کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2524137 1557973 2015 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The association between the SNP rs763110 and the risk of gynecological cancer: A meta-analysis
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی تومور شناسی
پیش نمایش صفحه اول مقاله
The association between the SNP rs763110 and the risk of gynecological cancer: A meta-analysis
چکیده انگلیسی

FAS and FAS ligand (FASL) are the principal genes of the apoptosis pathway, which play a vital role in the etiology of various gynecological cancers. Studies have revealed that polymorphism of FASL promoter -844C>T (rs763110) influences FASL transcription process, which involving in cancer risk. Moreover, estrogen has been proved to trigger T-cell apoptosis by up-regulating FAS/FASL system in cancer cells. However, results from the published studies on the association between FASL -844C>T polymorphism and risk of gynecological cancer are conflicting. We performed a meta-analysis based on 13 case-control studies, including a total of 6256 cancer cases and 5573 controls. We used odd ratios (ORs) with 95% confidence intervals (CIs) to assess the association strength. Overall, the FASL -844CT and TT genotypes were associated with a significantly reduced risk of gynecological cancer types in homozygote comparison (OR = 0.80, 95% CI = 0.64–0.99), heterozygote comparison (OR = 0.81, 95% CI = 0.67–0.98), and dominant model (OR = 0.81, 95% CI = 0.67–0.98). In the stratified analyses, we observed a similar association among Asian population (heterozygote comparison: OR = 0.73, 95% CI = 0.56–0.95; dominant model: OR = 0.75, 95% CI = 0.57–0.98) and hospital-based studies (homozygote comparison: OR = 0.61, 95% CI = 0.43–0.86). When stratified by cancer type, there was also a significantly lower risk of the ovarian cancer in different genetic models except the recessive one. The results suggested that the FASL -844C>T polymorphism may reduce the risk of gynecological cancer.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biomedicine & Pharmacotherapy - Volume 69, February 2015, Pages 208–213
نویسندگان
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