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 Table of Contents  
REVIEW ARTICLE
Year : 2014  |  Volume : 1  |  Issue : 1  |  Page : 5-8

Magnanimous effects and role of dietary nutrition on carcinogenesis: A comprehensive review of literature


1 Department of Periodontics, Shree Bankey Bihari Dental College and Research Centre, Ghaziabad, Uttar Pradesh, India
2 Department of Oral and Maxillofacial Surgery, Rama Dental College Hospital and Research Centre, Kanpur, Uttar Pradesh, India
3 Department of Pedodontics and Preventive Dentistry, DJ Dental College, Modinagar, Ghaziabad, Uttar Pradesh, India
4 Department of Prosthodontics, Shree Bankey Bihari Dental College and Research Centre, Ghaziabad, Uttar Pradesh, India

Date of Web Publication17-Feb-2014

Correspondence Address:
Prashant Tyagi
Department of Periodontics, Shree Bankey Bihari Dental College and Research Centre, Masuri, N.H. 24, Ghaziabad - 201 302, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2148-7731.127219

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  Abstract 

Oral cancer is one of the most critical health problems faced by the mankind today. Cancer is a result of multiple genetic defects resulting from exposure to environmental and infectious agents. Most of the oral cancers are associated with tobacco use and some are attributed to inappropriate nutritional habits. Tobacco chewing is a unique habit of Indian, southeast Asian subcontinent and is consumed commonly in the form of pan, gutka, etc. Furthermore, cancer prevention strategies can be applied by upregulating the defense mechanism, inducing cancer cells to apoptosis and decreasing angiogenesis of cancer cells. Nutritional factors play a key role in cancer impediment by increasing the intake of vegetables and fruits. This paper is an effort to draw the attention towards the significant role of diet in cancer prevention and associated mechanisms with its carcinogenesis.

Keywords: Cancer, carcinogenesis, nutrition


How to cite this article:
Tyagi P, Shrama G, Hussain S, Kundu A, Gaur A, Kumar P. Magnanimous effects and role of dietary nutrition on carcinogenesis: A comprehensive review of literature. Sifa Med J 2014;1:5-8

How to cite this URL:
Tyagi P, Shrama G, Hussain S, Kundu A, Gaur A, Kumar P. Magnanimous effects and role of dietary nutrition on carcinogenesis: A comprehensive review of literature. Sifa Med J [serial online] 2014 [cited 2019 Mar 23];1:5-8. Available from: http://www.imjsu.org/text.asp?2014/1/1/5/127219


  Introduction Top


Relative advantages of a balanced diet on general body health are well-known. Rising incidence of cancer is an alarming cause of concern in today's world. Dietary factors have been thought to account for about 30% of cancers in Western countries, making diet second only to tobacco as a preventable cause of cancer. [1] According to the World Health Report (2002) tobacco is the most important preventable cause of overall mortality as well as cardiovascular mortality worldwide. [2] The contribution of diet to cancer risk in developing countries has been considered to be lower, perhaps around 20%. [3] Cancers of the oral cavity, pharynx, and esophagus were estimated to account for 867,000 cases and 582,000 deaths in 2000. [4]

Each year, about 550,000 Americans die of cancer; fully one-third of these deaths are linked to poor diet, physical inactivity, and obesity. In developed countries like India, the main risk factors are alcohol and tobacco, and up to 75% of these cancers are attributable to these two lifestyle factors. [5] Diet is an important factor in cancer etiology and prevention in India. In developing countries, around 60% of cancers of the oral cavity, pharynx, and esophagus are thought to be due to micronutrient deficiencies related to a restricted diet that is low in fruits and vegetables and animal products. [6],[7]

