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肺癌中谷胱甘肽S-转移酶M1和T1缺失的研究。

Investigation of glutathione S-transferase M1 and T1 deletions in lung cancer.

作者信息

Altinisik Julide, Balta Zinnet B, Aydin Gunay, Ulutin Turgut, Buyru Nur

机构信息

Cerrahpasa Medical Faculty, Department of Medical Biology, Istanbul University, Temel Bilimler Binasi Kat:2 Tibbi Biyoloji ABD., Kocamustafapasa, Istanbul, Turkey.

出版信息

Mol Biol Rep. 2010 Jan;37(1):263-7. doi: 10.1007/s11033-009-9673-5. Epub 2009 Aug 8.

DOI:10.1007/s11033-009-9673-5
PMID:19669596
Abstract

Glutathione S-transferases (GSTs) M1 and T1 are known to be polymorphic in humans. Both polymorphisms are due to gene deletions which are responsible for the existence of null genotypes. Previous studies have suggested that GST genotypes may play a role in determining susceptibility to a number of unrelated cancers, including lung cancer. The GSTM1 and GSTT1 polymorphisms were determined by PCR-based analysis in 75 lung cancer patients and 55 controls. The unconditional logistic regression analysis was used to calculate ORs and 95% CI. The frequencies of GSTM1 and GSTT1 null genotypes were 37.3 and 22.7% in lung cancer patients and 27.3 and 16.4% in controls, respectively. When analyzed by histology the GSTM1 null genotype was more prevalent in squamous-cell carcinoma and adenocarcinoma patients. Whereas, GSTT1 null genotype frequency was lower in small-cell lung cancer patients than controls. But these differences were not statistically significant. According to smoking status, null genotype for both gene are associated with an increase in risk for lung cancer. Our results suggest that GSTM1 and GSTT1 polymorphisms may play a role in the development of lung cancer for some histological subtypes and modifies the risk of smoking-related lung cancer.

摘要

已知谷胱甘肽S-转移酶(GSTs)M1和T1在人类中具有多态性。这两种多态性均由基因缺失引起,基因缺失导致了无效基因型的存在。先前的研究表明,GST基因型可能在决定对包括肺癌在内的多种不相关癌症的易感性方面发挥作用。通过基于聚合酶链反应(PCR)的分析,在75例肺癌患者和55例对照中确定了GSTM1和GSTT1多态性。采用非条件逻辑回归分析来计算比值比(ORs)和95%可信区间(CI)。肺癌患者中GSTM1和GSTT1无效基因型的频率分别为37.3%和22.7%,对照中分别为27.3%和16.4%。按组织学分析时,GSTM1无效基因型在鳞状细胞癌和腺癌患者中更为普遍。而小细胞肺癌患者中GSTT1无效基因型频率低于对照。但这些差异无统计学意义。根据吸烟状况,两个基因的无效基因型均与肺癌风险增加相关。我们的结果表明,GSTM1和GSTT1多态性可能在某些组织学亚型的肺癌发生中起作用,并改变吸烟相关肺癌的风险。

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