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Comprehensive genomic profiling of tumor tissue and cfDNA of patients enrolled in the phase 2 study of infigratinib underscored the heterogeneity of CCA and the potential clinical utility of cfDNA to identify FGFR2 fusions.

Meta-analysis identifies upregulation of several novel genes that have not been previously described, and suggests the potential role of ERBB2 and extracellular genes in the pathogenesis of CCA.

The multidrug combination of toripalimab, lenvatinib plus chemotherapy with gemcitabine and oxaliplatin showed promising efficacy and tolerability in patients with intrahepatic CCA.

Comprehensive genomic profiling data indicate that genetic profile of primary intrahepatic CCA was significantly different from metastatic intrahepatic CCA, with different rates of potentially targetable genetic alterations.

Retrospective chart review data indicate that intrahepatic CCA and extrahepatic CCA exhibit disparate clinical features and molecular profile, and divergent treatment patterns.

Real-world data indicate that genetic testing and personalized medicine is rarely applied in the community setting for patients with hepatobiliary and pancreatic cancers.

Emerging data suggest that patient-derived 3-dimensional organoid model of intrahepatic CCA may allow personalized drug screening for active single agents or drug combinations similar to patient-derived xenograft models.

Patient-derived tumor organoids may have clinical application to predict drug responses in a personalized treatment setting; they have shown concordance with actionable genomic anchors and retrospective treatment outcomes.

Preclinical evidence presented at the AACR meeting implicates PKN2 signaling in resistance mechanisms in patients with FGFR2 fusion–positive intrahepatic CCA.

Preclinical data indicate that genetic analysis of ctDNA from patients with advanced CCA harboring IDH mutations was concordant with those of tissue samples and could detect emerging mutations associated with treatment resistance.