ArticleInternational journal of cancer2020
Molecular changes during progression from nonmuscle invasive to advanced urothelial carcinoma.
Article in International journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Association Between Estrogen Receptors and GATA3 in Bladder Cancer: A Systematic Review and Meta-Analysis of Their Clinicopathological Significance.Frontiers in endocrinology · 2021Pooled it
- Multiomic profiling links L1 retrotransposition to genomic instability and ecDNA in bladder cancer.Nature communications · 2026Article
- Ethnicity-specific molecular subtypes and a machine-learning risk model in Asian patients with non-muscle-invasive bladder cancer.Scientific reports · 2026Article
- An integrated molecular classification system identifies distinct prognostic clusters of non-muscle-invasive bladder cancer.Functional & integrative genomics · 2026Article
- A molecular landscape tracking the progression of non-muscle invasive bladder cancer.World journal of urology · 2026Review
- Multi-omic profiling defines three distinct molecular subtypes of urothelial carcinoma with implications for precision therapy.Clinical and translational medicine · 2026Article
- Field cancerization in urothelial carcinoma: molecular alterations and clinical implications.Journal of Cancer · 2026Review
- Identification of multicohort-based predictive signature for NMIBC recurrence reveals SDCBP as a novel oncogene in bladder cancer.Annals of medicine · 2025Article
- Droplet digital PCR assay for precise determination of FRS2 gene copy number in bladder cancer.BMC cancer · 2025Article
- Bladder cancer subtypes exhibit limited plasticity across different microenvironments and in metastases.Experimental hematology & oncology · 2025Article
- Molecular biomarkers of progression in non-muscle-invasive bladder cancer - beyond conventional risk stratification.Nature reviews. Urology · 2025Review
- Proteomic profiling identifies muscle-invasive bladder cancers with distinct biology and responses to platinum-based chemotherapy.Nature communications · 2025Article
- Clinical significance of tumor location in non-muscle-invasive bladder cancer: A single-center longitudinal cohort analysis.Bladder (San Francisco, Calif.) · 2025Article
- Epigenetic dysregulation-induced metabolic reprogramming fuels tumor progression in bladder cancer.Frontiers in molecular biosciences · 2025Article
- Immunophenotypic and molecular changes during progression of papillary urothelial carcinoma.Investigative and clinical urology · 2024Article
- Article
- Lysine Methyltransferase 9 (KMT9) Is an Actionable Target in Muscle-Invasive Bladder Cancer.Cancers · 2024Article
- The Evolving Role of PD-(L)1 Inhibition in Optimizing Outcomes for High-Risk Non-Muscle-Invasive Bladder Cancer (NMIBC): A Podcast.Advances in therapy · 2024Article
- Unveiling the mechanisms and challenges of cancer drug resistance.Cell communication and signaling : CCS · 2024Review
- Identification of ECM and EMT relevant genes involved in the progression of bladder cancer through bioinformatics analysis.American journal of clinical and experimental urology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Molecular changes occurring during invasion and clinical progression of cancer are difficult to study longitudinally in patient-derived material. A unique feature of urothelial bladder cancer (UBC) is that patients frequently develop multiple nonmuscle invasive tumors, some of which may eventually progress to invade the muscle of the bladder wall. Here, we use a cohort of 73 patients that experienced a total of 357 UBC diagnoses to study the stability or change in detected molecular alterations during cancer progression. The tumors were subtyped by gene expression profiling and analyzed for hotspot mutations in FGFR3, PIK3CA and TERT, the most frequent early driver mutations in this tumor type. TP53 alterations, frequent in advanced UBC, were inferred from p53 staining pattern, and potential genomic alterations were inferred by gene expression patterns at regions harboring frequent copy number alterations. We show that early driver mutations were largely preserved in UBC recurrences. Changes in FGFR3, PIK3CA or TERT mutation status were not linked to changes in molecular subtype and aggressive behavior. Instead, changes into a more aggressive molecular subtype seem to be associated with p53 alterations. We analyze changes in gene expression from primary tumors, to recurrences and progression tumors, and identify two modes of progression: Patients for whom progression is preceded by or coincides with a radical subtype shift, and patients who progress without any systematic molecular changes. For the latter group of patients, progression may be either stochastic or depending on factors already present at primary tumor initiation.
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