Event Abstract Back to Event GST polymorphisms and lung cancer risk Ahmet O. Ada1* 1 Ankara University, Department of Toxicology, Turkey There are a lot of studies focused on investigating genetic polymorphisms in order to estimate genetic contribution to various pathologies including lung cancer. Possible cancer susceptibility genes have been sought among oncogenes, tumor suppressor genes, DNA repair genes and genes encoding phase I and phase II enzymes. Among them, glutathione S-transferases (GSTs), a multiple gene family of phase II enzymes, catalyze detoxifying endogenous reactions with glutathione and protect cellular macromolecules from damage caused by cytotoxic and carcinogenic agents. Cytosolic GST enzymes occupy a key position in biological detoxification processes especially in the detoxification of major classes of tobacco carcinogens. The cytosolic GST enzymes are classified according to their genetic and biochemical properties like alpha (GSTA), mu (GSTM), theta (GSTT), pi (GSTP) and omega (GSTO). GSTM1 and GSTT1 are genetically deleted in a high percentage of the human population with major ethnic differences resulting in loss of corresponding enzyme activities. GSTM1 is particularly relevant in the deactivation of carcinogenic intermediates of polycyclic aromatic hydrocarbons. GSTT1 plays a major role in phase II biotransformation of a number of drugs and industrial chemicals, e.g. cytostatic drugs, hydrocarbons and halogenated hydrocarbons. There is cumulating evidence that combinations of the GSTM1 null genotype with other genetic traits affecting the metabolism of carcinogens may predispose the aero-digestive tract and lung, especially in smokers, to a higher risk of cancer. GSTP1, the most abundant GST isoform in the lung, metabolizes numerous carcinogenic compounds including benzo[a]pyrene, a tobacco carcinogen. Previous studies suggest that genetic polymorphisms of GSTP1 exon 5 (Ile105Val) and exon 6 (Ala114Val) have functional effects on the GST gene product resulting in reduced enzyme activity. Therefore individuals with reduced or loss of GST enzymatic activity may be at a greater risk for cancer due to decreased detoxification of carcinogenic and mutagenic compounds. Substantial evidence indicates that there is interindividual variation in the susceptibility to lung cancer. As lung cancer is an important health problem of global proportions, associations between GST genotypes and lung cancer risk are herein evaluated from recent epidemiological studies, namely case control studies (This study was supported by the Research Fund of Ankara University, Grant no: 2006-08-03-002HPD). Keywords: GST polymorphisms, lung cancer Conference: 8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010, Thessaloniki, Greece, 1 Oct - 5 Oct, 2010. Presentation Type: Invited speaker Topic: Genomics - Proteomics - Metabolomics Citation: Ada AO (2010). GST polymorphisms and lung cancer risk. Front. Pharmacol. Conference Abstract: 8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010. doi: 10.3389/conf.fphar.2010.60.00095 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 05 Mar 2011; Published Online: 04 Nov 2010. * Correspondence: Dr. Ahmet O Ada, Ankara University, Department of Toxicology, Ankara, Turkey, ada@pharmacy.ankara.edu.tr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ahmet O Ada Google Ahmet O Ada Google Scholar Ahmet O Ada PubMed Ahmet O Ada Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
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