Abstract
Hepatocellular carcinoma (HCC) is the seventh most common cancer worldwide and the second leading cause of cancer-related mortality. HCC typically arises within a cirrhotic liver, but in about 20% of cases occurs in absence of cirrhosis. Among non-cirrhotic risk factors, non-alcoholic fatty liver disease (NAFLD) currently represents the most important emerging cause of HCC in developed countries. It has been estimated that annual incidence of HCC among patients with non-cirrhotic NAFLD is approximately 0.1–1.3 per 1000 patients/year and ranges from 0.5% to 2.6% among patients with non-alcoholic steatohepatitis (NASH) cirrhosis. However, only a few clinical trials enrolling HCC patients actually distinguished NAFLD/NASH-related cases from other non-cirrhotic causes and therefore evidence is still lacking in this subset of patients. This review aims to describe the biology underpinning NAFLD development, to investigate the main molecular pathways involved in its progression to NASH and HCC and to describe how different pathogenetic mechanisms underlying the onset of HCC can have an impact in clinical practice. We hereby also provide an overview of current HCC treatment options, with a particular focus on the available data on NAFLD-related cases in practice-changing clinical trials.
Highlights
Hepatocellular carcinoma (HCC) is the seventh most common cancer worldwide and the second leading cause of cancer-related mortality, with substantial differences across geographical areas due to the different prevalence of risk factors [1].HCC typically arises within a cirrhotic liver, but about 20% of cases occurs within a non-cirrhotic liver [2].Main risk factors for HCC are represented by the presence of viral hepatitis due to hepatitis B virus (HBV) or hepatitis C virus (HCV) infection [3,4]
The cornerstone of non-alcoholic fatty liver disease (NAFLD) treatment is the control of insulin resistance in conjunction with weight loss and lifestyle modification: reduction of caloric intake, high fiber and low red meat diet, animal fats and refined sugars intake; and an active lifestyle with daily physical activity [23]. Drawing from these considerations, this review aims to describe the main molecular mechanisms underlying the development of NAFLD and its progression to HCC, not necessarily through the classical progression from fibrosis to cirrhosis to HCC
Cells 2021, 10, x Cells 2021, 10, 2034 caloric intake, high fiber and low red meat diet, animal fats and refined sugars intake; and an active lifestyle with daily physical activity [23]
Summary
Hepatocellular carcinoma (HCC) is the seventh most common cancer worldwide and the second leading cause of cancer-related mortality, with substantial differences across geographical areas due to the different prevalence of risk factors [1]. The cornerstone of NAFLD treatment is the control of insulin resistance in conjunction with weight loss and lifestyle modification: reduction of caloric intake, high fiber and low red meat diet, animal fats and refined sugars intake; and an active lifestyle with daily physical activity [23] Drawing from these considerations, this review aims to describe the main molecular mechanisms underlying the development of NAFLD and its progression to HCC, not necessarily through the classical progression from fibrosis to cirrhosis to HCC. Cells 2021, 10, x Cells 2021, 10, 2034 caloric intake, high fiber and low red meat diet, animal fats and refined sugars intake; and an active lifestyle with daily physical activity [23]
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