Wang S.-H.Shiou-Hwei YehPEI-JER CHEN2021-07-032021-07-032016#VALUE!https://www.scopus.com/inward/record.uri?eid=2-s2.0-85018058361&doi=10.1007%2f978-4-431-56101-9_4&partnerID=40&md5=fe888ffaf00ce360ce61e9e652e9de68https://scholars.lib.ntu.edu.tw/handle/123456789/568387Hepatocellular carcinoma (HCC) is an important health issue worldwide. It is a liver malignancy with heterogeneous etiologies. Among them, chronic hepatitis C virus (HCV) infection is one major cause. In chronically infected hepatocytes, HCV directly induces oxidative stress, impairs DNA damage response, manipulates cell cycle control and generates insulin resistance, possibly promoting DNA mutations accumulated in host genome from hepatitis stages in a long time. The predisposing polymorphisms or genetic mutations in critical proto-oncogenes and tumor suppressor genes, in synergy with epigenetic alterations after HCV invasion, would eventually transform hepatocytes to HCC tumor cells. Therefore, this chapter focuses on reviewing the virologic role of HCV in disease progression, as well as the host genetic changes for HCC development. Besides, the oncogenic mechanisms evoked by HCV at cellular level and the sex disparity of HCV-related HCC based on sex hormone effects are discussed individually. The comprehensive understanding of HCV-induced hepatocarcinogenesis paves the way to develop novel prophylactic or therapeutic strategies for HCC in future. ? 2016 Springer Japan.Androgen receptor (AR); Chronic hepatitis C (CHC); Estrogen receptor α (ERα); Hepatitis C virus (HCV); Hepatocellular carcinoma (HCC); Sustained virologic response (SVR)[SDGs]SDG3book part10.1007/978-4-431-56101-9_42-s2.0-85018058361