What question did this study set out to answer?

To clarify the clinical-pathological significance of FGFR2 abnormalities in solid tumors using the C-CAT database.

April 5, 2026

Abstract 3918: FGFR2 might be a promising therapeutic target for some types of carcinomas: Analysis of 1312 tumors with FGFR2 abnormalities.

Key Points

To clarify the clinical-pathological significance of FGFR2 abnormalities in solid tumors using the C-CAT database.
Analyzed 1312 cases with FGFR2 gene abnormalities from a database of 101,231 solid cancer patients.
Assessed tumor type distribution, co-mutations, and responses to FGFR inhibitors.
Evaluated disease control rates (DCR) in patients receiving FGFR-targeted therapy.
FGFR2 alterations included amplification in 515 cases, fusions in 280 cases, and mutations in 568 cases.
The most frequent tumors with FGFR2 abnormalities were in the biliary tract, esophagus/stomach, and breast.
DCR was achieved in 49 of 85 cases treated with FGFR inhibitors, particularly in biliary tract cancer.

Abstract

Abstract Background: 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. Materials Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3918.

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Cite This Study

Nishikubo et al. (Fri,) studied this question.

synapsesocial.com/papers/69d1fdf7a79560c99a0a45f1 https://doi.org/https://doi.org/10.1158/1538-7445.am2026-3918

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