FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies

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 tumor...

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Main Authors: Maxim Noeraparast, Katarina Krajina, Renate Pichler, Dora Niedersüß‐Beke, Shahrokh F Shariat, Viktor Grünwald, Sascha Ahyai, Martin Pichler
Format: Article
Language:English
Published: Wiley 2024-10-01
Series:Cancer Communications
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Online Access:https://doi.org/10.1002/cac2.12602
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author Maxim Noeraparast
Katarina Krajina
Renate Pichler
Dora Niedersüß‐Beke
Shahrokh F Shariat
Viktor Grünwald
Sascha Ahyai
Martin Pichler
author_facet Maxim Noeraparast
Katarina Krajina
Renate Pichler
Dora Niedersüß‐Beke
Shahrokh F Shariat
Viktor Grünwald
Sascha Ahyai
Martin Pichler
author_sort Maxim Noeraparast
collection DOAJ
description 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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spelling doaj-art-9e3eb5c1f9b94eb79fa47e4b178e90be2025-08-20T01:47:48ZengWileyCancer Communications2523-35482024-10-0144101189120810.1002/cac2.12602FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapiesMaxim Noeraparast0Katarina Krajina1Renate Pichler2Dora Niedersüß‐Beke3Shahrokh F Shariat4Viktor Grünwald5Sascha Ahyai6Martin Pichler7Translational Oncology II. Med Clinics Hematology and Oncology Augsburg GermanyTranslational Oncology II. Med Clinics Hematology and Oncology Augsburg GermanyDepartment of Urology Medical University of Innsbruck Innsbruck AustriaDepartment of Hematology and Oncology Clinics Ottakring Vienna AustriaDepartment of Urology Medical University of Vienna Vienna AustriaInterdisciplinary Genitourinary Oncology Clinic for Urology, Clinic for Medical Oncology University Hospital Essen, Hufelandstraße 55 Essen GermanyDepartment of Urology Medical University of Graz Graz AustriaTranslational Oncology II. Med Clinics Hematology and Oncology Augsburg GermanyAbstract 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.https://doi.org/10.1002/cac2.12602Bladder CancerErdafitinibFGFR inhibitionFGFR3 mutationsResistance to ErdafitinibTumor Microenvironment
spellingShingle Maxim Noeraparast
Katarina Krajina
Renate Pichler
Dora Niedersüß‐Beke
Shahrokh F Shariat
Viktor Grünwald
Sascha Ahyai
Martin Pichler
FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies
Cancer Communications
Bladder Cancer
Erdafitinib
FGFR inhibition
FGFR3 mutations
Resistance to Erdafitinib
Tumor Microenvironment
title FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies
title_full FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies
title_fullStr FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies
title_full_unstemmed FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies
title_short FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies
title_sort fgfr3 alterations in bladder cancer sensitivity and resistance to targeted therapies
topic Bladder Cancer
Erdafitinib
FGFR inhibition
FGFR3 mutations
Resistance to Erdafitinib
Tumor Microenvironment
url https://doi.org/10.1002/cac2.12602
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