Hino Okio
Department of Pathology, Juntendo University School of Medicine, Tokyo, Japan.
Intervirology. 2005;48(1):6-9. doi: 10.1159/000082088.
Human hepatocellular carcinomas (HCCs) are preceded by chronic hepatitis and cirrhosis. Despite a clear viral etiology [hepatitis B virus (HBV) and hepatitis C virus (HCV)] of human hepatocarcinogenesis, the mechanism is complex and the distinct molecular pathway or molecules to explain this phenomenon are not yet known. Hepatitis viral, 'inflammation-mediated' hepatocarcinogenesis greatly influences the incidence of somatic genetic events in hepatocytes by increasing the number of target cells, or the proliferation of once-hit hepatocytes, eventually leading to HCCs. These conditions may be designated as the 'hypercarcinogenic state'. Our goal is to lead the 'hypercarcinogenic state' to the 'normo- or hypocarcinogenic' state and to prevent HCC development (intentional delay of HCC).
人类肝细胞癌（HCC）之前会出现慢性肝炎和肝硬化。尽管人类肝癌发生有明确的病毒病因[乙型肝炎病毒（HBV）和丙型肝炎病毒（HCV）]，但其机制复杂，目前尚不清楚解释这一现象的独特分子途径或分子。病毒性肝炎“炎症介导”的肝癌发生通过增加靶细胞数量或曾经受损肝细胞的增殖，极大地影响肝细胞中体细胞遗传事件的发生率，最终导致肝细胞癌。这些情况可被称为“高致癌状态”。我们的目标是将“高致癌状态”转变为“正常或低致癌状态”，并预防肝细胞癌的发生（有意延缓肝细胞癌）。
