ArticleJournal of clinical oncology : official journal of the American Society of Clinical Oncology2013
Prevalence and co-occurrence of actionable genomic alterations in high-grade bladder cancer.
Article in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03745911 (Phase II Study of Paclitaxel and TAK-228 in Metastatic Urothelial Carcinoma), which is not on this map. Cited by 159 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Phase II Study of Paclitaxel and TAK-228 in Metastatic Urothelial Carcinoma (UC) and the Impact of PI3K-mTOR Pathway Genomic Alterations
Who cites it
159 citing papers in PubMed, 1 synthesis or guideline pooled it, 304 citations in OpenAlex.
- Update for the practicing pathologist: The International Consultation On Urologic Disease-European association of urology consultation on bladder cancer.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015Guideline
- Phase II trial of afatinib in patients with advanced urothelial carcinoma with genetic alterations in ERBB1-3 (LUX-Bladder 1).British journal of cancer · 2024Trial
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- Safety and efficacy of temsirolimus as second line treatment for patients with recurrent bladder cancer.BMC cancer · 2018Trial
- Afatinib Activity in Platinum-Refractory Metastatic Urothelial Carcinoma in Patients With ERBB Alterations.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2016Trial
- Trial
- Trial
- Expression of ribosomal S6 kinase 4 in bladder cancer and its correlation with clinicopathological features.Frontiers in oncology · 2026Article
- Determinants of sensitivity to HER2-targeted antibody drug conjugates in urothelial cancer.Nature communications · 2025Article
- Genomic Characteristics of Bladder Cancer: An AACR Project GENIE Study.International journal of molecular sciences · 2025Article
- Toxicity Profile of New Therapies in Metastatic Urothelial Carcinoma and Its Impact on Treatment Selection.Cancers · 2025Review
- KDM6A expression loss is frequent in low grade non-invasive urothelial carcinomas of the urinary bladder.Pathologica · 2025Article
- Mechanism of action and future perspectives of ADCs in combination with immune checkpoint inhibitors for solid tumors.Clinical and experimental medicine · 2025Review
- Redefining bladder cancer treatment: innovations in overcoming drug resistance and immune evasion.Frontiers in immunology · 2025Review
- Clinicopathological significance of c-MET and HER2 altered expression in bladder cancer.Journal of the Egyptian National Cancer Institute · 2024Article
- Genetic Alterations in Chromatin Regulatory Genes in Upper Tract Urothelial Carcinoma and Urothelial Bladder Cancer.Cancer medicine · 2024Article
- Prolonged Response to Osimertinib in EGFR-Mutated Metastatic Urothelial Carcinoma, a Case Report.Current oncology (Toronto, Ont.) · 2024Article
- Advancements in First-Line Treatment of Metastatic Bladder Cancer: EV-302 and Checkmate-901 Insights and Future Directions.Cancers · 2024Review
- Article
99 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeWe sought to define the prevalence and co-occurrence of actionable genomic alterations in patients with high-grade bladder cancer to serve as a platform for therapeutic drug discovery. PATIENTS AND
methodsAn integrative analysis of 97 high-grade bladder tumors was conducted to identify actionable drug targets, which are defined as genomic alterations that have been clinically validated in another cancer type (eg, BRAF mutation) or alterations for which a selective inhibitor of the target or pathway is under clinical investigation. DNA copy number alterations (CNAs) were defined by using array comparative genomic hybridization. Mutation profiling was performed by using both mass spectroscopy-based genotyping and Sanger sequencing.
resultsSixty-one percent of tumors harbored potentially actionable genomic alterations. A core pathway analysis of the integrated data set revealed a nonoverlapping pattern of mutations in the RTK-RAS-RAF and phosphoinositide 3-kinase/AKT/mammalian target of rapamycin pathways and regulators of G1-S cell cycle progression. Unsupervised clustering of CNAs defined two distinct classes of bladder tumors that differed in the degree of their CNA burden. Integration of mutation and copy number analyses revealed that mutations in TP53 and RB1 were significantly more common in tumors with a high CNA burden (P < .001 and P < .003, respectively).
conclusionHigh-grade bladder cancer possesses substantial genomic heterogeneity. The majority of tumors harbor potentially tractable genomic alterations that may predict for response to target-selective agents. Given the genomic diversity of bladder cancers, optimal development of target-specific agents will require pretreatment genomic characterization.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.