<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(2)</volume><submitter>Huang SF</submitter><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>The correlation between chronic hepatitis B virus (HBV) infection and hepatocellular carcinoma (HCC) has been well-established. But the roles of viral factor remain uncertain. Only HBV X gene and nonsense mutations of S gene (C-terminal truncation of HBV surface protein) have been demonstrated to have transforming activity. Whether they play a significant role in hepatocarcinogenesis is still uncertain.&lt;h4>Methods&lt;/h4>Twenty-five HBV-related HCC patients were positive for hepatitis B core antigen (HBcAg) in the cancerous parts of their HCC liver tissues by immunohistochemistry studies, and had available tissue for whole HBV genome sequence analysis. The results were compared with 25 gender and age-matched HBcAg negative HCCs. Plasmids encoding HBV S gene nonsense </pubmed_abstract><journal>PloS one</journal><pagination>e89753</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3933656</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma.</pubmed_title><pmcid>PMC3933656</pmcid><pubmed_authors>Lai MW</pubmed_authors><pubmed_authors>Wu HD</pubmed_authors><pubmed_authors>Yuh CH</pubmed_authors><pubmed_authors>Yeh CT</pubmed_authors><pubmed_authors>Matsuura I</pubmed_authors><pubmed_authors>Chang Y</pubmed_authors><pubmed_authors>Shih LY</pubmed_authors><pubmed_authors>Lee WC</pubmed_authors><pubmed_authors>Tu HC</pubmed_authors><pubmed_authors>Chen MF</pubmed_authors><pubmed_authors>Chen YT</pubmed_authors><pubmed_authors>Huang SF</pubmed_authors><pubmed_authors>Chiu YT</pubmed_authors><pubmed_authors>Chang IC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma.</name><description>&lt;h4>Background &amp; aims&lt;/h4>The correlation between chronic hepatitis B virus (HBV) infection and hepatocellular carcinoma (HCC) has been well-established. But the roles of viral factor remain uncertain. Only HBV X gene and nonsense mutations of S gene (C-terminal truncation of HBV surface protein) have been demonstrated to have transforming activity. Whether they play a significant role in hepatocarcinogenesis is still uncertain.&lt;h4>Methods&lt;/h4>Twenty-five HBV-related HCC patients were positive for hepatitis B core antigen (HBcAg) in the cancerous parts of their HCC liver tissues by immunohistochemistry studies, and had available tissue for whole HBV genome sequence analysis. The results were compared with 25 gender and age-matched HBcAg negative HCCs. Plasmids encoding HBV S gene nonsense </description><dates><release>2014-01-01T00:00:00Z</release><publication>2014</publication><modification>2026-04-30T10:55:22.066Z</modification><creation>2019-03-26T23:23:51Z</creation></dates><accession>S-EPMC3933656</accession><cross_references><pubmed>24587012</pubmed><doi>10.1371/journal.pone.0089753</doi></cross_references></HashMap>