Research & Innovation
Publications
Translating Fibrosis to Malignancy
PMU Authors
Daniel Neureiter, Tobias Kiesslich
All Authors
Daniel Neureiter, Tobias Kiesslich, Matthias Ocker
Journal association
MED SCI-BASEL
Abstract
Background/Objectives: Hepatocellular carcinoma (HCC) commonly arises from chronic liver diseases that show progressing fibrosis and cirrhosis. The molecular mechanisms driving the transition from advanced fibrosis to overt malignancy remain poorly defined, representing a key knowledge gap in current hepatology research. This review delineates shared pathways like TGF beta/SMAD, WNT/beta-catenin, Hedgehog, NOTCH, Hippo/YAP-TAZ and MAPK, linking fibrosis to HCC and opening avenues for dual antifibrotic/antitumor therapies. Results and Conclusions: So far, validated biomarker tools for fibrosis, like FIB-4, Enhanced Liver Fibrosis (ELF) and combined direct/indirect markers of liver damage and tissue remodeling, are used for fibrosis staging, while HCC detection leverages serum parameters like alpha-fetoprotein (AFP) or, more recently, multi-omics approaches (miRNA, cfDNA, metabolomics). Understanding the interconnection of these pathways can lead to novel targeted therapies (e.g., TGF beta inhibitors) that may show dual antifibrotic and antitumor activity in future studies.
Keywords
Humans, Signal Transduction, Carcinoma, Hepatocellular/metabolism, Liver Neoplasms/metabolism, Liver Cirrhosis/metabolism, Biomarkers, Tumor/metabolism, Biomarkers/metabolism