ArticleNature communications2024
The molecular interaction pattern of lenvatinib enables inhibition of wild-type or kinase-mutated FGFR2-driven cholangiocarcinoma.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Sequencing of Fibroblast Growth Factor Receptor Inhibitors in Cholangiocarcinoma: A Review of Published Cases.JCO precision oncology · 2026Review
- Selective Inhibition of VEGFR2 in Preference to Other Receptor Tyrosine Kinases by Diosgenin, a Natural Steroidal Sapogenin.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- [Clinician and medical scientists in internal medicine: gastroenterology].Innere Medizin (Heidelberg, Germany) · 2026Review
- Personalized signaling pathway analysis of gastrointestinal tumors for patient stratification and drug target evaluation using clinically derived core biopsies.NPJ precision oncology · 2026Article
- Amino acid metabolic reprogramming: future prospects for cholangiocarcinoma therapy.Cell death discovery · 2026Review
- Lenvatinib after progression on pemigatinib and futibatinib in FGFR2 fusion-positive biliary tract cancer with an acquired kinase point mutation.The oncologist · 2025Article
- Efficacy and safety of transarterial chemoembolization with chemotherapy, PD-1/PD-L1 inhibitors, and tyrosine kinase inhibitors in unresectable intrahepatic cholangiocarcinoma.World journal of gastrointestinal oncology · 2025Article
- Functional Characterization of Variants of Unknown Significance of Fibroblast Growth Factor Receptors 1-4 and Comparison With AI Model-Based Prediction.JCO precision oncology · 2025Article
- Lenvatinib-activated NDUFA4L2/IL33/PADI4 pathway induces neutrophil extracellular traps that inhibit cuproptosis in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism.Cell death discovery · 2025Article
- Effect of Electric Fields on the Mechanical Mechanism of Regorafenib-VEGFR2 Interaction to Enhance Inhibition of Hepatocellular Carcinoma.Biomolecules · 2025Article
- Case Report: FGFR2 inhibitor resistance viaFrontiers in oncology · 2025Article
- Targeting FGFR for cancer therapy.Journal of hematology & oncology · 2024Review
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
Abstract
Fibroblast growth factor receptor (FGFR)-2 can be inhibited by FGFR-selective or non-selective tyrosine kinase inhibitors (TKIs). Selective TKIs are approved for cholangiocarcinoma (CCA) with FGFR2 fusions; however, their application is limited by a characteristic pattern of adverse events or evocation of kinase domain mutations. A comprehensive characterization of a patient cohort treated with the non-selective TKI lenvatinib reveals promising efficacy in FGFR2-driven CCA. In a bed-to-bench approach, we investigate FGFR2 fusion proteins bearing critical tumor-relevant point mutations. These mutations confer growth advantage of tumor cells and increased resistance to selective TKIs but remain intriguingly sensitive to lenvatinib. In line with clinical observations, in-silico analyses reveal a more favorable interaction pattern of lenvatinib with FGFR2, including an increased flexibility and ligand efficacy, compared to FGFR-selective TKIs. Finally, the treatment of a patient with progressive disease and a newly developed kinase mutation during therapy with a selective inhibitor results in a striking response to lenvatinib. Our in vitro, in silico, and clinical data suggest that lenvatinib is a promising treatment option for FGFR2-driven CCA, especially when insurmountable adverse reactions of selective TKIs or acquired kinase mutations occur.
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