Response to Capmatinib in a MET Fusion-positive Cholangiocarcinoma

Anthony Turpin; Clotilde Descarpentries; Valérie Grégoire; Olivier Farchi; Alexis B Cortot; Philippe Jamme

doi:10.1093/oncolo/oyac194

Response to Capmatinib in a MET Fusion-positive Cholangiocarcinoma

Oncologist. 2023 Jan 18;28(1):80-83. doi: 10.1093/oncolo/oyac194.

Authors

Anthony Turpin¹, Clotilde Descarpentries², Valérie Grégoire³, Olivier Farchi², Alexis B Cortot⁴, Philippe Jamme⁵

Affiliations

¹ Medical Oncology Department, CHU Lille, University of Lille, Lille, France.
² Department of Biochemistry and Molecular Biology, Hormonology Metabolism Nutrition Oncology, CHU Lille, University of Lille, Lille, France.
³ Pathology Department, CHU Lille, University of Lille, Lille, France.
⁴ Thoracic Oncology Department, CHU Lille, University of Lille, Lille, France.
⁵ Department of Dermatology, Hopital Claude Huriez, CHU Lille, University of Lille, France.

Abstract

Cholangiocarcinoma is the second most common liver cancer after hepatocellular carcinoma. In case of metastatic or unresectable disease, the recommended first-line treatment is gemcitabine-based doublet, most commonly gemcitabine and cisplatin. There is no standard treatment for further lines. MET fusions are rare alterations described in many cancers. The efficacy of specific MET inhibitors is poorly studied. We present the case of a patient with chemotherapy-refractory metastatic cholangiocarcinoma harboring a CAPZA-2-MET fusion along with MET amplification who dramatically responded to capmatinib, a specific MET tyrosine kinase inhibitor.

Keywords: MET; cholangiocarcinoma; precision medicine; resistance.

Publication types

Case Reports

MeSH terms

Bile Duct Neoplasms* / drug therapy
Bile Duct Neoplasms* / genetics
Bile Ducts, Intrahepatic
Cholangiocarcinoma* / drug therapy
Cholangiocarcinoma* / genetics
Humans
Liver Neoplasms* / drug therapy
Liver Neoplasms* / genetics

Substances

capmatinib
MET protein, human