The association of phosphatase and tensin homolog deleted on chromosome 10 polymorphisms and lifestyle habits with colorectal cancer risk in a Chinese population

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• 作者：Fangyuan Jing ; Yingying Mao ; Zhenyu Zhang ; Yingjun Li ; Shaofang Cai…
• 关键词：PTEN ; Single ; nucleotide polymorphism ; Colorectal cancer ; Susceptibility
• 刊名：Tumor Biology
• 出版年：2014
• 出版时间：September 2014
• 年：2014
• 卷：35
• 期：9
• 页码：9233-9240
• 全文大小：174 KB
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• 作者单位：Fangyuan Jing (1)
  Yingying Mao (1)
  Zhenyu Zhang (1)
  Yingjun Li (1)
  Shaofang Cai (1)
  Qilong Li (2)
  Xinyuan Ma (2)
  Mingjuan Jin (1)
  Kun Chen (1)
  
  1. Department of Epidemiology and Biostatistics, Zhejiang University School of Public Health, Hangzhou, 310058, Zhejiang, China
  2. Institute for Cancer Prevention of Jiashan County, Jiashan, Zhejiang, China
  
• ISSN：1423-0380

文摘

The PI3K signaling pathway plays an important role in the development of colorectal cancer (CRC) and other neoplasm. Somatic phosphatase and tensin homolog deleted on chromosome 10 (PTEN) mutations and deletions or epigenetic silencing have been observed in multiple tumor types including CRC. To assess the association of PTEN polymorphisms and lifestyle habits with CRC risk in Chinese population, we carried out a case-control study which included 545 cases and 522 controls. In the present study, we genotyped eight single-nucleotide polymorphisms (SNPs) in PTEN and found that rs11202607 was associated with increased CRC risk (odds ratio (OR)--.40, 95?% confidence interval (CI)--.04-.90). Stratification analysis by lifestyle habits showed a stronger association between rs11202607 and CRC risk among never tea drinkers than that among tea-drinkers (OR--.04, 95?% CI 1.29-.22), and significant additive interaction between rs10490920 and tea drinking status was observed. Our study provided the evidence of an association between PTEN polymorphisms and the risk of CRC and significant additive interaction between PTEN polymorphism and tea drinking. Studies with larger sample size and further investigations into the mechanism are warranted to clarify the role of PTEN in colorectal carcinogenesis and the association between PTEN genetic variations, environment exposure, and CRC risk.