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Influence of glutathione‐ S ‐transferase theta (GSTT1) and mu (GSTM1) gene polymorphisms on the susceptibility of hepatocellular carcinoma in Taiwan
Author(s) -
Kao ChiaChun,
Chen MuKuan,
Kuo WuHsien,
Chen TzyYen,
Su ShihChi,
Hsieh YiHsien,
Liu ChuenLan,
Chou MingChih,
Tsai HsiuTing,
Yang ShunFa
Publication year - 2010
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21643
Subject(s) - hepatocellular carcinoma , genotype , medicine , pathological , genetic predisposition , glutathione s transferase , gene , oncology , liver cancer , gastroenterology , glutathione , biology , genetics , enzyme , disease , biochemistry
Background and Objectives Hepatocellular carcinoma (HCC) is one of the most frequent malignant neoplasms worldwide and is the second leading cause of cancer death in Taiwan. Genetic polymorphism has been reported as a factor for increased susceptibility of HCC. Glutathione‐ S ‐transferases theta (GSTT1) and mu (GSTM1) play essential roles in detoxification of ingested xenobiotics and modulation of the susceptibility of gene‐related cancer. The aim of this study was to estimate the relationships between these two gene polymorphisms and HCC risk and clinicopathological status in Taiwanese. Methods Polymerase chain reaction (PCR) was used to determine gene polymorphisms of 102 patients with HCC and 386 healthy controls. Results Both gene polymorphisms were not associated with the clinical pathological status of HCC and serum levels of liver‐related clinical pathological markers. While no relationship between GSTM1 gene polymorphism and HCC susceptibility was found, individuals of age < 56 years old with GSTT1 present genotype have a risk of 2.77‐fold (95% CI: 1.09–7.09) for HCC compared to that with null variant, after adjustment for other confounders. Conclusions GSTT1 and GSTM1 null genotypes do not associate with increased risk of HCC. J. Surg. Oncol. 2010;102:301–307. © 2010 Wiley‐Liss, Inc.