As a society, Indians have one of the most interesting diets, with many unique dietary constituents that have promise for cancer prevention. There is also consistent evidence that consuming drinks and foods at a very high temperature increases the risk for these cancers. [8] Since long time, it is believed that certain foods have potential components which augment our immune system and thus effectively combat various infectious diseases. [9] Genotoxic agent begins their action at the deoxyribonucleic acid (DNA) level, causing DNA damage through several mechanisms, e.g., gene point mutations, deletions and insertions, recombinations, rearrangements and amplifications, as well as chromosomal aberrations. [10] However, literature has evidenced several studies stating that abundant consumption of foods of plant origin, such as fruit, vegetables, whole grains, nuts, seeds, and tea can decrease the risk of developing various cancers. [11]

Human beings are often being exposed to carcinogenic factors during their life, whether they realize it or not. It was long discovered that the carcinogenesis process is complex and multistep process of which several genetic and molecular defects are needed to manifest as cancer. The three major stages of carcinogenic process are initiation, promotion, and progression Carcinogenesis is a multistep process which has checkpoint controls at each step. Thus, the process of carcinogenesis can be intercepted at all these various levels by a variety of molecular events. [12] Various steps involved in carcinogenesis are initiation, promotion, progression, and growth. Initiation results from exposure to a carcinogen, which leads to promotion of a normal cell to cancer cell. This further advances progression and growth of the cancer cells. These cancerous cells must accumulate several mutations in the genes involved in cell cycle arrest, resistance to apoptosis, and induction of angiogenesis in order to grow and invade the host tissues. The nutrients with their active components can act on genetic alterations occurring in cancer cells. They can also alter regulation of apoptosis, cause cell cycle arrest and control angiogenesis in tumor cells. Certain nutrients even restrict tumor growth potential. [13] The present paper describes the significant role of diet in cancer prevention along with an elaborate overview of various mechanisms by which several active nutrient molecules intercept carcinogenesis.


  Nutritional Carcinogenic Agents and the Source from Diet Top


Aflatoxin B1

Aflatoxin is a type of mycotoxins produced by the mold Aspergillus flavus. It is frequently found in legumes, corns, soybeans, rice, milk, and cheese. In different animal study models, aflatoxins B1 had been proved to induce liver cancer. Moreover, guanine interaction with adducts will create mutational effects to p53 tumor suppressor gene at specific codon 249. Such transversion is almost found in liver cancer patients with high levels of aflatoxins contamination. [14],[15]

Heterocyclic amines (HCA)

HCA are the most notorious carcinogenic chemicals usually formed inside muscle meats during various types of high temperature cooking. The underlying mechanism is frequently related to pyrolisis process from amino acids, proteins, and creatines. [16],[17],[18],[19],[20] HCA formation is mainly affected by four factors: Type of food, cooking method, temperature, and time. However, the HCA are found in cooked muscle meats (beef, pork, of fish). Other sources of protein (milk, eggs, tofu, and organ meats such as liver) have very little or no HCA content naturally or when cooked. Method of cooking, such as frying, broiling, and barbecuing produce the largest amounts of HCAs on the other hand oven, roasting, and baking produce smaller amount of HCAs. 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. [15]

Polycyclic aromatic hydrocarbons (PAHs)

PAH compounds are generally produced during incomplete combustion of organic matter. These compounds are also usually found in tobacco smoking. Benzopirene is the best-characterized PAH compound available from the diet. Several animal and human studies suggest that dietary PAH is distributed to organ besides the locally exposed tissues, so it is plausible to consider that dietary PAH may contribute to lung or breast cancer risk, for example. [14]

N-nitrosamines

Nitrosamine-based compounds are readily formed by nitrate- and nitrite-based elements. Carcinomas of the lung, liver, kidney, mammary gland, stomach, pancreas, bladder, or esophagus are understood on the basis of nitrosamine-related mechanisms. [21] 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 derived from nicotine of tobacco smoking. [22],[23]

