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Year : 2009 | Volume
: 20
| Issue : 2 | Page : 249 |
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Open questions on carcinogenesis of oral cancer: Interaction between the environmental and genetic aspects |
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Dennis de Carvalho Ferreira, Jose Alexandre da Rocha Curvelo, Mauro Romero Leal Passos
Department of Microbiology, Sector of Sexually Transmitted Diseases, Federal University of Fluminense (UFF), Rio de Janeiro, Brazil
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Date of Web Publication | 23-Jun-2009 |
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How to cite this article: Ferreira D, Curvelo Jd, Passos ML. Open questions on carcinogenesis of oral cancer: Interaction between the environmental and genetic aspects. Indian J Dent Res 2009;20:249 |
How to cite this URL: Ferreira D, Curvelo Jd, Passos ML. Open questions on carcinogenesis of oral cancer: Interaction between the environmental and genetic aspects. Indian J Dent Res [serial online] 2009 [cited 2021 Mar 5];20:249. Available from: https://www.ijdr.in/text.asp?2009/20/2/249/52882 |
Sir,
Recently, an article was published in this journal entitled "Estimation of nicotine content in popular Indian brands of smoking andchewing tobacco products [1] ," measuring and comparing the nicotine present in this habit. Although the relationship between smoking habit and prevalence of oral cancer has already been established for many years, [2],[3] we would like to discuss the relevance of these kinds of measurements at this point in time, if we still do not reach experimental models studies that can answer questions such as: Is the expression of cytochrome p450 enzymes similar on different sites of the oral cavity? Is the inflammatory response similar on the different sites of the oral cavity? What is the expression and activity of the phase II enzymes involved in the oxidative metabolism involved? Have the genetic polymorphisms of these enzymes already been evaluated in India and Brazilian populations, which are known to have high oral cancer rates?
Carcinogenesis is a highly complex process involving both environmental and inherited risk factors. The inter-individual genetic differences and individual susceptibility to human cancer triggered by environmental exposures has already been studied and reported elsewhere. This carcinogenesis environment-gene interaction is well reflected by phase I and II enzymes that are involved in the metabolism of carcinogens. Therefore, the measure of nicotine levels inside objects of smoking habits may not be enough for the elucidation of these risks, mainly because the major carcinogens present in tobacco are polycyclic aromatic hydrocarbons, nitrosamines and aromatic amines. [2],[3]
It is clear that more studies are required at the molecular and genetic basis in order to investigate susceptibility and therapeutics, such as the expression and the polymorphism of enzymes related to the oxidative metabolism (Cytochrome p450, GSTS, NATs); adducts formation, characterized by impressions on DNA originated from carcinogens; gene mutations associated with cell cycle control; viral infections (Epstein-Barr virus, human papilloma virus, human immunodeficiency virus, human T-cell leukemia virus); congenital features like congenital immunodeficiency and genodermatosis, which are knowingly associated to malignancy. These studies could formulate strategies that can determinate a new criteria for the approach of this situation and, therefore, avoid misdiagnosis and etiologies previously considered idiopathic among pre-malignant and malignant lesions. [2],[3],[4],[5]
The complexity around the diagnosis of this type of cancer probably begins under the professional graduation, which does not always provide a connection between basic science and clinical practice. Continuous professional education and a systematic approach considering genetics and biomolecular aspects must be considered for the evaluation of these patients. [2],[3]
References | |  |
1. | Reddy SS, Shaik Hyder Ali KH. Estimation of nicotine content in popular Indian brands of smoking and chewing tobacco products. Indian J Dent Res 2008;19:88-91. [PUBMED]  |
2. | Ali S, El-Rayes BF, Heilbrun LK, Sarkar FH, Ensley JF, Kucuk O, et al . Cytochrome p450 and glutathione transferase expression in squamous cell cancer. Clin Cancer Res 2004;10:4412-6. [PUBMED] [FULLTEXT] |
3. | Llewellyn CD, Johnson NW, Warnakulasuriya KA. Risk factors for squamous cell carcinoma of the oral cavity in young people: A comprehensive literature review. Oral Oncol 2001;37:401-18. [PUBMED] [FULLTEXT] |
4. | Sroussi HY, Villines D, Epstein J, Alves MC, Alves ME. Oral lesions in HIV-positive dental patients - one more argument for tobacco smoking cessation. Oral Dis 2007;13:324-8. [PUBMED] [FULLTEXT] |
5. | Nemes JA, Deli L, Nemes Z, Mαrton IJ. Expression of p16(INK4A), p53, and Rb proteins are independent from the presence of human papillomavirus genes in oral squamous cell carcinoma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:344-52. |

Correspondence Address: Dennis de Carvalho Ferreira Department of Microbiology, Sector of Sexually Transmitted Diseases, Federal University of Fluminense (UFF), Rio de Janeiro Brazil
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0970-9290.52882

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This article has been cited by | 1 |
Genital and oral human papillomavirus infection in a patient from the group of women who have sex with women |
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| dos Reis, H.L.B., Ferreira, D.C., Forattini, A.G., Souza, P.G., Curvelo, J.A.R., Passos, M.R.L. | | Clinics. 2010; 65(12): 1383-1385 | | [Pubmed] | |
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