fig1

Glucose metabolic dysregulation and oxidative stress in cholangiocarcinoma: molecular mechanisms, oncogenic drivers, and novel therapeutic targets

Figure 1. Classification of CCA based on its anatomical site of origin. iCCA originates in the periphery of the second-order bile ducts, pCCA arises in the right and/or left hepatic ducts and their junction, and dCCA involves the common bile duct (choledochus). CCA presents with three growth patterns: mass-forming, periductal-infiltrating, and intraductal-growing. Mass-forming CCA appears as a hepatic mass lesion, periductal-infiltrating iCCA grows along the duct wall, and intraductal-growing CCA forms a polypoid or papillary tumor extending into the duct lumen. Common oncogenic mutations contributing to CCA include: KRAS, TP53, IDH, ARID1A, FGFR2, HER2. These mutations drive tumorigenesis by altering key cellular pathways. Created in BioRender. Chanda M. (2025) https://BioRender.com/s4pk8iv. CCA: Cholangiocarcinoma; iCCA: intrahepatic cholangiocarcinoma; pCCA: perihilar cholangiocarcinoma; dCCA: distal cholangiocarcinoma; KRAS: Kirsten rat sarcoma viral oncogene homolog; TP53: tumor protein p53; IDH: isocitrate dehydrogenase; ARID1A: AT-rich interaction domain 1A; FGFR2: fibroblast growth factor receptor 2; HER2: human epidermal growth factor receptor 2.

Hepatoma Research
ISSN 2454-2520 (Online) 2394-5079 (Print)

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