Association between a functional polymorphism rs712 within let-7-binding site and risk of papillary thyroid cancer

被引:0
作者
Hong Jin
Yundan Liang
Xunli Wang
Jingqiang Zhu
Ruifen Sun
Peng Chen
Xinwen Nie
Linbo Gao
Lin Zhang
机构
[1] Sichuan University,Department of Immunology, West China School of Preclinical and Forensic Medicine
[2] Hospital of Yunnan University of Nationalities,Department of Thyroid and Breast Surgery
[3] West China Hospital of Sichuan University,Laboratory of Molecular and Translational Medicine, West China Institute of Women and Children’s Health; West China Second University Hospital
[4] Sichuan University,undefined
[5] Key Laboratory of Obstetric & Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education,undefined
来源
Medical Oncology | 2014年 / 31卷
关键词
Let-7; Polymorphism; Papillary thyroid cancer;
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摘要
KRAS mutation is frequently detected in a series of cancers, including papillary thyroid cancer (PTC). Recently, a genetic variant of rs712 in the 3′ untranslated region of the KRAS gene has been reported to be functional in the regulation of KRAS by disrupting complementary site of let-7 and miR-181. We aimed to investigate whether the polymorphism is a risk factor for PTC. We conducted an association study, including 252 PTC patients and 290 healthy controls. The KRAS rs712 polymorphism was genotyped by polymerase chain reaction–restriction fragment length polymorphism. Although no significant difference of the KRAS rs712 distribution was observed between cases and controls in overall analysis, stratification analysis showed that patients carrying the KRAS rs712TT genotype were less likely to develop stages T3 and T4 under a recessive genetic model (OR 0.26, 95 % CI 0.08–0.82). These results supported the role of the KRAS rs712 polymorphism as a potential genetic biomarker for the extension of PTC. Further population-based association studies are of great value to confirm the results in diverse ethnicities.
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