Published online Apr 14, 2022. doi: 10.3748/wjg.v28.i14.1384
Peer-review started: December 5, 2021
First decision: January 8, 2022
Revised: January 9, 2022
Accepted: March 6, 2022
Article in press: March 6, 2022
Published online: April 14, 2022
Processing time: 121 Days and 11.7 Hours
Hepatocellular adenoma (HCA) is a benign hepatocellular neoplasm, commonly occurs in young women with a history of oral contraceptive use. Complications including hemorrhage and malignant transformation necessitate the need for a thorough understanding of the underlying molecular signatures in this entity. Recent molecular studies have significantly expanded our knowledge of HCAs. The well-developed phenotype-genotype classification system improves clinical management through identifying “high risk” subtype of HCAs. In this article, we attempt to provide updated information on clinical, pathologic and molecular features of each subtype of HCAs.
Core Tip: Hepatocellular adenoma (HCA) has been well recognized as a benign liver neoplasm with risks of hemorrhage and malignant transformation. Studies revealed that different HCA subtypes with specific genetic mutation and pathologic findings are associated with different clinical features. Currently HCAs are classified into at least 5 major subtypes, involving 4 different pathways driving HCA pathogenesis: Hepatocyte nuclear factor 1A, interleukin-6/the Janus kinase/signal transducer and activator of transcription, β-catenin, and Sonic hedgehog pathway.