Remarkable response to capmatinib in a patient with intrahepatic cholangiocarcinoma harboring TFG - MET fusion.
Akira UetaAtsushi YamadaMasahiro YoshiokaMasashi KanaiManabu MutoNatsuko OkitaPublished in: International cancer conference journal (2024)
Dysregulation of mesenchymal-epithelial transition factor ( MET ) gene due to amplification, mutation, and fusion has been reported in various types of human cancers. Recently, the efficacy of small-molecule tyrosine kinase inhibitors (TKIs) targeting MET has been demonstrated in a wide range of MET -dysregulated tumors. The majority of biliary tract cancers including intrahepatic cholangiocarcinoma (iCCA) are diagnosed at an advanced stage, and the utility of conventional chemotherapy is limited. Here, we present a case of metastatic iCCA harboring TFG-MET gene fusion, which demonstrated a remarkable response to treatment with capmatinib, a selective MET inhibitor. The patient was a 46-year-old man diagnosed with iCCA with hepatic, intraabdominal lymph nodes, and peritoneal metastases. Comprehensive genomic profiling (CGP) revealed TFG-MET gene fusion in his tumor. After becoming refractory to standard chemotherapy, he received capmatinib, which resulted in a marked shrinkage of the liver masses and lymph node metastases, as well as a drastic decrease in serum CA19-9 level. Our case reinforces the importance of CGP in exploring targeted therapy and supports the potential role of capmatinib in the treatment of tumors harboring MET fusions.
Keyphrases
- lymph node
- tyrosine kinase
- small molecule
- copy number
- genome wide
- small cell lung cancer
- stem cells
- case report
- magnetic resonance imaging
- risk assessment
- dna methylation
- early stage
- magnetic resonance
- climate change
- drug delivery
- young adults
- sentinel lymph node
- cancer therapy
- chronic myeloid leukemia
- induced pluripotent stem cells