Endocrine Abstracts

Metabolic-associated fatty liver disease (MAFLD) is a growing cause of hepatocellular carcinoma (HCC), but the molecular mechanisms associated with the pathological progression from MAFLD to HCC are still to be fully elucidated. The genomic and transcriptomic profile of HCC samples have been widely described; however, the proteomic landscape of MAFLD-derived HCC samples is mostly unknown. Here, we sought to perform the first quantitative proteomic analysis of HCC samples from ...

Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing cause of hepatocellular carcinoma (HCCs); however, the molecular characteristics of MAFLD-derived HCCs are still to be elucidated. To provide novel insights in this field, we performed the first quantitative proteomic analysis of HCC samples from different aetiologies. Particularly, cytosolic and nuclear proteome of liver tissues from HCC patients (n=42; HCC vs adjacent tissue) and healthy contr...

Hormonal signalling plays a key role in the progression of metabolic (dysfunction)-associated fatty liver disease (MAFLD) to hepatocellular carcinoma (HCC). However, the role of somatostatin (SST), cortistatin (CORT), neuronostatin (NST) and ghrelin systems in MAFLD-HCC progression has not yet been elucidated. We characterized the role of SST/CORT/NST and ghrelin systems in chronic liver disease and evaluated their clinical potential. The expression of the components of the SS...

Background: Hormonal signalling plays a key role in the progression of non-alcoholic fatty liver disease (NAFLD) to hepatocellular carcinoma (HCC). However, the role of somatostatin (SST), cortistatin (CORT), neuronostatin (NST) and ghrelin systems in NAFLD-HCC progression has not been elucidated.Objectives: To characterize the role of SST/CORT/NST and ghrelin systems in chronic liver disease and evaluate its clinical potential.Met...

Development and progression of liver diseases, from non-alcoholic fatty liver disease (NAFLD) to steatohepatitis (NASH), and hepatocellular carcinoma (HCC), seem to be accompanied by a dysregulation of the expression of alternative splicing variants (SVs) and appearance of aberrant SVs. The splicing factor 3B subunit 1 (SF3B1) represents a crucial player for the functional assembly of the spliceosome, the core machinery that controls the splicing process, and its activity can ...