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To understand the molecular mechanisms underlying dysregulation of SAA metabolism during liver cancer development, we first investigated the relationship between the expression levels of five well-established hepatic HNF4 target genes, five general mesenchymal markers, and eight SAA metabolic enzymes in the TCGA LIHC dataset of 373 HCC patients
This information is key for identifying pathway-biased agonists that avoid beta-arrestin-mediated side effects (e.g., tolerance), thereby supporting lead optimization and selection of safer, more efficacious candidates before preclinical studies
K., Johansen, V