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Its asymptomatic onset and the lack of reliable early diagnostic tools contribute to delayed detection and poor clinical outcomes. Although epidemiological and genetic studies have identified numerous risk factors, the molecular mechanisms linking these factors to tumor initiation and progression remain incompletely understood. This review integrates current evidence on the multifactorial etiology of GBC\u2014including geographic variation, genetic predisposition, environmental exposures, chronic inflammation, and infections\u2014with emerging insights into metabolic and molecular dysregulation. Particular focus is placed on metabolic reprogramming as a central driver of carcinogenesis. Altered lipid metabolism, bile acid signaling, and redox imbalance interact with inflammatory and oncogenic pathways, fostering a permissive microenvironment for malignant transformation. Key molecular cascades include inflammation-driven NF-\u03baB activation, bile acid\u2013induced oxidative stress, PI3K\/AKT-mediated metabolic remodeling, and DNA damage and repair defects. 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