DNA损伤与肝癌发生

DNA damage and liver cancer

肝癌是最常见的恶性肿瘤之一,其发生是一个复杂的生物学过程,具体机制尚未完全阐明.研究表明,乙、丙型肝炎病毒感染,黄曲霉毒素污染,饮酒,电离辐射以及具有有遗传毒性的人体代谢产物等能够诱导肝癌的发生,他们大都直接作用于肝细胞的遗传物质,引起DNA的损伤,这是发生肝癌的重要分子基础.DNA损伤后引起细胞一系列的反应,包括损伤信号的传导,损伤修复,诱导细胞死亡.这些诱因也能作用于损伤修复系统中的某个环节,使DNA损伤不能修复或不能正确修复,细胞发生恶性转化.因此,损伤DNA的累积就成为肝癌发生的重要分子机制,对其深入研究将会为肝癌的治疗奠定基础.

Hepatocellular carcinoma （HCC） is one of the most common malignant tumors. Carcinogenesis of HCC involves complex biological processes for which the mechanism/s remains to be completely clarified. Research has shown that hepatitis B and C virus infections, aflatoxin contamination, alcohol abuse, ionizing radiation and human metabolic products toxic to the human genome can induce HCC. Most of these cause DNA damage by having direct impacts on the genetic materials of hepatocytes. This constitutes an important molecular basis for the carcinogenesis of HCC. DNA damage causes a series of cell responses, including injury signal transduction, damage repair, and induction of cell death. The factors involved in DNA damage can also affect some aspects of the DNA injury repair system, preventing the damage from being repaired or correctly repaired, leading to malignant transformations. Therefore, the accumulation of damaged DNA becomes an important molecular mechanism underlying the carcinogenesis of HCC. Further studies should lay a foundation for research into treatments for HCC.