Nutritional carcinogenesis

The nutrients such as β-carotene and α-tocopherol solely stimulate the immune cells like macrophages, mast cells, lymphocytes; which in turn are responsible for the release of cytokines tumor necrosis factor (TNF)-α and TNF-β. These chemical mediators identify cancer cells and destroy them by apoptosis mechanism. [24],[25] Moreover, the extracts of Allium sativum (garlic) are known to enhance the immune system significantly by stimulating the proliferation of lymphocytes by increasing interleukin (IL)-2 and IL-4 production. [26] Additionally, the p53 is a tumor suppressor gene which is accountable for the repair of damaged DNA at G1 phase of the cell cycle. The main cause of tumor progression is dysfunction of p53 gene resulting in uncontrolled check points and failure in apoptosis of tumor cells. There is an experimental evidence that nutrients, like β-carotene, stimulate some "heat shock" proteins such as hsp 70 and hsp 90 possibly G proteins, which may act as signals to turn on the p53 tumor suppressor system and this may be a major mechanism for the anticancer action of antioxidant nutrients. The relationship of heat shock proteins to the p53 system has been demonstrated. [27],[28] In real terms, the dysregulated cell proliferation and apoptosis lead to cancer development progressively. However, initiation of apoptosis process is one of the novel therapeutic concepts which is known to be effective against cancer cells. At the molecular level apoptosis takes place by two pathways. The intrinsic apoptotic pathway involving the mitochondrial membrane permeabilization, release of cytochrome C into the cytosol, followed by activation of caspase-3 mechanism causing cell death. [29] Resveratrol found in grapes usually induces apoptosis and inhibits the growth of various human tumor cells, including oral squamous cell carcinoma. [30] The allyl sulfur compounds derived from garlic have a significant antiproliferative activity against human cancers. [31],[32] Luteolin, a flavonoid present in apples and carrots and selenium present in broccoli kills cancer cells by inducing apoptotic cell death in many types of cancers like epidermoid carcinoma and leukemia. [33] Curcumin is a major active polyphenolic component of turmeric (Curcuma longa). It is established that curcumin induces apoptosis in tumor cells. [34]

Cell division and cell-cycle progression is a sequential process that directs dividing mammalian cells through G1, S, G2, and M phases. Transitions between G1-S or G2-M phases function as checkpoints to halt cell division if necessary. Examples of dietary components that modulate cell proliferation include phenolic compounds, such as genistein and epigallocatechin-3-gallate, that elicit cell-cycle arrest through the induction of CDIs (p21 and p27) and the inhibition of CDK4, CDK2, cyclin D1, and cyclin E. [35] Flavonoids have been found to inhibit the proliferation of many cancer cells by arresting cell cycle progression either at the G1/S or G2/M checkpoints. Organosulfur compound called isothiocyanates found in papaya restore the cell cycle to eliminate cancer. Isothiocyanates can induce p21 expression and inhibit cell proliferation at the G2-M checkpoint. [36],[37] Allyl sulfur compounds present in garlic and onion has a potential to slow or prevent the growth of tumor cells. These compounds make cells vulnerable to the stress created by the products of cell division. As cancer cells divide rapidly, they create more stress compared to their normal counterparts. Hence cancer cells are damaged by the presence of allyl sulfur compounds. [38],[39]


  Summary Top


Diet and nutritional factors are one of several major causes of carcinogenesis. A large number of studies indicate that an abundant consumption of foods of plant origin reduce the risk of cancer. Food mutagen is working through genotoxic and non-genotoxic pathway in carcinogenesis. Genotoxic pathway works on the level of DNA causing DNA damage. Moreover, non-genotoxic pathway affects the cell through tumor promoters such as inflammation, immunosupression, free radical, and so on. The chemopreventive effect is related to the high content of nutrients like phytochemicals, lycopene, phenolic compounds, β-carotene, flavonoids, etc. These foods have a potent anticancer property. Therefore, one must have thorough knowledge of diet, nutrition, and lifestyles as they play vital role reducing cancer risk in the society.

