2020 Year in Review - Cholangiocarcinoma

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.
First results of the multicohort phase 2 LEAP-005 study suggest that lenvatinib plus pembrolizumab combination immunotherapy has promising antitumor activity in patients with biliary tract cancer.
Preclinical evidence using an genetically engineered mouse model of IDH1-mutated intrahepatic CCA indicates that the selective IDH1 inhibitor ivosidenib mediates its antitumor activity by promoting hepatic progenitor-cell differentiation, and inducing T-cell–mediated antitumor immune response.
Data reported at the ASCO 2020 GI Cancers Symposium indicate that treatment with neoadjuvant definitive chemoradiation followed by orthotopic liver transplantation was associated with better outcomes compared with definitive chemoradiation alone in patients with unresectable extrahepatic/hilar CCA.
Molecular analyses of biliary tract cancers indicate that neurotrophic tyrosine receptor kinase (NTRK) gene fusions are rare, suggesting that it is not a major driver of BTC pathogenesis.
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