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Article

The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-β/Smad signaling pathway.

Virology journal - 2 Apr 2018

Wang Meng-Lan, Wu Dong-Bo, Tao Ya-Chao, Chen Lan-Lan, Liu Cui-Ping, Chen En-Qiang, Tang Hong

Abstract excerpt

BACKGROUND: It has been reported that the emergence of HBV rtA181T/sW172* mutant could result in a dominant secretion defect of HBsAg and increase the risk of HCC development. This study was designed to reveal the role and possible pathogenic mechanism of truncated mutant HBsAg in tumorigenesis of HBV rtA181T/sW172* mutant. RESULTS: As compared to wide type or substituted mutant HBsAg, the ratio of cell clones...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 29609638
DOI: 10.1186/s12985-018-0972-0
PMCID: PMC5879756

Genes

TGFBI

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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