 
  References Top

1.Doll R, Peto R. The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst 1981;66:1191-308.  Back to cited text no. 1
    
2.WHO. Global cancer rates could increase by 50% to 15 million by 2020 [serial online]. 2003 Available from: http://www.who.int/mediacentre/news/releases/2003/pr27/en/ [Last accessed on 2001 Jan 13, last cited on 2009 Jun 2].  Back to cited text no. 2
    
3.Miller AB. Diet in cancer prevention. Available from: http://www.who.int/ ncd/cancer/publications/abstracts/abs9810_05. [Last accessed on 2001 Jan 13].  Back to cited text no. 3
    
4.Parkin DM, Bray F, Ferlay J, Pisani P. Estimating the world cancer burden: Globocan 2000. Int J Cancer 2001;94:153-6.  Back to cited text no. 4
    
5.International Agency for Research on Cancer. Cancer: Causes, Occurrence and Control. IARC Scientific Publications No. 100. Lyon: IARC; 1990.  Back to cited text no. 5
    
6.World Cancer Research Fund. Food, Nutrition, and the Prevention of Cancer: A Global Perspective. Washington: American Institute for Cancer Research; 1997.  Back to cited text no. 6
    
7.Luch A. Nature and nurture - lessons from chemical carcinogenesis. Nat Rev Cancer 2005;5:113-25.  Back to cited text no. 7
    
8.World Health Organisation: International Agency for Research on Cancer. Cancer: Causes, Occurrence and Control. Lyon: IARC; 1990.  Back to cited text no. 8
    
9.Tsuda H, Ohshima Y, Nomoto H, Fujita K, Matsuda E, Iigo M, et al. Cancer prevention by natural compounds. Drug Metab Pharmacokinet 2004;19:245-63.  Back to cited text no. 9
    
10.Weisburger JH. Antimutagens, anticarcinogens and effective worldwide cancer prevention. J Environ Pathol Toxicol Oncol 1999;18:85-93.  Back to cited text no. 10
    
11.Taghavi N, Yazdi I. Type of food and risk of oral cancer. Arch Iran Med 2007;10:227-32.  Back to cited text no. 11
    
12.Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000;100:57-70.  Back to cited text no. 12
    
13.Hsu S, Singh B, Schuster G. Induction of apoptosis in oral cancer cells: Agents and mechanisms for potential therapy and prevention. Oral Oncol 2004;40:461-73.  Back to cited text no. 13
    
14.Goldman R, Shields PG. Food mutagens. J Nutr 2003;133:965S-73S.  Back to cited text no. 14
    
15.Sugimura T. Nutrition and dietary carcinogens. Carcinogenesis 2000;21:387-95.  Back to cited text no. 15
    
16.Skog KI, Johansson MA, Jagestad MI. Carcinogenic heterocyclic amines in model systems and cooked foods: A review on formation, occurrence, and intake. Food Chem Toxicol 1998;36:879-96.  Back to cited text no. 16
    
17.Keating GA, Layton DW, Felton JS. Factors determining dietary intakes of heterocyclic amines in cooked foods. Mutat Res 1999;443:149-56.  Back to cited text no. 17
    
18.Knize MG, Salmon CP, Pais P, Felton JS. Food heating and the formation of heterocyclic aromatic amine and polycylic aromatic hydrocarbon mutagens/carcinogens. Adv Exp Med Biol 2000;459:179-93.  Back to cited text no. 18
    
19.Schut HA, Snyderwine EG. DNA adducts of heterocyclic amine food mutagens: Implication for mutagenesis and carcinogenesis. Carcinogenesis 1999;20:353-68.  Back to cited text no. 19
    
20.Park BK, Kitteringham NR, Maggs JL, Pirmohamed M, Williams DP. The role of metabolic activation in drug-induced hepatotoxicity. Annu Rev Pharmacol Toxicol 2005;45:177-202.  Back to cited text no. 20
    
21.Lijinsky W. In vivo testing for carcinogenicity. In: Cooper CS, Grover PL, editors. Chemical carcinogenesis and mutagenesis I. Berlin: Springer-Verlag; 1999. p. 179-209.  Back to cited text no. 21
    
22.Fiddler W. The occurrence and determination of N-nitroso compounds. Toxicol Appl Pharmacol 1995;31:352-60.  Back to cited text no. 22
    
