ArticleInternational journal of clinical oncology2026
Prevalence and complementary distribution of FGFR3 alterations and ERBB2 amplification in metastatic urothelial carcinoma: a nationwide registry analysis.
Article in International journal of clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundFibroblast growth factor receptor 3 (FGFR3) alterations and ERBB2 (HER2) amplification are clinically actionable genomic events in metastatic urothelial carcinoma (mUC). However, their prevalence and overlap in metastatic-specific cohorts remain incompletely defined. We evaluated their nationwide distribution and co-occurrence using the Japanese C-CAT registry.
methodsThis retrospective study included patients with histologically confirmed mUC who underwent comprehensive genomic profiling with tissue-based FoundationOne assays between January 2019 and June 2025. FGFR3 positivity was defined as pathogenic mutations or fusions meeting companion diagnostic criteria, and HER2 positivity as ERBB2 amplification. Associations with clinicopathological variables were assessed using logistic regression. Co-occurrence was analyzed with Fisher's exact test.
resultsAmong 1014 patients, FGFR3 alterations were identified in 157 (15.5%) and HER2 amplification in 150 (14.8%). Concurrent alterations occurred in 13 patients (1.3%). Under statistical independence, the expected co-occurrence rate was 2.3%; the observed frequency was significantly lower (P = 0.010; crude OR 0.47). In multivariable analysis, female sex (OR 0.58, 95% CI 0.36-0.93; P = 0.024) and upper tract origin (OR 0.57, 95% CI 0.39-0.84; P = 0.005) were independently associated with lower odds of HER2 amplification. HER2 amplification was independently associated with reduced odds of FGFR3 alterations (adjusted OR 0.49, 95% CI 0.27-0.88; P = 0.018).
conclusionsIn this nationwide metastatic cohort, FGFR3 alterations and ERBB2 amplification were each detected in approximately 15% of cases and showed a significant but partial negative association. These findings clarify the molecular epidemiology of mUC and support comprehensive genomic profiling to guide biomarker-driven therapy.
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