Abstract
Hepatocellular adenomas (HCAs) are benign tumors developed in normal liver most frequently in women before menopause. HCAs lead to diagnostic pitfalls and several difficulties to assess the risk of malignant transformation in these young patients. Recent advances in basic knowledge have revealed a molecular classification related to risk factors, pathological features, and risk of transformation in hepatocellular carcinoma. Three major molecular pathways have been identified altered in specific HCA subgroups that are defined by either (1) inactivation of hepatocyte nuclear factor 1A (HNF1A) transcription factor, (2) activation of the WNT/β-catenin by CTNNB1 mutations, or (3) activation of the IL6/STAT3 pathway by somatic mutation of IL6ST, GNAS, or STAT3. Here, we will review the different molecular classes of HCA.
Highlights
Hepatocellular tumors deriving from monoclonal proliferation of hepatocytes are classically divided in benign hepatocellular adenoma (HCA) and malignant hepatocellular carcinoma (HCC)
A long path has been walked in the area of hepatocellular benign tumors since Edmonson described the association between HCA and oral contraception [4]
The discovery of genetic drivers of HCA has re ned our knowledge of the life history of HCA from risk factors and clinical features to the risk of malignant transformation
Summary
Hepatocellular tumors deriving from monoclonal proliferation of hepatocytes are classically divided in benign hepatocellular adenoma (HCA) and malignant hepatocellular carcinoma (HCC). HCAs are rare tumors most frequentlydeveloped in women before menoaupose and a er a longterm use of oral contraception [1]. Other risk factors such as glycogen storage diseases and androgen intake are classically associated with HCA development. Is new classi cation linked speci c risk factor, clinical history, and histological features to each molecular subgroup of HCA [6,7,8,9]. In this paper we aimed to describe how genomic analyses enabled us to identify the different HCA molecular subgroups and their speci c molecular defects
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
