Role of Nucleotide Polymorphism in TLL1 Gene in Development of Hepatocellular Carcinoma in Patients Achieving Sustained Virological Response after Direct Acting Antiviral Drugs for HCV

Abstract

ncidence of Hepatocellular carcinoma (HCC) has rapidly increased worldwide. HCC is the sixth most common malignancy and the third most common cause of cancer related death. Recent investigations in Egypt have shown the increasing importance of HCV infection in the etiology of liver cancer, estimated to account for 40–50% of cases. Chronic infection with HCV is the leading cause of end-stage liver disease, HCC and liver-related death in Egypt. Direct-acting antiviral agents for chronic hepatitis C have initiated a revolution in the management and control of this important liver disease with cure rates over 90%. Highly effective DAA were expected to dramatically decrease HCV related liver disease progression to end-stage liver disease and HCC. In fact, the risk of developing HCC continues to persist in those patients with HCV cirrhosis even after they have achieved SVR. In contrast to these initial observations, several larger studies found different results. Recent studies have suggested that DAA may accelerate the occurrence of HCC in patients with liver cirrhosis. In contrast to these observations, several larger studies found different results. Over the past decade, much progress has been made in elucidating the molecular mechanisms underlying hepatocarcinogenesis. The impact of genetic variations on risk of HCC remains largely undefined although hepatocarcinogenesis arises from complex interactions between genetic and environmental factors.