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Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer
PURPOSE: Oral cancer is the fifth most common form of cancer in the world and comprises 6.5% of all cancer deaths. Since one of the major risk factors for oral cancer is tobacco use, we hypothesized that polymorphic genes coding for tobacco carcinogen-metabolizing enzymes may play a role in oral can...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Yonsei University College of Medicine
2007
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628133/ https://www.ncbi.nlm.nih.gov/pubmed/17461521 http://dx.doi.org/10.3349/ymj.2007.48.2.233 |
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author | Cha, In-Ho Park, Jong Yun Chung, Won-Yoon Choi, Min-Ah Kim, Hyung-Jun Park, Kwang-Kyun |
author_facet | Cha, In-Ho Park, Jong Yun Chung, Won-Yoon Choi, Min-Ah Kim, Hyung-Jun Park, Kwang-Kyun |
author_sort | Cha, In-Ho |
collection | PubMed |
description | PURPOSE: Oral cancer is the fifth most common form of cancer in the world and comprises 6.5% of all cancer deaths. Since one of the major risk factors for oral cancer is tobacco use, we hypothesized that polymorphic genes coding for tobacco carcinogen-metabolizing enzymes may play a role in oral cancer susceptibility. MATERIALS AND METHODS: To investigate the association between polymorphisms of the CYP1A1 and GSTM1 genes and risks for oral squamous cell carcinoma (OSCC) in the Korean population, the prevalence of the CYP1A1 Mspl and GSTM1 null polymorphisms were examined in 72 patients with histologically confirmed primary OSCC, as well as in 221 healthy control subjects. RESULTS: A significant risk increase for oral cancer was observed among subjects with the homozygous CYP1A1 (m2/m2) genotype (OR = 3.8, 95% CI = 1.9-7.7), but not the GSTM1 null genotype (OR = 0.7, 95% CI = 0.4-1.3). Risk for oral cancer was significantly increased in subjects with the homozygous CYP1A1 (m2/m2) genotype, regardless of smoking history (smokers; OR = 4.4; 95% CI = 1.2-16.3; non-smokers OR = 4.9; 95% CI=1.9-12.5). Using the potentially most protective genotype GSTM1 (+)/CYP1A1 [(m1/m1)+(m1/m2)] as the reference group, an increased risk for oral cancer was observed among subjects with the GSTM1 (+)/ CYP1A1 (m2/m2) (OR = 2.0, 95% CI = 0.8-5.2), and GSTM1 (-)/ CYP1A1 (m2/m2) (OR=4.9, 95% CI = 1.5-15.5) genotypes (p < 0.009, (χ(2) trend test). CONCLUSION: Our results suggest that individuals with a genotype of CYP1A1 (m2/m2) and GSTM1 (-) are highly susceptible for OSCC and that the CYP1A1 (m2/m2) genotype is closely associated with increased risk of OSCC in Koreans. |
format | Text |
id | pubmed-2628133 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | Yonsei University College of Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-26281332009-02-02 Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer Cha, In-Ho Park, Jong Yun Chung, Won-Yoon Choi, Min-Ah Kim, Hyung-Jun Park, Kwang-Kyun Yonsei Med J Original Article PURPOSE: Oral cancer is the fifth most common form of cancer in the world and comprises 6.5% of all cancer deaths. Since one of the major risk factors for oral cancer is tobacco use, we hypothesized that polymorphic genes coding for tobacco carcinogen-metabolizing enzymes may play a role in oral cancer susceptibility. MATERIALS AND METHODS: To investigate the association between polymorphisms of the CYP1A1 and GSTM1 genes and risks for oral squamous cell carcinoma (OSCC) in the Korean population, the prevalence of the CYP1A1 Mspl and GSTM1 null polymorphisms were examined in 72 patients with histologically confirmed primary OSCC, as well as in 221 healthy control subjects. RESULTS: A significant risk increase for oral cancer was observed among subjects with the homozygous CYP1A1 (m2/m2) genotype (OR = 3.8, 95% CI = 1.9-7.7), but not the GSTM1 null genotype (OR = 0.7, 95% CI = 0.4-1.3). Risk for oral cancer was significantly increased in subjects with the homozygous CYP1A1 (m2/m2) genotype, regardless of smoking history (smokers; OR = 4.4; 95% CI = 1.2-16.3; non-smokers OR = 4.9; 95% CI=1.9-12.5). Using the potentially most protective genotype GSTM1 (+)/CYP1A1 [(m1/m1)+(m1/m2)] as the reference group, an increased risk for oral cancer was observed among subjects with the GSTM1 (+)/ CYP1A1 (m2/m2) (OR = 2.0, 95% CI = 0.8-5.2), and GSTM1 (-)/ CYP1A1 (m2/m2) (OR=4.9, 95% CI = 1.5-15.5) genotypes (p < 0.009, (χ(2) trend test). CONCLUSION: Our results suggest that individuals with a genotype of CYP1A1 (m2/m2) and GSTM1 (-) are highly susceptible for OSCC and that the CYP1A1 (m2/m2) genotype is closely associated with increased risk of OSCC in Koreans. Yonsei University College of Medicine 2007-04-30 2007-04-30 /pmc/articles/PMC2628133/ /pubmed/17461521 http://dx.doi.org/10.3349/ymj.2007.48.2.233 Text en Copyright © 2007 The Yonsei University College of Medicine http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Cha, In-Ho Park, Jong Yun Chung, Won-Yoon Choi, Min-Ah Kim, Hyung-Jun Park, Kwang-Kyun Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer |
title | Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer |
title_full | Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer |
title_fullStr | Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer |
title_full_unstemmed | Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer |
title_short | Polymorphisms of CYP1A1 and GSTM1 Genes and Susceptibility to Oral Cancer |
title_sort | polymorphisms of cyp1a1 and gstm1 genes and susceptibility to oral cancer |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628133/ https://www.ncbi.nlm.nih.gov/pubmed/17461521 http://dx.doi.org/10.3349/ymj.2007.48.2.233 |
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