared with those with a low level of these micronutrients. [33],[34]

Prostate cancer prevention

Three population-based, randomized, placebo-controlled clinical trials conducted also report encouraging results for the bioactive food components vitamin E and selenium. In a secondary analysis of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, it was reported that men (smokers) who received 50 g daily vitamin E (alpha-tocopherol) supplements had a 41% decrease in prostate cancer mortality and a 36% decrease in incidence. Other bioactive food components also are being investigated in prostate cancer prevention trials. For example, lycopene, abundant in tomato-based products, has been the subject of numerous experimental and animal studies showing a possible reduction in prostate cancer risk with high levels of lycopene intake. [33],[34]

Gastrointestinal cancer prevention

While combined treatments with selenium (50 μg), α-carotene (15 mg) and vitamin E (α-tocopherol, 30 mg) resulted in a lower incidence of cancer and a 10% reduction in cancer mortality from esophageal and gastric cancer in the China study. β-carotene, vitamin A, vitamin C and vitamin E supplements given alone or in combinations do not seem to have much effect in the prevention of gastrointestinal cancers. [33],[34]

Oral cancer prevention

The evidence of a beneficial effect of fruit and vegetables on oral and pharyngeal cancer risk has been consistently observed for raw and green/leafy vegetables and citrus fruit. Several case-control studies also found consistent inverse associations with carrots while for other specific vegetables or fruit (such as cruciferous vegetables or apples/pears) the evidence is more limited. [35]

Probiotics

The bacteria that reside in the intestinal tract generally have a symbiotic relationship with their host. Beneficial bacteria produce natural antibiotics to keep pathogenic bugs in check (preventing diarrhea and infections) and produce some B vitamins in the small intestine where they can be utilized. There is a solid theoretical basis for why probiotics should help prevent cancer, especially colon cancer and even reverse cancer. Probiotics produce short chain fatty acids in the colon, which acidify the environment. Lower colon pH is associated with a lower incidence of colon cancer. Probiotic bacteria reduce the level of procarcinogenic enzymes such as beta-glucuronidase, nitroreductase and azoreductase. [36],[37],[38]

Dietary fibers

Burkitt proposed that a high-fiber diet would effectively dilute out carcinogens.

He also proposed that diets low in fiber lead to a slow transmission of dietary components through the gut. The slow transit time may allow a longer time during which carcinogens present in the gut may be in contact with the gut wall. [39]

Selenium

Selenium is a mineral with anti-cancer properties. Many studies in the last several years have shown that selenium is a potent protective nutrient for some forms of cancer. Overall, it appears that poor selenium levels, especially for men, are a cancer risk. If a person has low selenium levels and other antioxidant defenses are also low the cancer risk is increased even further. Good vegetarian sources of selenium are whole grains and legumes grown in selenium-rich soil, nuts, nutritional yeast, brewer's yeast and sunflower seeds. [40],[41],[42]


   Conclusion Top


Diet and nutritional factors are one of several major causes of carcinogenesis. Carcinogenic processes themselves are known to involve multi steps process (initiation, promotion, progression) and influenced by various factors. Chemoprevention by dietary substances is now considered to be an inexpensive, readily applicable, acceptable and accessible approach to cancer control and management. With health-care costs being a key issue today, it would be cost-effective to promote awareness and consumption of such substances as a cancer-preventive strategy for the general public. Hence, a good knowledge of diet, nutrition and life-styles are important to reduce cancer risk in the society.

