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首页> 外文期刊>Journal of dermatological science >Polymorphisms of FAS and FAS ligand genes and risk of skin cancer.
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Polymorphisms of FAS and FAS ligand genes and risk of skin cancer.

机译：FAS和FAS配体基因的多态性与皮肤癌的风险。

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摘要

Skin cancer is the most common form of cancer in the United States among Caucasians. DNA damage induced by ultraviolet (UV) exposure has been shown to be involved in the etiology of melanoma, squamous cell carcinoma (SCC), and basal cell carcinoma (BCC) [1]. Under normal conditions, UV-induced DNA damage is repaired by DNA repair mechanisms, or cells with damaged DNA undergo apoptosis [2]. Apoptosis can be triggered by one of the two pathways: an intrinsic pathway or an extrinsic pathway. In the extrinsic pathway, a death-ligand binds a death-receptor that is displayed on the cell surface of the damaged cell. FAS ligand (FASL [also known as CD95LG and TNFSF6]) is one such death-ligand, and FAS (also known as CD95, APO-1, and TNFRSF6) is the corresponding death-receptor. Without the ability to undergo death-signal-induced apoptosis, mutations can rapidly accumulate, potentially leading to uncontrolled growth and tumor formation.
机译：皮肤癌是美国白种人中最常见的癌症形式。紫外线（UV）暴露引起的DNA损伤已被证明与黑色素瘤，鳞状细胞癌（SCC）和基底细胞癌（BCC）的病因有关[1]。在正常情况下，紫外线诱导的DNA损伤可以通过DNA修复机制修复，或者DNA受损的细胞会发生凋亡[2]。凋亡可以通过两种途径之一触发：内在途径或外在途径。在外在途径中，死亡配体结合显示在受损细胞的细胞表面上的死亡受体。 FAS配体（FASL [也称为CD95LG和TNFSF6]）就是这样一种死亡配体，而FAS（也称为CD95，APO-1和TNFRSF6）是相应的死亡受体。没有能力进行死亡信号诱导的细胞凋亡，突变会迅速积累，可能导致不受控制的生长和肿瘤形成。

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