23.Tannenbaum SR. Endogenous formation of N-nitroso compounds: A current perspective. The relevance of N-nitroso compounds to human cancer exposures and mechanisms. In: Bartsch H, O'Neill I and Schulte-Hermann R, editors. IARC scientific publications no. 84. Lyon: International Agency for Research on Cancer; 1997. p. 292-5.  Back to cited text no. 23
    
24.Beliveau R, Gingras D. Role of nutrition in preventing cancer. Can Fam Physician 2007;53:1905-11.  Back to cited text no. 24
    
25.Jawanda MK. Antitumor activity of antioxidants - an overview. Int J Dent Clin 2009;1:11-17.  Back to cited text no. 25
    
26.Ejaz S, Woong LC, Ejaz A. Extracts of garlic (ALLIUM SATIVUM) in cancer chemoprevention. Experi Oncol 2003;25:93-97.  Back to cited text no. 26
    
27.Schwartz JL, Singh RP, Teicher B, Wright JE, Trites DH, Shklar G, et al. The induction of a 70 kD protein associated with the selective cytotoxic activity of beta carotene in human epidermal carcinoma. Biochem Biophys Res Commun 1990;169:941-6.  Back to cited text no. 27
    
28.Morimoto RI. Heat shock: The role of transient inducible response in cell damage, transformation, and di€erentiation. Cancer Cell 1991;3:295-301.  Back to cited text no. 28
    
29.Kumar V, Abbas AK, Fausto N, Robbins SL, Cotran RS. Robbins Basic Pathology. 8 th ed. 2007. Philadelphia: Elsevier Saunders. p. 19-22.  Back to cited text no. 29
    
30.Elattar TM, Virji AS. The effect of red wine and its components on growth and proliferation of human oral squamous carcinoma cells. Anticancer Res 1999;19:5407-14.  Back to cited text no. 30
    
31.Pinto JT, Rivlin RS. Antiproliferative effects of allium derivatives from garlic. J Nutr 2001;131:1058-60S.  Back to cited text no. 31
    
32.Knowles LM, Milner JA. Possible mechanism by which allyl sulfides suppress neoplastic cell proliferation. J Nutr 2001;131:1061-6S.  Back to cited text no. 32
    
33.Cheng AC, Huang TC, Lai CS, Pan MH. Induction of apoptosis by luteolin through cleavage of Bcl-2 family in human leukemia HL-60 cells. Eur J Pharmacol 2005;509:1-10.  Back to cited text no. 33
    
34.Carroll KK. Dietary fats and cancer. Am J Clin Nutr 1991;53:1064-7S.  Back to cited text no. 34
    
35.Visanji JM, Duthie SJ, Pirie L, Thompson DG, Padfield PJ. Dietary isothiocyanates inhibit Caco-2 cell proliferation and induce G2/M phase cell cycle arrest, DNA damage, and G2/M checkpoint activation. J Nutr 2004;134:3121-6.  Back to cited text no. 35
    
36.Bianchini F, Vainio H. Isothiocyanates in cancer prevention. Drug Metab Rev 2004;36:655-67.  Back to cited text no. 36
    
37.Lau BH, Tadi PP, Tosk JM. Allium sativum (garlic) and cancer prevention. Nutr Res 1990;21:937-48.  Back to cited text no. 37
    
38.Weinhouse S, Bal DG, Adamson R, Dwyer J, Kleinman RE, Kritchevsky D, et al. American Cancer Society guidelines on diet, nutrition, and cancer. The Work Study Group on Diet, Nutrition, and Cancer. CA Cancer J Clin 1991;41:334-8.  Back to cited text no. 38
    
39.Doll R, Peto R. Epidemiology of cancer. In: Weatherall DJ, Ledingham JG, Warrell DA, editors. Oxford Textbook of Medicine. Oxford: Oxford University Press; 1996. p. 197-221.  Back to cited text no. 39
    




 

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