Gene polymorphisms, tobacco exposure and oral cancer susceptibility: a study from Gujarat, West India

Abstract

Polymorphic variability in the enzymes involved in biotransformation of tobacco-related pro-carcinogens plays an important role in modulating oral cancer susceptibility. CYP1A1*2A, CYP1A1*2C, GSTM1 and GSTT1 polymorphisms were determined in 122 oral carcinoma cases and 127 controls from Gujarat, West India using PCR-based methods. The results revealed that the polymorphic variants of CYP1A1 gene did not show association towards oral cancer risk. The GSTM1 and GSTT1 null genotypes were found to be over-represented in patients than controls, suggesting a moderate increase in risk of oral cancer. The oral cancer risk was significantly increased in the patients having either alone or concurrent deletion of GSTM1 and GSTT1. The results also suggested significant association between tobacco habits, especially chewing, variant genotypes of CYP1A1, GSTM1 and GSTT1 and oral cancer risk. Our data have provided evidence that GST polymorphism modified the susceptibility to oral cancer and individuals with variant genotypes of the three genes with tobacco habits are at significant risk of developing oral cancer.

Gene–environment interaction and susceptibility in head and neck cancer patients and in their first‐degree relatives: a study of Northeast Indian population

“…Other tobacco products like gutkha , paan‐masala , and khaini are regularly consumed by people from this part of India. The GST superfamily enzymes are the major phase‐II xenobiotic metabolizing enzymes and known to be involved in detoxification of procarcinogens like PAHs, nitroamines, and other chemical carcinogens present in tobacco . Our previous study conducted on oral squamous cell carcinoma also showed a possible role of GSTM1 and GSTT1 null genotypes .…”

Association of CYP1A1 MspI polymorphism with oral cancer risk in Asian populations: a meta-analysis

“…According to the inclusion and exclusion criteria mentioned above, and after screening the type, title, abstract, and full text of each article, 12 relevant articles were ultimately included in the meta-analysis (Sato et al, 1999;Tanimoto et al, 1999;Sreelekha et al, 2001;Kao et al, 2002;Anantharaman et al, 2007;Cha et al, 2007;Sam et al, 2008;Chatterjee et al, 2010;Guo et al, 2012;Shukla et al, 2012;Shukla et al, 2013;Singh et al, 2014). In total, those articles included 1925 oral cancer patients and 2335 controls.…”

“…Cytochrome P450 1A1 (CYP1A1), a vital phase I xenobiotic metabolizing enzyme, is widely distributed in many epithelial tissues (Totlandsdal et al, 2010;Newland et al, 2011). It is involved in the biotransformation of several tobacco-related pro-carcinogens into reactive electrophilic intermediate metabolites that can damage DNA (Singh et al, 2014). The CYP1A1 MspI polymorphism has been reported to be related to higher risk of tobaccorelated lung cancer (Hashibe et al, 2003).…”

Networks development between nicotinic chemical probes and Ca9–22 oral cancer cells by general proteomics analyses

“…With long‐term exposure, nicotine enhanced the development of cancer stem‐like cells (CSCs) and epithelial–mesenchymal transdifferentiation (EMT) properties by positively regulating aldehyde dehydrogenase 1 (ALDH 1) expression in normal gingival epithelial cells, and CSCs and their properties will be reduced via knockdown of SNAIL . It has been reported that tobacco users carrying specific polymorphisms in tobacco metabolism and modulation of DNA repair genes have high risk of oral cancer . Furthermore, numerous studies have reported that oral cancer and precancer synergistic effects were caused by free radicals caused by the consumption of tobacco , alcoholic beverages with tobacco abuse , BQ, BQ with or without tobacco , and BQ with tobacco and alcoholic beverages .…”