Premium
Hepatitis B × antigen and p53 in the development of hepatocellular carcinoma
Author(s) -
Feitelson Mark A.
Publication year - 1998
Publication title -
journal of hepato‐biliary‐pancreatic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 0944-1166
DOI - 10.1007/s005340050060
Subject(s) - hepatocellular carcinoma , hepatitis b virus , apoptosis , cancer research , hepatitis b , cell cycle , cell cycle checkpoint , antigen , virology , genome instability , biology , virus , medicine , immunology , dna , dna damage , genetics
Hepatitis B virus (HBV) is one of the major etiological agents responsible for the appearance of chronic liver diseases, including hepatocellular carcinoma (HCC). There is increasing evidence that the HBV excoded × antigen (HBxAg) is involved in one or more steps that contribute to multistep hepatocarcinogenesis. Recent work has now defined one of these steps as the physical binding and functional inactivation of the tumor suppressor protein, p53, by HBxAg. The centrality of p53 to genomic stability, cell cycle arrest, induction of apoptosis, and in senescence related pathways, suggests that its disruption by HBxAg will result in genomic instability, loss of cell cycle control, a lower apoptotic rate, and an extension in the life span of HBV‐infected cells. It is proposed that HBxAg/p53 complex formation represents one of several steps whereby HBV contributes to the development of HCC.