Functional regulatory variants of MCL1 contribute to enhanced promoter activity and reduced risk of lung cancer in nonsmokers: Implications for context‐dependent phenotype of an antiapoptotic and antiproliferative gene in solid tumor
Functional regulatory variants of MCL1 contribute to enhanced promoter activity and reduced risk of lung cancer in nonsmokers: Implications for context‐dependent phenotype of an antiapoptotic and antiproliferative gene in solid tumor
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DOI：
10.1002/cncr.26502
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发表时间：
2012-04
期刊：
影响因子：
6.2
通讯作者：
Yan Jiang;Wenjing Wang;Jiucun Wang;Ye Lu;Yan-Min Chen;Li Jin;D. Lin;F. He;Haijian Wang
中科院分区：
文献类型：
--
作者：
Yan Jiang;Wenjing Wang;Jiucun Wang;Ye Lu;Yan-Min Chen;Li Jin;D. Lin;F. He;Haijian Wang
调节细胞凋亡和增殖的分子的功能障碍与肿瘤发生有关。BCL 2家族基因MCL1启动子区常见的插入多态性与白血病的发生有关，但其与白血病易感性及预后的关系尚不清楚。我们假设MCL1启动子变异可能改变实体癌的风险。
Dysfunction of molecules that regulate both apoptosis and proliferation is involved in tumorigenesis. A common insertional polymorphism in promoter of MCL1, a member of BCL2 family gene with the dual regulatory functions, has been shown to be functional in leukemia, but its association with cancer predisposition and prognosis has not been well established. We hypothesized that MCL1 promoter variants may modify risk of solid cancer.