Epigenetic mechanism of chronic inflammation-associated human carcinogenesis

本研究的重点是表观基因组改变在与慢性炎症相关的多阶段癌变中的意义。在从肺腺癌患者获得的癌性和非癌性组织样本中进行全基因组DNA甲基化分析。为了进行比较，我们还分析了无原发性肺肿瘤患者的正常肺组织样本。在重度吸烟者慢性阻塞性肺疾病的炎症背景下，DNA甲基化谱可能产生侵袭性腺癌。全基因组DNA甲基化分析还确定了与乙型肝炎病毒（HBV）感染和丙型肝炎病毒（HCV）感染相关的肝癌发生特异性的DNA甲基化谱，以及HBV阳性和HCV阳性患者共有的DNA甲基化谱。

This study has focused on the significance of epigenome alterations in multistage carcinogenesis associated with chronic inflammation. Genome-wide DNA methylation analysis was performed in cancerous and non-cancerous tissue samples obtained from patients with adenocarcinomas of the lung. For comparison, normal lung tissue samples from patients without any primary lung tumor were also analyzed. DNA methylation profiles, which may generate aggressive adenocarcinomas from the inflammatory background in chronic obstructive pulmonary disease in heavy smokers, were identified. Genome-wide DNA methylation analysis also identified DNA methylation profiles each specific to hepatocarcinogenesis associated with hepatitis B virus (HBV) infection and hepatitis C virus infection (HCV) and DNA methylation profiles shared by HBV-positive and HCV-positive patients.