MET signaling drives acquired resistance to erdafitinib in muscle-invasive bladder cancer cells.
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ABSTRACT: Muscle-invasive bladder cancer (MIBC) is an aggressive malignancy with high recurrence and poor survival, accounting for the majority of bladder cancer-related deaths. A subset of MIBC harbors FGFR1 amplification or overexpression, associated with increased proliferation and poor prognosis. Although the pan-FGFR inhibitor erdafitinib has demonstrated clinical benefit in patients with FGFR3/FGFR2 alterations, primarily in non-MIBC, its efficacy is limited by resistance and toxicity. Moreover, its effectiveness in FGFR1-driven MIBC remains unclear. To address this gap, we investigated erdafitinib response and resistance mechanisms in JMSU1 cells, a model of FGFR1-amplified MIBC. While erdafitinib initially suppressed tumor growth, prolonged treatment led to resistance, characterized by persi
SUBMITTER: Makabe S
PROVIDER: S-EPMC12663377 | biostudies-literature | 2025 Nov
REPOSITORIES: biostudies-literature
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