 
   References Top

1.Ma X, Yu H. Global burden of cancer. Yale J Biol Med 2006;79:85-94.  Back to cited text no. 1
[PUBMED]    
2.Anand P, Kunnumakkara AB, Sundaram C, Harikumar KB, Tharakan ST, Lai OS, et al. Cancer is a preventable disease that requires major lifestyle changes. Pharm Res 2008;25:2097-116.  Back to cited text no. 2
[PUBMED]    
3.Goldman R, Shields PG. Food mutagens. J Nutr 2003;133 Suppl 3:965S-73.  Back to cited text no. 3
[PUBMED]    
4.Ames BN. Dietary carcinogens and anticarcinogens. Oxygen radicals and degenerative diseases. Science 1983;221:1256-64.  Back to cited text no. 4
[PUBMED]    
5.Sutandyo N. Nutritional carcinogenesis. Acta Med Indones 2010;42:36-42.  Back to cited text no. 5
[PUBMED]    
6.Turner PC, Mendy M, Whittle H, Fortuin M, Hall AJ, Wild CP. Hepatitis B infection and aflatoxin biomarker levels in Gambian children. Trop Med Int Health 2000;5:837-41.  Back to cited text no. 6
[PUBMED]    
7.Sugimura T. Nutrition and dietary carcinogens. Carcinogenesis 2000;21:387-95.  Back to cited text no. 7
[PUBMED]    
8.Marasas WF, Riley RT, Hendricks KA, Stevens VL, Sadler TW, Gelineau-van Waes J, et al. Fumonisins disrupt sphingolipid metabolism, folate transport, and neural tube development in embryo culture and in vivo: A potential risk factor for human neural tube defects among populations consuming fumonisin-contaminated maize. J Nutr 2004;134:711-6.  Back to cited text no. 8
[PUBMED]    
9.van der Merwe KJ, Steyn PS, Fourie L, Scott DB, Theron JJ. Ochratoxin A, a toxic metabolite produced by Aspergillus ochraceus Wilh. Nature 1965;205:1112-3.  Back to cited text no. 9
[PUBMED]    
10.Kuiper-Goodman T, Scott PM. Risk assessment of the mycotoxin ochratoxin A. Biomed Environ Sci 1989;2:179-248.  Back to cited text no. 10
[PUBMED]    
11.Fiddler W. The occurrence and determination of N-nitroso compounds. Toxicol Appl Pharmacol 1975;31:352-60.  Back to cited text no. 11
    
12.Tannenbaum SR. Endogenous formation of N-nitroso compounds: A current perspective. In: Bartsch H, O'Neill I, Schulte-Hermann R, editors. The Relevance of N-nitroso Compounds to Human Cancer Exposures and Mechanisms. Lyon, France: IARC Scientific Publications No. 84, International Agency for Research on Cancer; 1997. p. 292-5.  Back to cited text no. 12
    
13.Lijinsky W. In vivo testing for carcinogenicity. In: Cooper CS, Grover PL, editors. Chemical Carcinogenesis and Mutagenesis 1. Berlin: Springer-Verlag; 1999. p. 179-209.  Back to cited text no. 13
    
14.Pöschl G, Seitz HK. Alcohol and cancer. Alcohol Alcohol 2004;39:155-65.  Back to cited text no. 14
    
15.Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 2003;348:1625-38.  Back to cited text no. 15
    
16.Donaldson MS. Nutrition and cancer: A review of the evidence for an anti-cancer diet. Nutr J 2004;3:19.  Back to cited text no. 16
[PUBMED]    
17.Devi PU. Basics of carcinogenesis. Health Adm 1998;17:16-24.  Back to cited text no. 17
    
18.Ioannides C, Lewis DF. Cytochromes P450 in the bioactivation of chemicals. Curr Top Med Chem 2004;4:1767-88.  Back to cited text no. 18
[PUBMED]    
19.Conney AH. Enzyme induction and dietary chemicals as approaches to cancer chemoprevention: The seventh DeWitt S. Goodman lecture. Cancer Res 2003;63:7005-31.  Back to cited text no. 19
[PUBMED]    
20.Talalay P. Chemoprotection against cancer by induction of phase 2 enzymes. Biofactors 2000;12:5-11.  Back to cited text no. 20
[PUBMED]    
21.Thornalley PJ. Isothiocyanates: Mechanism of cancer chemopreventive action. Anticancer Drugs 2002;13:331-8.  Back to cited text no. 21
[PUBMED]    
22.Karunagaran D, Rashmi R, Kumar TR. Induction of apoptosis by curcumin and its implications for cancer therapy. Curr Cancer Drug Targets 2005;5:117-29.  Back to cited text no. 22
[PUBMED]    
23.Jang M, Cai L, Udeani GO, Slowing KV, Thomas CF, Beecher CW, et al. Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Science 1997;275:218-20.  Back to cited text no. 23
[PUBMED]    
24.Tosetti F, Ferrari N, De Flora S, Albini A. Angioprevention': Angiogenesis is a common and key target for cancer chemopreventive agents. FASEB J 2002;16:2-14.  Back to cited text no. 24
[PUBMED]    
25.Sapra R, Bansal R, Bansal P. Dietary phytochemicals in cell cycle arrest and apoptosis: An insight. J Drug Deliv Ther 2012;2:8-17.  Back to cited text no. 25
    
