| Literature DB >> 24120759 |
Yang Deng1, Yan Du1, Qi Zhang1, Xue Han2, Guangwen Cao3.
Abstract
During hepatitis B virus (HBV)-induced hepatocarcinogenesis, chronic inflammation facilitates the evolution of hepatocellular carcinoma (HCC)-promoting HBV mutants. Cytidine deaminases, whose expression is stimulated by inflammatory cytokines and/or chemokines, play an important role in bridging inflammation and HCC. Through G-to-A hypermutation, cytidine deaminases inhibit HBV replication and facilitate the generation of HCC-promoting HBV mutants including C-terminal-truncated HBx. Cytidine deaminases also promote cancer-related somatic mutations including TP53 mutations. Their editing efficiency is counteracted by uracil-DNA glycosylase. Understanding the effects of cytidine deaminases in HBV-induced hepatocarcinogenesis and HCC progression will aid in developing efficient prophylactic and therapeutic strategies against HCC in HBV-infected population.Entities:
Keywords: Chronic HBV infection; Cytidine deaminase; Evolution; HBV mutation; Hepatocellular carcinoma; Somatic mutation
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Year: 2013 PMID： 24120759 DOI： 10.1016/j.canlet.2013.09.041
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679