Characterizing the Mechanism Behind the Progression of NAFLD to Hepatocellular Carcinoma

Abstract

Hepatocellular carcinoma (HCC) developed in non-alcoholic fatty liver disease (NAFLD) individuals presents substantial clinical and biological characteristics, which remain to be elucidated. Its occurrence in noncirrhotic patients raises issues regarding surveillance strategies, which cannot be considered as cost-effective given the high prevalence of obesity and metabolic syndrome, and furthermore delineates specific oncogenic process that could be targeted in the setting of primary or secondary prevention. In this context, the identification of a genetic heterogeneity modulating HCC risk as well as specific biological pathways have been made possible through genome-wide association studies, development of animal models and in-depth analyses of human samples at the pathological and genomic levels. These advances must be confirmed and pursued to pave the way for personalized management of NAFLD-related HCC.

Keywords::

• cirrhosis
• fibrosis
• functional genomics
• genetic association studies
• hepatocellular carcinoma
• inflammation
• mouse models
• steatosis

Author contributions

P Nahon, M Allaire, J-C Nault and V Paradis participated in all stages of manuscript production, design, figures, tables, writing and review of final version.

Financial & competing interests disclosure

P Nahon has received honoraria or grants from Abbvie, Astra-Zeneca, Bayer, Bristol-Myers Squibb, EISAI, Gilead, Ipsen and Roche. He consults for Bristol-Myers Squibb and Roche. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

P Nahon has received honoraria or grants from Abbvie, Astra-Zeneca, Bayer, Bristol-Myers Squibb, EISAI, Gilead, Ipsen and Roche. He consults for Bristol-Myers Squibb and Roche. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.