食管癌
DNA甲基化
医学
优势比
甲基化
内科学
癌症
肿瘤科
生物标志物
癌变
置信区间
胃肠病学
基因
生物
遗传学
基因表达
作者
Mandakini Das,Basanta Saikia,Sandeep Sharma,Gaganpreet Singh Sekhon,Jagadish Mahanta,Rup Kumar Phukan
出处
期刊:Tumor Biology
[SAGE]
日期:2014-11-01
卷期号:36 (3): 1627-1642
被引量:18
标识
DOI:10.1007/s13277-014-2762-7
摘要
Esophageal cancer is one of the most common cancers in North East India. The molecular mechanisms of esophageal cancer susceptibility in North East India have not been fully understood. There is a need for identification of biomarkers to identify people at risk of esophageal cancer. p16 is an essential G1 cell cycle regulatory gene whose loss of function is associated with carcinogenesis. Therefore, we conducted this study to determine the prevalence of p16 gene methylation in patients with esophageal cancer to assess the feasibility of using gene methylation as a biomarker. A total of 100 newly diagnosed esophageal cancer cases along with equal number of age, sex, and ethnicity-matched controls were included in this study. Methylation-specific PCR was used to determine the p16 methylation status. Aberrant promoter methylation of the p16 gene was detected in 81 of 100 (81 %) esophageal cancer cases. Hypermethylation of p16 gene was found to be influenced by lifestyle factors. Betel quid and tobacco chewing habit synergistically with p16 methylation elevated the risk for esophageal cancer development (adjusted odds ratio (OR) = 6.88, 95 % confidence interval (CI) = 1.64–28.81, p = 0.003 for betel quid chewing and adjusted OR = 7.02, 95 % CI = 1.87–26.38, p = 0.001 for tobacco chewing). Further, intake of green leafy vegetables and fruits lowered the risk of esophageal cancer (adjusted OR = 0.16, 95 % CI = 0.04–0.58, p = 0.05 for green leafy vegetables and adjusted OR = 0.15, 95 % CI = 0.04–0.64, p = 0.01 for fruits). Thus, p16 hypermethylation may aid as a biomarker in identifying habitués at greater risk for esophageal cancer susceptibility in high incidence region of North East India.
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