The Metabolic Dysfunction–Associated Steatotic Liver Disease and Hepatocellular Carcinoma Continuum: Fibrosis, Inflammation, and Clinical Decision-Making, Part 2

Metabolic dysfunction–associated steatotic liver disease (MASLD) is a leading driver of fibrosis progression and hepatocellular carcinoma (HCC), with implications that extend beyond the liver. This joint session traces the clinical continuum from MASLD/metabolic dysfunction–associated steatohepatitis (MASH) to liver cancer, highlighting how metabolic inflammation, fibrosis, and comorbidity shape cancer risk, prevention, and treatment. The first part of the session focuses on MASLD/MASH as a systemic, pro-oncogenic condition. Topics include: (1) epidemiologic links between MASLD and hepatic and extrahepatic malignancies; (2) inflammation as a clinical framework connecting metabolic dysfunction, fibrosis progression, and cancer risk; (3) fibrosis as the key inflection point for risk stratification using noninvasive tools; and (4) the impact of contemporary MASH therapies on inflammation, fibrosis dynamics, and long-term oncologic outcomes. The second part of the session follows the MASLD/MASH fibrosis to cancer continuum across liver cancer. Topics include: (1) mechanistic insights into how fibroinflammatory signaling and stromal remodeling enable tumor initiation and immune evasion; (2) risk-stratified HCC surveillance that moves beyond cirrhosis only paradigms, integrating fibrosis assessment with practical pathways when ultrasound visualization is inadequate; (3) cancer prevention and interception strategies in advanced fibrosis, including chemopreventive signals and pragmatic trial designs; and (4) immuno-oncology–era treatment of MASLD/MASH–associated HCC, emphasizing how fibrosis burden and metabolic comorbidity influence selection and sequencing of systemic and locoregional therapies.