26.Béliveau R, Gingras D. Green tea: Prevention and treatment of cancer by nutraceuticals. Lancet 2004;364:1021-2.  Back to cited text no. 26
    
27.Coussens LM, Werb Z. Inflammation and cancer. Nature 2002;420:860-7.  Back to cited text no. 27
[PUBMED]    
28.Surh YJ, Chun KS, Cha HH, Han SS, Keum YS, Park KK, et al. Molecular mechanisms underlying chemopreventive activities of anti-inflammatory phytochemicals: Down-regulation of COX-2 and iNOS through suppression of NF-kappa B activation. Mutat Res 2001;480-1:243-68.  Back to cited text no. 28
    
29.Farombi EO. Diet-related cancer and prevention using anticarcinogens. Afr J Biotechnol 2004;3:651-61.  Back to cited text no. 29
    
30.Béliveau R, Gingras D. Role of nutrition in preventing cancer. Can Fam Physician 2007;53:1905-11.  Back to cited text no. 30
    
31.Johary A, Jain V, Misra S. Role of lycopene in the prevention of cancer. Int J Nutr Pharmacol Neurol Dis 2012;2:167-70.  Back to cited text no. 31
  Medknow Journal  
32.Mullaicharam AR, Maheshwaran A. Pharmacologic effects of curcumin. Int J Nutr Pharmacol Neurol Dis 2012;2:92-9.  Back to cited text no. 32
  Medknow Journal  
33.Nebeling L. Phytochemicals: The color of a healthy diet. Pediatr Basics Spring 2002;99:1-4.  Back to cited text no. 33
    
34.Borek C. Dietary antioxidants and human cancer. Integr Cancer Ther 2004;3:333-41.  Back to cited text no. 34
[PUBMED]    
35.Bjelakovic G, Nikolova D, Simonetti RG, Gluud C. Antioxidant supplements for prevention of gastrointestinal cancers: A systematic review and meta-analysis. Lancet 2004;364:1219-28.  Back to cited text no. 35
[PUBMED]    
36.Lucenteforte E, Garavello W, Bosetti C, La Vecchia C. Dietary factors and oral and pharyngeal cancer risk. Oral Oncol 2009;45:461-7.  Back to cited text no. 36
[PUBMED]    
37.Finegold SM, Sutter VL, Sugihara PT, Elder HA, Lehmann SM, Phillips RL. Fecal microbial flora in Seventh Day Adventist populations and control subjects. Am J Clin Nutr 1977;30:1781-92.  Back to cited text no. 37
[PUBMED]    
38.Goldin BR, Gorbach SL. The effect of milk and Lactobacillus feeding on human intestinal bacterial enzyme activity. Am J Clin Nutr 1984;39:756-61.  Back to cited text no. 38
[PUBMED]    
39.Saini R. Role of probiotics in colorectal cancer. Int J Nutr Pharmacol Neurol Dis 2011;1:81-2.  Back to cited text no. 39
  Medknow Journal  
40.Burkitt DP, Walker AR, Painter NS. Effect of dietary fibre on stools and the transit-times, and its role in the causation of disease. Lancet 1972;2:1408-12.  Back to cited text no. 40
[PUBMED]    
41.Selenium Information Sheet. Available from: http://www.selenium.arizona.edu/INFOse.htm. [Accessed on 2012 Sep 01].  Back to cited text no. 41
    
42.Duffield-Lillico AJ, Reid ME, Turnbull BW, Combs GF Jr, Slate EH, Fischbach LA, et al. Baseline characteristics and the effect of selenium supplementation on cancer incidence in a randomized clinical trial: A summary report of the nutritional prevention of cancer trial. Cancer Epidemiol Biomarkers Prev 2002;11:630-9.  Back to cited text no. 42
[PUBMED]    


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