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;

D O I：

暂无

中图分类号：

学科分类号：

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.

引用

共 131 条

[1]

Pazaitou-Panayiotou K(2013)The increase in thyroid cancer incidence is not only due to papillary microcarcinomas: a 40-year study in 1 778 patients Exp Clin Endocrinol Diabetes 121 397-401

[2]

Iliadou PK(2009)Exposure to ionizing radiation in adulthood and thyroid cancer incidence Epidemiology 20 181-187

[3]

Chrisoulidou A(2006)Radiation-epidemiological studies of thyroid cancer incidence among children and adolescents in the Bryansk oblast of Russia after the Chernobyl accident (1991–2001 follow-up period) Radiat Environ Biophys 45 9-16

[4]

Mitsakis P(2008)Common SNP in pre-miR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma Proc Natl Acad Sci USA 105 7269-7274

[5]

Doumala E(2014)Association between a functional insertion/deletion polymorphism in IL1A gene and risk of papillary thyroid carcinoma Tumour Biol 35 3861-3865

[6]

Richardson DB(2013)Requirement for interaction of PI3-kinase p110alpha with RAS in lung tumor maintenance Cancer Cell 24 617-630

[7]

Ivanov VK(2005)The Ras-MAPK signal transduction pathway, cancer and chromatin remodeling Biochem Cell Biol 83 1-14

[8]

Gorski AI(2005)Reduction in the requirement of oncogenic Ras signaling to activation of PI3 K/AKT pathway during tumor maintenance Cancer Cell 8 381-392

[9]

Tsyb AF(2005)Activation of RalA is critical for Ras-induced tumorigenesis of human cells Cancer Cell 7 533-545

[10]

Maksioutov MA(2013)BRAF and RAS mutations in follicular variants of papillary thyroid carcinoma Endocr Pathol 24 69-76

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