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谷胱甘肽 S-转移酶 Mu 多态性与葡萄牙人群的胃癌。

Glutathione S transferase mu polymorphism and gastric cancer in the Portuguese population.

出版信息

Biomarkers. 1998;3(6):441-7. doi: 10.1080/135475098231084.

DOI:10.1080/135475098231084
PMID:23899396
Abstract

The glutathione S-transferases appear to form part of a protective mechanism against the development of cancer where environmental chemical carcinogens are involved. In humans one member of the mu class gene family (GSTM1) has been shown to be polymorphic and is only expressed in ~50% of individuals. Previous studies have shown a possible link between the null phenotype and susceptibility to cancer but have been equivocal regarding stomach cancer. To evaluate any association in Portuguese gastric cancer individuals with GSTM1 variability, we performed GST M 1 polymorphism by PCR amplification in 148 gastric cancer patients and in 84 healthy control individuals. We found no statistical differences between the gastric cancer and control populations (wild type phenotype: 52%, 48%; null phenotype: 48%, 52%, respectively). A subset analysis into site of tumour also revealed no significant differences between the groups, although we found a slight increase of the wild type phenotype in the samples of the antrum compared with the control population (57% vs 48%, respectively; 2= 1.18; p 0.28) and a slight increase of the null phenotype in the signet ring cells/mucocellular group (2= 1.05; p 0.3). However, in both cases it did not reach statistical significance. A subset analysis of the histological groups following the WHO criteria revealed a statistically significant difference (2= 3.704; p 0.05) between the moderately differentiated gastric adenocarcinoma and the presence of the wild type phenotype. These results do not support the hypothesis that the GSTM1 null phenotype predisposes to gastric cancer in the Portuguese population and the moderately differentiated gastric adenocarcinoma seems to be associated with the presence of the G STM 1 wild type phenotype.

摘要

谷胱甘肽 S-转移酶似乎是一种保护机制的一部分,可防止涉及环境化学致癌物的癌症发展。在人类中,已经表明 mu 类基因家族的一个成员(GSTM1)具有多态性,并且仅在约 50%的个体中表达。先前的研究表明,缺失表型与癌症易感性之间可能存在联系,但对于胃癌则存在争议。为了评估葡萄牙胃癌个体中 GSTM1 变异性与胃癌的任何关联,我们通过 PCR 扩增在 148 例胃癌患者和 84 例健康对照个体中检测 GST M1 多态性。我们发现胃癌和对照组之间没有统计学差异(野生型表型:52%,48%;缺失型表型:48%,52%)。肿瘤部位的亚组分析也没有显示两组之间存在显著差异,尽管我们发现与对照组相比,胃窦部的野生型表型略有增加(分别为 57%和 48%;2=1.18;p=0.28),印戒细胞/黏液细胞组的缺失型表型略有增加(2=1.05;p=0.3)。然而,在这两种情况下,差异均未达到统计学意义。根据世卫组织标准对组织学组进行的亚组分析显示,中度分化胃腺癌与野生型表型之间存在统计学显著差异(2=3.704;p=0.05)。这些结果不支持 GSTM1 缺失型表型易患葡萄牙人群胃癌的假设,并且中度分化胃腺癌似乎与 GST M1 野生型表型的存在相关。

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