ArticleAnnals of oncology : official journal of the European Society for Medical Oncology2016
Tumor heterogeneity of fibroblast growth factor receptor 3 (FGFR3) mutations in invasive bladder cancer: implications for perioperative anti-FGFR3 treatment.
Article in Annals of oncology : official journal of the European Society for Medical Oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 60 citations in OpenAlex.
- Prospective multicenter study of ctDNA versus tumor tissue guiding FGFR-targeted therapy in metastatic urothelial cancer.Nature communications · 2026Article
- A Novel FGFR3-Targeting Antibody-Drug Conjugate Induces Tumor Cell Apoptosis through the cGAS-STING Pathway in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- The role of focal adhesion kinase in bladder cancer: translation fromRadiology and oncology · 2025Article
- Are primary tumors suitable for biomarker-guided treatment of metastatic urothelial cancer?Translational andrology and urology · 2024Article
- The roles of FGFR3 and c-MYC in urothelial bladder cancer.Discover oncology · 2024Review
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- Profiling the Biological Characteristics and Transitions through Upper Tract Tumor Origin, Bladder Recurrence, and Muscle-Invasive Bladder Progression in Upper Tract Urothelial Carcinoma.International journal of molecular sciences · 2022Article
- New Directions and Challenges in Targeted Therapies of Advanced Bladder Cancer: The Role of FGFR Inhibitors.Cancers · 2022Review
- Non-muscle invasive bladder cancer biomarkers beyond morphology.Frontiers in oncology · 2022Review
- A hypoxia related long non-coding RNA signature could accurately predict survival outcomes in patients with bladder cancer.Bioengineered · 2021Article
- Review
- Therapeutic and prognostic implications of NOTCH and MAPK signaling in bladder cancer.Cancer science · 2021Article
- Plasma ctDNA is a tumor tissue surrogate and enables clinical-genomic stratification of metastatic bladder cancer.Nature communications · 2021Article
- Development and Validation of a Hypoxia-Related Signature for Predicting Survival Outcomes in Patients With Bladder Cancer.Frontiers in genetics · 2021Article
- Genomic heterogeneity in bladder cancer: challenges and possible solutions to improve outcomes.Nature reviews. Urology · 2020Review
- Genomic Subtyping in Bladder Cancer.Current urology reports · 2020Review
- Genomic characterization for familial cases with urothelial carcinoma.International cancer conference journal · 2019Article
- Circular RNA hsa_circ_0068871 regulates FGFR3 expression and activates STAT3 by targeting miR-181a-5p to promote bladder cancer progression.Journal of experimental & clinical cancer research : CR · 2019Article
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Authors and funding
39 authors at 13 institutions in 8 countries.
Funding
Abstract
backgroundFibroblast growth factor receptor 3 (FGFR3) is an actionable target in bladder cancer. Preclinical studies show that anti-FGFR3 treatment slows down tumor growth, suggesting that this tyrosine kinase receptor is a candidate for personalized bladder cancer treatment, particularly in patients with mutated FGFR3. We addressed tumor heterogeneity in a large multicenter, multi-laboratory study, as this may have significant impact on therapeutic response. PATIENTS AND
methodsWe evaluated possible FGFR3 heterogeneity by the PCR-SNaPshot method in the superficial and deep compartments of tumors obtained by transurethral resection (TUR, n = 61) and in radical cystectomy (RC, n = 614) specimens and corresponding cancer-positive lymph nodes (LN+, n = 201).
resultsWe found FGFR3 mutations in 13/34 (38%) T1 and 8/27 (30%) ≥T2-TUR samples, with 100% concordance between superficial and deeper parts in T1-TUR samples. Of eight FGFR3 mutant ≥T2-TUR samples, only 4 (50%) displayed the mutation in the deeper part. We found 67/614 (11%) FGFR3 mutations in RC specimens. FGFR3 mutation was associated with pN0 (P < 0.001) at RC. In 10/201 (5%) LN+, an FGFR3 mutation was found, all concordant with the corresponding RC specimen. In the remaining 191 cases, RC and LN+ were both wild type.
conclusionsFGFR3 mutation status seems promising to guide decision-making on adjuvant anti-FGFR3 therapy as it appeared homogeneous in RC and LN+. Based on the results of TUR, the deep part of the tumor needs to be assessed if neoadjuvant anti-FGFR3 treatment is considered. We conclude that studies on the heterogeneity of actionable molecular targets should precede clinical trials with these drugs in the perioperative setting.
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