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541 results on '"Hu, Rey-Heng"'

8. HBV DNA integration and somatic mutations in HCC patients with HBV-HCV dual infection reveals profiles intermediate between HBV- and HCV-related HCC.

Author

Li, Chiao-Ling, Hsu, Chia-Lang, Lin, You-Yu, Ho, Ming-Chih, Hu, Rey-Heng, Tzeng, Sheng-Tai, Wang, Ya-Chun, Tanaka, Yasuhito, Chen, Pei-Jer, and Yeh, Shiou-Hwei

Subjects
NUCLEOTIDE sequencing, HEPATITIS C virus, TELOMERASE reverse transcriptase, HEPATITIS B virus, CHRONIC hepatitis B
Abstract

Background: In regions with a high prevalence of chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, coinfected patients face a heightened risk of developing hepatocellular carcinoma (HCC), termed HBV/HCV-related HCC (HBCV-HCC). We aimed to investigate the contribution of preexisting chronic hepatitis B (CHB) and subsequent chronic hepatitis C (CHC) to the development of HBCV-HCC. Methods: We examined HBV's involvement in 93 HBCV-HCC cases by analyzing HBV DNA integration as an indicator of HCC originating from HBV-infected hepatocytes, compared with 164 HBV-HCCs and 56 HCV-HCCs as controls. Results: Next generation sequencing revealed that 55% of HBCV-HCCs exhibited clonal HBV integration, which falls between the rates observed in HBV-HCCs (88%) and HCV-HCCs (7%), with similar integration patterns to HBV-HCCs. Common HCC somatic mutation analysis indicated HCV superinfection in HBCV-HCCs correlated with increased mutation rates in the telomerase reverse transcriptase (TERT) promoter and beta-catenin genes. Transcriptome analysis showed a prevalence of replicating HCV over HBV in HBCV-HCCs, with preexisting HBV exerting a proliferative role. The comparison of clinical characteristics revealed similarities between HBCV-HCC and HCV-HCC patients, including later onset for HBCV-HCC, possibly due to HCV superinfection slowing carcinogenesis. Notably, HBCV-HCCs with the same driver mutation, HBV integration at the TERT promoter, tended to develop later and showed a better prognosis post-tumor resection than HBV-HCCs. Conclusions: Our findings shed light on the interplay between preexisting CHB and subsequent CHC in elevating the risk of HBCV-HCC. These insights are crucial for understanding viral etiology-specific carcinogenesis and guiding surveillance policies for HBCV-HCC post-antiviral therapy. [ABSTRACT FROM AUTHOR]

Published
2025
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32. Supplementary Figures 1-4 from Mucin Glycosylating Enzyme GALNT2 Regulates the Malignant Character of Hepatocellular Carcinoma by Modifying the EGF Receptor

Author

Wu, Yao-Ming, primary, Liu, Chiung-Hui, primary, Hu, Rey-Heng, primary, Huang, Miao-Juei, primary, Lee, Jian-Jr, primary, Chen, Chi-Hau, primary, Huang, John, primary, Lai, Hong-Shiee, primary, Lee, Po-Huang, primary, Hsu, Wen-Ming, primary, Huang, Hsiu-Chin, primary, and Huang, Min-Chuan, primary

Published
2023
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36. Supplementary Figure Legends 1-4 from Mucin Glycosylating Enzyme GALNT2 Regulates the Malignant Character of Hepatocellular Carcinoma by Modifying the EGF Receptor

Author

Wu, Yao-Ming, primary, Liu, Chiung-Hui, primary, Hu, Rey-Heng, primary, Huang, Miao-Juei, primary, Lee, Jian-Jr, primary, Chen, Chi-Hau, primary, Huang, John, primary, Lai, Hong-Shiee, primary, Lee, Po-Huang, primary, Hsu, Wen-Ming, primary, Huang, Hsiu-Chin, primary, and Huang, Min-Chuan, primary

Published
2023
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37. Supplementary Tables 1-2 from Mucin Glycosylating Enzyme GALNT2 Regulates the Malignant Character of Hepatocellular Carcinoma by Modifying the EGF Receptor

Author

Wu, Yao-Ming, primary, Liu, Chiung-Hui, primary, Hu, Rey-Heng, primary, Huang, Miao-Juei, primary, Lee, Jian-Jr, primary, Chen, Chi-Hau, primary, Huang, John, primary, Lai, Hong-Shiee, primary, Lee, Po-Huang, primary, Hsu, Wen-Ming, primary, Huang, Hsiu-Chin, primary, and Huang, Min-Chuan, primary

Published
2023
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50. Hepatitis C treatment and long‐term outcome of patients with hepatocellular carcinoma after resection.

Author

Cheng, Hou‐Ying, Hu, Rey‐Heng, Hsiao, Chih‐Yang, Ho, Ming‐Chih, Wu, Yao‐Ming, Lee, Po‐Huang, and Ho, Cheng‐Maw

Subjects
*LIVER surgery, *HEPATOCELLULAR carcinoma, *HEPATITIS C, *HEPATITIS C virus, *ANTIVIRAL agents, *OVERALL survival
Abstract

Background and Aim: This study aimed to investigate the survival outcomes of antiviral agents (direct‐acting antivirals [DAAs] or interferon [IFN]) in patients with hepatitis C virus who underwent liver resection for primary hepatocellular carcinoma. Methods: This retrospective single‐center study included 247 patients, between 2013 and 2020, being treated with DAAs (n = 93), IFN (n = 73), or no treatment (n = 81). Overall survival (OS), recurrence‐free survival (RFS), and risk factors were analyzed. Results: After a median follow‐up time of 50.4 months, the rates of 5‐year OS and RFS in the IFN, DAA, and no treatment groups were 91.5% and 55.4%, 87.2% and 39.8%, and 60.9% and 26.7%, respectively. One hundred and twenty‐eight (51.6%) patients developed recurrence; recurrence was mostly (86.7%) intrahepatic, and 58 (23.4%) developed early recurrence, most of which received no antiviral treatment. The OS and RFS were similar between patients who received antiviral treatment before (50.0%) and after surgery, but longer survival was observed in patients achieving sustained virologic response. In multivariate analysis, antiviral treatment was protective for OS (hazard ratio [HR] 0.475, 95% confidence interval [CI]: 0.242–0.933) with significance but not RFS, in contrast to microvascular invasion (OS HR 3.389, 95% CI: 1.637–7.017; RFS HR 2.594, 95% CI: 1.520–4.008). In competing risk analysis, DAAs (subdistribution HR 0.086, 95% CI: 0.007–0.991) were protective against hepatic decompensation events but not recurrence events. Conclusion: In patients with hepatitis C virus, antiviral treatment suggested OS benefit for primary hepatocellular carcinoma after resection, and DAAs might be protective against hepatic decompensation. Following adjustment for oncological factors, IFN and DAA treatment was not significantly advantageous relative to the other. [ABSTRACT FROM AUTHOR]

Published
2023
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