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논문 기본 정보

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학술저널
저자정보
Chung-Feng Huang (Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital; College of Medicine and Center for Liquid Biopsy and Cohort Research, Kaohsiung Medical Univer) Manar Hijaze Awad (Molecular Virology Lab, The Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel) Meital Gal-Tanamy (Molecular Virology Lab, The Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel) Ming-Lung Yu (Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital; College of Medicine and Center for Liquid Biopsy and Cohort Research, Kaohsiung Medical Univer)
저널정보
대한간학회 Clinical and Molecular Hepatology Clinical and Molecular Hepatology Vol.30 No.3
발행연도
2024.7
수록면
326 - 344 (19page)

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초록· 키워드

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Hepatitis C virus (HCV) infection is one of the major etiologies of hepatocellular carcinoma (HCC) with approximately 30% of HCC being due to HCV infection worldwide. HCV eradication by antivirals greatly reduces the risk of HCC; nevertheless, HCC remains to occur in chronic hepatitis C (CHC) patients who have achieved a sustained virological response (SVR). The proportion of post-SVR HCC among newly diagnosed HCC patients is increasing in the direct-acting antiviral (DAA) era and might be due to preexisting inflammatory and fibrotic liver backgrounds, immune dysregulation between host and virus interactions, as well as host epigenetic scars, genetic predispositions and alternations. By means of applying surrogate markers and adopting risk stratification, HCC surveillance should be consistently performed in high-risk populations. In this review, we discuss the possible molecular mechanism, risk factors, and HCC surveillance strategy for HCC development after HCV eradication in CHC patients.

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