BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the fastest-growing etiology of hepatocellular carcinoma (HCC). Understanding the metabolic heterogeneity of MASLD-driven tumors is crucial to inform strategies for future treatment options. METHODS: Paired tumor (n=8) and adjacent non-tumor tissue (n=8) were collected from patients with steatohepatitic HCC at the University of Kentucky Markey Cancer Center. Hematoxylin and eosin (H 186 gene-lipid) across tumor and nontumor tissue. CONCLUSIONS: Taken together, this integrative analysis reveals novel relationships between steady-state gene transcripts and specific metabolites in steatohepatitic tumors, thereby identifying new pharmacological targets that may be exploited for therapeutic benefit.
Anspach et al. (Mon,) studied this question.
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