ArticleCancer prevention research (Philadelphia, Pa.)2023
Analysis of Several Common APOBEC-type Mutations in Bladder Tumors Suggests Links to Viral Infection.
Article in Cancer prevention research (Philadelphia, Pa.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Virus-induced APOBEC3 transmutagenesis in bladder cancer initiation.Science advances · 2025Article
- Solvent Exposure, Genetic Susceptibility, and Risk of Bladder Cancer.Cancer prevention research (Philadelphia, Pa.) · 2025Article
- Single-cell analysis reveals host S phase drives large T antigen expression during BK polyomavirus infection.PLoS pathogens · 2024Article
- Massive entry of BK Polyomavirus induces transient cytoplasmic vacuolization of human renal proximal tubule epithelial cells.PLoS pathogens · 2024Article
- Integrating Genetic Alterations and Histopathological Features for Enhanced Risk Stratification in Non-Muscle-Invasive Bladder Cancer.Diagnostics (Basel, Switzerland) · 2024Article
- Unveiling the Role of Human Papillomavirus in Urogenital Carcinogenesis a Comprehensive Review.Viruses · 2024Review
- The Intricate Interplay between APOBEC3 Proteins and DNA Tumour Viruses.Pathogens (Basel, Switzerland) · 2024Review
- Viral infection, APOBEC3 dysregulation, and cancer.Frontiers in genetics · 2024Review
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Authors and funding
21 authors at 9 institutions in 4 countries.
Funding
Abstract
FGFR3 and PIK3CA are among the most frequently mutated genes in bladder tumors. We hypothesized that recurrent mutations in these genes might be caused by common carcinogenic exposures such as smoking and other factors. We analyzed 2,816 bladder tumors with available data on FGFR3 and/or PIK3CA mutations, focusing on the most recurrent mutations detected in ≥10% of tumors. Compared to tumors with other FGFR3/PIK3CA mutations, FGFR3-Y375C was more common in tumors from smokers than never-smokers (P = 0.009), while several APOBEC-type driver mutations were enriched in never-smokers: FGFR3-S249C (P = 0.013) and PIK3CA-E542K/PIK3CA-E545K (P = 0.009). To explore possible causes of these APOBEC-type mutations, we analyzed RNA sequencing (RNA-seq) data from 798 bladder tumors and detected several viruses, with BK polyomavirus (BKPyV) being the most common. We then performed IHC staining for polyomavirus (PyV) Large T-antigen (LTAg) in an independent set of 211 bladder tumors. Overall, by RNA-seq or IHC-LTAg, we detected PyV in 26 out of 1,010 bladder tumors with significantly higher detection (P = 4.4 × 10-5), 25 of 554 (4.5%) in non-muscle-invasive bladder cancers (NMIBC) versus 1 of 456 (0.2%) of muscle-invasive bladder cancers (MIBC). In the NMIBC subset, the FGFR3/PIK3CA APOBEC-type driver mutations were detected in 94.7% (18/19) of PyV-positive versus 68.3% (259/379) of PyV-negative tumors (P = 0.011). BKPyV tumor positivity in the NMIBC subset with FGFR3- or PIK3CA-mutated tumors was also associated with a higher risk of progression to MIBC (P = 0.019). In conclusion, our results support smoking and BKPyV infection as risk factors contributing to bladder tumorigenesis in the general patient population through distinct molecular mechanisms. PREVENTION RELEVANCE: Tobacco smoking likely causes one of the most common mutations in bladder tumors (FGFR3-Y375C), while viral infections might contribute to three others (FGFR3-S249C, PIK3CA-E542K, and PIK3CA-E545K). Understanding the causes of these mutations may lead to new prevention and treatment strategies, such as viral screening and vaccination.
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