ArticleScientific reports2022
Targeted-sequence of normal urothelium and tumor of patients with non-muscle invasive bladder cancer.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Role of Spatial Heterogeneity in Muscle-Invasive Bladder Cancer on Overall Survival and Immunotherapy Response.Cancers · 2026Article
- Field cancerization in urothelial carcinoma: molecular alterations and clinical implications.Journal of Cancer · 2026Review
- Article
- Comparison of genetic mutations in bladder cancers that arose following radiotherapy for prostate cancer with those in primary bladder cancers.Scientific reports · 2025Article
- Article
- From Detection to Cure - Emerging Roles for Urinary Tumor DNA (utDNA) in Bladder Cancer.Current oncology reports · 2024Review
- Mutation Hotspots Found in Bladder Cancer Aid Prediction of Carcinogenic Risk in Normal Urothelium.International journal of molecular sciences · 2023Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During tumorigenesis, certain tissues are colonized by mutant clones with oncogenic driver mutations as precancer lesions. These mutations can facilitate clonal expansion and may contribute to malignant transformation. The molecular features of low-grade non-muscle invasive bladder cancer (NMIBC) and high-grade bladder cancer are so distinct that they are thought to follow different evolutionary tumorigenesis pathways. Although NMIBC accounts for most bladder tumors, the somatic mutation patterns in "precancer" urothelium of patients with NMIBC remain unclear. Here, we analyzed specimens of normal urothelium and bladder tumors from patients with low-grade and high-grade NMIBC and investigated the genomic evolution of the cancer. Somatic mutations were analyzed using 50 oncogene-targeted sequences and droplet digital polymerase chain reaction for TERT promoter mutations. Somatic mutations in TERT promoter, FGFR3, and CDKN2A were characteristically identified in the normal urothelium of patients with NMIBC. These mutations, consistently identified in both tumor and normal specimens, likely affect clonal expansion during the malignant transformation of NMIBC. Though larger samples and comprehensive study are warranted to confirm our results, the difference in mutational landscape of the precancerous urothelium of patients with bladder cancer could offer deeper understandings of genomic evolution in bladder tumorigenesis.
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