Associated Papers
Saturation mutagenesis identifies activating and resistance-inducing FGFR kinase domain mutations.
Tangermann C et al.
Nature Genetics, 2026
41361008 (PubMed )
Supplement: 41588_2025_2431_MOESM5_ESM.xlsx › Figure_1d
Prevalence and biological impact of clinically relevant gene fusions in head and neck cancers.
Hoskins EL et al.
Npj Precision Oncology, 2025
40610725 (PubMed )
Supplement: 41698_2025_889_MOESM5_ESM.xlsx › Sheet1
A Phase I Study of KIN-3248, an Irreversible Small-molecule Pan-FGFR Inhibitor, in Patients with Advanced FGFR2/3-driven Solid Tumors.
Garmezy B et al.
Cancer Research Communications, 2024
38602417 (PubMed )
Supplement: crc-24-0137-s07.pdf
Characterization of the cholangiocarcinoma drug pemigatinib against FGFR gatekeeper mutants.
Lin Q et al.
Communications Chemistry, 2022
Truncated FGFR2 is a clinically actionable oncogene in multiple cancers.
Zingg D et al.
Nature, 2022
35948633 (PubMed )
Supplement: 41586_2022_5066_MOESM16_ESM.xlsx › ED_Fig._2a
Identification of pathogenic missense mutations using protein stability predictors.
Gerasimavicius L et al.
Scientific Reports, 2020
32958805 (PubMed )
Supplement: 41598_2020_72404_MOESM2_ESM.xlsx › ClinVar
The N550K/H mutations in FGFR2 confer differential resistance to PD173074, dovitinib, and ponatinib ATP-competitive inhibitors.
Byron SA et al.
Neoplasia (new York, N.y.), 2013
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