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首页> 外文期刊>Journal of Medical Genetics >Functional polymorphisms in cell death pathway genes FAS and FASL contribute to risk of lung cancer.
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Functional polymorphisms in cell death pathway genes FAS and FASL contribute to risk of lung cancer.

机译：细胞死亡途径基因FAS和FASL中的功能多态性会增加患肺癌的风险。

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BACKGROUND: The FAS and FASL system plays a key role in regulating apoptotic cell death and corruption of this signalling pathway has been shown to participate in immune escape and tumorigenesis. There is reduced expression of FAS but elevated expression of FASL in many types of human cancers including lung cancer. We recently reported an association between functional polymorphisms in FAS (-1377G-->A) and FASL (-844T-->C) and risk of oesophageal cancer. OBJECTIVE: To examine the contribution of these polymorphisms to risk of developing lung cancer. METHODS: Genotypes of 1000 lung cancer patients and 1270 controls were analysed by PCR based restriction fragment length polymorphism. Associations with risk of lung cancer were estimated by logistic regression. RESULTS: Compared with non-carriers, there was a 1.6 fold excess risk of developing lung cancer for carriers of the FAS -1377AA genotype (odds ratio (OR) 1.59, 95% confidence interval (CI) 1.21 to 2.10; p = 0.001), and 1.8 fold excess risk (OR 1.79,95% CI 1.26 to 2.52; p = 0.001) for carriers of FASL -844CC. Gene-gene interaction of FAS and FASL polymorphisms increased risk of lung cancer in a multiplicative manner (OR for the carriers of both FAS -1377AA and FASL -844CC genotypes 4.18, 95% CI 2.83 to 6.18). Gene-environment interaction of FAS or FASL polymorphism and smoking associated with increased risk of lung cancer was also found. CONCLUSION: These results are consistent with our initial findings in oesophageal cancer and further support the hypothesis that the FAS and FASL triggered apoptosis pathway plays an important role in human carcinogenesis.
机译：背景：FAS和FASL系统在调节凋亡细胞死亡中起关键作用，该信号通路的破坏已显示参与免疫逃逸和肿瘤发生。在许多类型的人类癌症（包括肺癌）中，FAS的表达降低，但FASL的表达升高。我们最近报道了FAS（-1377G-> A）和FASL（-844T-> C）中的功能多态性与食道癌风险之间的关联。目的：研究这些多态性对患肺癌风险的影响。方法：采用基于PCR的限制性片段长度多态性分析1000例肺癌患者和1270例对照的基因型。通过逻辑回归评估与肺癌风险的相关性。结果：与非携带者相比，FAS -1377AA基因型携带者患肺癌的风险高1.6倍（优势比（OR）为1.59，95％置信区间（CI）为1.21至2.10; p = 0.001） ，对于FASL -844CC的携带者，则有1.8倍的额外风险（或1.79,95％CI 1.26至2.52; p = 0.001）。 FAS和FASL多态性的基因-基因相互作用以乘法方式增加了肺癌的风险（对于FAS -1377AA和FASL -844CC基因型的携带者为4.18，95％CI为2.83至6.18）。还发现FAS或FASL多态性与吸烟的基因环境相互作用与肺癌风险增加有关。结论：这些结果与我们在食道癌中的初步发现相符，并进一步支持了FAS和​​FASL触发凋亡通路在人类致癌作用中起重要作用的假说。

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