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首页> 外文期刊>Journal of the National Cancer Institute >Polymorphisms of death pathway genes FAS and FASL in esophageal squamous-cell carcinoma.
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Polymorphisms of death pathway genes FAS and FASL in esophageal squamous-cell carcinoma.

机译：食管鳞状细胞癌死亡途径基因FAS和FASL的多态性。

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BACKGROUND: The FAS receptor-ligand system is a key regulator of apoptotic cell death, and loss of FAS expression and gain of FAS ligand (FASL) expression play important roles in the development and progression of cancer. Single-nucleotide polymorphisms in the promoter region of the FAS (G or A at position -1377 [FAS -1377G/A] and A or G at position -670 [FAS -670A/G]) and FASL (T or C at position -844 [FASL -844T/C]) genes alter the transcriptional activity of these genes. We examined the association between these polymorphisms and risk of the development and metastasis of esophageal squamous-cell carcinoma. METHODS: Genotypes of 588 case patients with esophageal squamous-cell carcinoma and 648 control subjects were determined by polymerase chain reaction-based restriction fragment length polymorphism. Associations with the risk of esophageal squamous-cell carcinoma were estimated by logistic regression. All statistical tests were two-sided. RESULTS: We observed a statistically significantly increasedrisk of esophageal squamous-cell carcinoma associated with the FAS -1377AA (odds ratio [OR] = 1.79, 95% confidence interval [CI] = 1.29 to 2.48; P<.001) or FAS -670GG (OR = 1.72, 95% CI = 1.26 to 2.34; P<.001) genotype, which are in strong linkage disequilibrium compared with the FAS -1377GA or GG or the FAS -670AG or AA genotype, respectively. An increased risk of esophageal squamous-cell carcinoma was also associated with the FASL -844CC genotype (OR = 2.06, 95% CI = 1.64 to 2.59; P<.001) compared with the FASL -844CT or TT genotype. Gene-gene interactions of FAS and FASL polymorphisms increased the risk of esophageal squamous-cell carcinoma in a multiplicative manner (OR for the presence of both FAS -1377AA and FASL -844CC genotypes = 4.55, 95% CI = 2.75 to 7.48; P =.001, test for homogeneity). Statistically significant interactions were found between these polymorphisms in FAS and FASL and tobacco smoking. None of the polymorphisms was associated with risk of differentiation or metastasis of esophageal squamous-cell carcinoma at diagnosis. CONCLUSION: Genetic polymorphisms in the death pathway genes FAS and FASL appear to be associated with an increased risk of developing esophageal squamous-cell carcinoma.
机译：背景：FAS受体-配体系统是凋亡细胞死亡的关键调节器，FAS表达的丧失和FAS配体（FASL）表达的增加在癌症的发展和进程中起着重要的作用。 FAS（-1377位置的G或A [FAS -1377G / A]和-670 [FAS -670A / G]位置的A或G）和FASL（T或C位置的启动子）单核苷酸多态性-844 [FASL -844T / C]）基因会改变这些基因的转录活性。我们检查了这些多态性与食管鳞状细胞癌发展和转移的风险之间的关联。方法：采用基于聚合酶链反应的限制性片段长度多态性分析方法，对588例食管鳞状细胞癌患者和648例对照者的基因型进行分析。通过逻辑回归分析估计与食管鳞状细胞癌风险的相关性。所有统计检验都是双面的。结果：我们观察到与FAS -1377AA相关的食道鳞状细胞癌的风险显着增加（几率[OR] = 1.79，95％置信区间[CI] = 1.29至2.48; P <.001）或FAS -670GG （OR = 1.72，95％CI = 1.26至2.34; P <.001）基因型，分别与FAS -1377GA或GG或FAS -670AG或AA基因型相比，具有很强的连锁不平衡。与FASL -844CT或TT基因型相比，FASL -844CC基因型（OR = 2.06，95％CI = 1.64至2.59; P <.001）也增加了食管鳞状细胞癌的风险。 FAS和FASL多态性的基因-基因相互作用以乘法方式增加了食管鳞状细胞癌的风险（ORS -1377AA和FASL -844CC基因型均存在的OR = 4.55，95％CI = 2.75至7.48; P = .001，测试同质性）。在FAS和FASL中的这些多态性与吸烟之间发现了统计学上显着的相互作用。诊断时，多态性均与食管鳞状细胞癌的分化或转移风险无关。结论：死亡途径基因FAS和FASL的遗传多态性似乎与食管鳞状细胞癌发生的风险增加有关。

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