Liver cancer, particularly hepatocellular carcinoma (HCC), is a major global health burden and often arises in the setting of chronic liver disease. Research shows that chronic infection with hepatitis B virus (HBV) or hepatitis C virus (HCV), heavy alcohol use, nonalcoholic fatty liver disease, aflatoxin exposure, and metabolic disorders such as obesity and diabetes are key risk factors. These conditions promote long term inflammation, fibrosis, and eventually cirrhosis, creating a microenvironment that favors malignant transformation of hepatocytes.

At the molecular level, studies highlight recurrent alterations in pathways controlling cell proliferation, survival, and genomic stability. Mutations in genes such as TP53 and CTNNB1, activation of Wnt and MAPK signaling, and dysregulation of epigenetic and microRNA networks contribute to tumor initiation and progression. The marked heterogeneity of HCC at the genetic and molecular level complicates prognosis and treatment selection.

Screening and early detection rely mainly on ultrasound imaging, often combined with serum alpha fetoprotein, in high risk patients. However, sensitivity is limited, and research is focusing on improved biomarkers, including panels of proteins, circulating tumor DNA, and other liquid biopsy approaches.

Treatment depends on tumor stage, liver function, and patient performance status. Curative options such as surgical resection, liver transplantation, and local ablative techniques are usually restricted to early stages. For advanced disease, systemic therapies have evolved from multikinase inhibitors to immunotherapies targeting PD 1, PD L1, and CTLA 4, often in combination with antiangiogenic agents. Current research emphasizes optimizing combinations, sequencing therapies, and integrating molecular profiling to move toward more personalized management of liver cancer.