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Hepatic tumorigenesis, also known as hepatocarcinogenesis, is the complex, multi-step biological process involving the transformation of healthy hepatocytes into malignant tumor cells (PubMed, PMID: 31215234). It is characterized by the sequential accumulation of genetic and epigenetic alterations that disrupt normal cellular homeostasis, leading to the development of liver cancer, most commonly hepatocellular carcinoma (HCC) (NIH, Cancer.gov). This process is typically driven by chronic liver injury and inflammation resulting from viral hepatitis, alcohol abuse, or metabolic disorders, which create a pro-tumorigenic microenvironment (Nature Reviews Disease Primers, 2021). Key pathways involved include Wnt/beta-catenin, PI3K/Akt/mTOR, and various growth factor signaling cascades that promote survival and angiogenesis (PubMed, PMID: 28416041). Because it is a physiological process rather than a discrete molecular entity, it is not considered a single therapeutic target. Instead, pharmacological interventions focus on inhibiting specific receptors and enzymes, such as multikinase inhibitors like sorafenib, to arrest the progression of the disease (StatPearls, 2023).
Not applicable as a single target; therapeutic agents inhibit specific downstream molecular drivers such as VEGFR, PDGFR, and Raf kinases to disrupt the tumorigenic process.
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