H
Han Chieh Wu
Researcher at National Institutes of Health
Publications - 31
Citations - 1227
Han Chieh Wu is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Hepatitis B virus & Hepatocellular carcinoma. The author has an hindex of 17, co-authored 31 publications receiving 1014 citations. Previous affiliations of Han Chieh Wu include National Health Research Institutes & National Cheng Kung University.
Papers
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Journal ArticleDOI
Different Types of Ground Glass Hepatocytes in Chronic Hepatitis B Virus Infection Contain Specific Pre-S Mutants that May Induce Endoplasmic Reticulum Stress
TL;DR: Laser capture microdissection demonstrates that different GGHs may contain specific mutants and exhibit differential biological activities.
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Ground glass hepatocytes contain pre-S mutants and represent preneoplastic lesions in chronic hepatitis B virus infection.
TL;DR: GGH, particularly type II GGH, may represent the preneoplastic lesions of HBV‐related HCC and transgenic mice harboring pre‐S2 mutant plasmids have been shown to develop a dysplastic change of hepatocytes and HCC.
Journal ArticleDOI
Hepatitis B virus pre‐S2 mutant upregulates cyclin A expression and induces nodular proliferation of hepatocytes
Hui Ching Wang,Wen Tsan Chang,Wen-Wei Chang,Han Chieh Wu,Wenya Huang,Huan Yao Lei,Ming Derg Lai,Nelson Fausto,Ih-Jen Su,Ih-Jen Su +9 more
TL;DR: In vitro and in vivo data support a role for ΔS2‐LHBs in the hepatocyte hyperplasia and a likely role in the process of HBV‐related tumorigenesis.
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Enhanced expression of vascular endothelial growth factor‐A in ground glass hepatocytes and its implication in hepatitis B virus hepatocarcinogenesis
Jui Chu Yang,Chiao Fang Teng,Han Chieh Wu,Hung Wen Tsai,Huai Chia Chuang,Huai Chia Chuang,Ting Fen Tsai,Yu Hsiang Hsu,Wenya Huang,Li Wha Wu,Ih-Jen Su,Ih-Jen Su +11 more
TL;DR: The enhanced expression of VEGF‐A in GGHs provides potential mechanism to explain the progression from preneoplastic G GHs to HCC in chronic HBV infection.
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Novel feedback inhibition of surface antigen synthesis by mammalian target of rapamycin (mTOR) signal and its implication for hepatitis B virus tumorigenesis and therapy
TL;DR: The activation of mTOR signal in GGHs may feedback suppress HBsAg synthesis during HBV tumorigenesis and explain the observed decrease or absence ofHBsAg in HCC tissues.