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FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies.
Noeraparast, Maxim; Krajina, Katarina; Pichler, Renate; Niedersüß-Beke, Dora; Shariat, Shahrokh F; Grünwald, Viktor; Ahyai, Sascha; Pichler, Martin.
Afiliación
  • Noeraparast M; Translational Oncology, II. Med Clinics Hematology and Oncology, Augsburg, Germany.
  • Krajina K; Translational Oncology, II. Med Clinics Hematology and Oncology, Augsburg, Germany.
  • Pichler R; Department of Urology, Medical University of Innsbruck, Innsbruck, Austria.
  • Niedersüß-Beke D; Department of Hematology and Oncology, Clinics Ottakring, Vienna, Austria.
  • Shariat SF; Department of Urology, Medical University of Vienna, Vienna, Austria.
  • Grünwald V; Interdisciplinary Genitourinary Oncology, Clinic for Urology, Clinic for Medical Oncology, University Hospital Essen, Hufelandstraße 55, Essen, Germany.
  • Ahyai S; Department of Urology, Medical University of Graz, Graz, Austria.
  • Pichler M; Translational Oncology, II. Med Clinics Hematology and Oncology, Augsburg, Germany.
Cancer Commun (Lond) ; 2024 Aug 19.
Article en En | MEDLINE | ID: mdl-39161208
ABSTRACT
In this review, we revisit the pivotal role of fibroblast growth factor receptor 3 (FGFR3) in bladder cancer (BLCA), underscoring its prevalence in both non-muscle-invasive and muscle-invasive forms of the disease. FGFR3 mutations in up to half of BLCAs play a well-established role in tumorigenesis, shaping distinct tumor initiation patterns and impacting the tumor microenvironment (TME). Emphasizing the importance of considering epithelial-mesenchymal transition profile and TME status, we revisit their relevance in predicting responses to immune checkpoint inhibitors in FGFR3-mutated BLCAs. This writing highlights the initially promising yet transient efficacy of the FGFR inhibitor Erdafitinib on FGFR3-mutated BLCA, stressing the pressing need to unravel resistance mechanisms and identify co-targets for future combinatorial studies. A thorough analysis of recent preclinical and clinical evidence reveals resistance mechanisms, including secondary mutations, epigenetic alterations in pathway effectors, phenotypic heterogeneity, and population-specific variations within FGFR3 mutational status. Lastly, we discuss the potential of combinatorial treatments and concepts like synthetic lethality for discovering more effective targeted therapies against FGFR3-mutated BLCA.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Cancer Commun (Lond) Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Cancer Commun (Lond) Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos