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Updated: Jan 11, 2026

Screening and Identification of Small Peptides Targeting Fibroblast Growth Factor Receptor2 using a Phage Display Peptide Library
Published on: September 30, 2019
FGFR2 Might Be a Promising Therapeutic Target for Some Solid Tumors: Analysis of 1312 Cancers with FGFR2
Hinano Nishikubo1, Dongheng Ma1, Tomoya Sano1
1Molecular Oncology and Therapeutics, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan.
Abstract:
Genetic abnormalities of the fibroblast growth factor receptor 2 (FGFR2) gene, including amplification, fusions, and mutations, have been reported in various solid tumors. While molecular targeted therapies against FGFR2 fusion have been proved to be useful in cholangiocarcinoma, the therapeutic significance of FGFR2 inhibitors remains unclear in other various solid cancers. Genomic and clinical information from solid tumor cancer gene panel testing cases is consolidated in the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database in Japan. This study aimed to utilize the C-CAT database to clarify the clinical-pathological significance of FGFR2 abnormalities. A total of 101,231 patients with solid cancer have been registered in the C-CAT database between June 2019 and June 2025. Of the 101,231 cases, 1312 cases with FGFR2 gene abnormalities were analyzed. FGFR2 alterations included amplification in 515 cases, fusion in 280 cases, and mutations in 568 cases. They were detected most frequently in the biliary tract (271 cases), esophagus/stomach (231 cases), and breast (211 cases). Amplification was frequent in the esophagus/stomach (205 cases) and breast (105 cases). Mutations were frequent in the uterus (111 cases), breast (89 cases), and biliary tract (86 cases). Among 515 FGFR2 alteration cases, FGFR2 inhibitors were administered in 85 cases. Of the 85 cases, disease control was achieved in 49 cases, 44 cases of which were biliary tract cancer. FGFR2 might be a promising therapeutic target not only for cholangiocarcinoma with fusion but also for esophagus/stomach cancer and breast cancer with FGFR2 alterations.
Insights
Fibroblast growth factor receptor 2 (FGFR2) gene abnormalities are found in various cancers. FGFR2 inhibitors show promise beyond cholangiocarcinoma, particularly in esophagus/stomach and breast cancers with FGFR2 alterations.
Area of Science:
- Oncology
- Genetics
- Pharmacology
Background:
- Genetic abnormalities in fibroblast growth factor receptor 2 (FGFR2), including amplification, fusions, and mutations, are implicated in diverse solid tumors.
- While FGFR2 fusions are targeted in cholangiocarcinoma, the efficacy of FGFR2 inhibitors in other solid cancers remains under investigation.
Purpose of the Study:
- To investigate the clinical-pathological significance of FGFR2 gene abnormalities in solid tumors using a large-scale Japanese database.
- To explore the therapeutic potential of FGFR2 inhibitors in cancers beyond cholangiocarcinoma.
Main Methods:
- Analysis of genomic and clinical data from 101,231 solid tumor patients in the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database.
- Identification and characterization of FGFR2 alterations (amplification, fusion, mutation) in 1312 patients.
- Evaluation of treatment outcomes for 85 patients receiving FGFR2 inhibitors.
Main Results:
- FGFR2 abnormalities were identified in 1312 out of 101,231 patients, with alterations including amplification (515), fusion (280), and mutation (568).
- The most frequent sites for FGFR2 alterations were the biliary tract (271), esophagus/stomach (231), and breast (211).
- Disease control was achieved in 49 of 85 patients treated with FGFR2 inhibitors, with 44 cases being biliary tract cancer.
Conclusions:
- FGFR2 alterations are prevalent across various solid tumors, with distinct patterns of amplification and mutation.
- FGFR2 inhibitors demonstrate therapeutic potential in biliary tract cancer and suggest promise for esophagus/stomach and breast cancers harboring FGFR2 alterations.
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