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首页> 外文期刊>Diseases of the esophagus: official journal of the International Society for Diseases of the Esophagus >Associations of risk factors obesity and occupational airborne exposures with CDKN2A/p16 aberrant DNA methylation in esophageal cancer patients.
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Associations of risk factors obesity and occupational airborne exposures with CDKN2A/p16 aberrant DNA methylation in esophageal cancer patients.

机译:食管癌患者肥胖和职业空气传播危险因素与CDKN2A / p16异常DNA甲基化的关联。

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摘要

It is known that obesity and occupational airborne exposure such as dust are among risk factors of esophageal cancer development, in particular squamous cell carcinoma (SCC) of esophagus. Here, we tested whether these factors could also affect aberrant DNA methylation. DNAs from 44 fresh tumor tissues and 19 non-tumor adjacent normal tissues, obtained from 44 patients affected by SCC of esophagus (SCCE), were studied for methylation at the CDKN2A/p16 gene promoter by methylation-specific polymerase chain reaction assay. Statistical methods were used to assess association of promoter methylation with biopathological, clinical, and personal information data, including obesity and airborne exposures. Methylation at the CDKN2A/p16 gene promoter was detected in 12 out of 44 tumor samples. None of the non-tumor tissues exhibited the aberrant methylation. Our results confirmed previously described significant association with low tumor stage (P= 0.002); in addition, we found that obesity (P= 0.001) and occupational exposure (P= 0.008) were both significantly associated with CDKN2A/p16 promoter methylation. This study provides evidence that obesity and occupational exposure increase the risk of developing esophageal cancer through an enhancement of CDKN2A/p16 promoter methylation.
机译:众所周知,肥胖和职业性空气传播的粉尘是食管癌发展的危险因素,特别是食道鳞状细胞癌(SCC)。在这里,我们测试了这些因素是否也可能影响异常的DNA甲基化。通过甲基化特异性聚合酶链反应分析研究了来自食管鳞状细胞癌(SCCE)的44例患者的44例新鲜肿瘤组织和19例非肿瘤邻近正常组织的DNA在CDKN2A / p16基因启动子上的甲基化情况。统计方法用于评估启动子甲基化与生物病理学,临床和个人信息数据(包括肥胖症和空气传播暴露)的关联。在44个肿瘤样本中的12个中检测到CDKN2A / p16基因启动子的甲基化。没有一个非肿瘤组织表现出异常的甲基化。我们的结果证实了先前描述的与低肿瘤分期的显着相关性(P = 0.002);此外,我们发现肥胖(P = 0.001)和职业暴露(P = 0.008)均与CDKN2A / p16启动子甲基化显着相关。这项研究提供了证据表明,肥胖和职业暴露会通过增强CDKN2A / p16启动子甲基化来增加发生食道癌的风险。

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