Introduction: Patients with non-muscle-invasive bladder tumor suffer from disease recurrence following transurethral surgery even with intravesical pharmacotherapy, while muscle-invasive disease is often deadly. It is therefore critical to elucidate the underlying molecular mechanisms responsible for not only bladder tumor progression but also its tumorigenesis. Indeed, various molecules and/or signaling pathways have been suggested to contribute to the pathogenesis of bladder cancer.
Areas Covered: We summarize the progress during the last few years on the initiation or development, but not progression, of urothelial cancer. The clinical implications of these available data, including prognostic significance and possible application for the prevention of the recurrence of non-muscle-invasive bladder tumors, are also discussed.
Expert Opinion: Bladder cancer is a heterogeneous group of neoplasms. The establishment of personalized therapeutic options based on the molecular profile in each case should thus be considered. On that account, further accumulation of data on urothelial tumorigenesis is warranted to identify promising targets for the prevention of postoperative tumor recurrence or tumor development in otherwise high-risk patients.
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http://dx.doi.org/10.1080/14737140.2023.2203388 | DOI Listing |
Transl Oncol
February 2025
Henan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, Henan 475004, China; Department of Stomatology, Huaihe Hospital of Henan University, School of Stomatology, Henan University, Kaifeng, Henan 475004, China. Electronic address:
The occurrence and development of tumor is mediated by a wide range of complex mechanisms. Subsequent to nitric oxide and carbon monoxide, hydrogen sulfide (HS) holds the distinction of being the third identified gasotransmitter. Alternation of HS level has been widely demonstrated to induce an array of disturbances in important cancer cell signaling pathways.
View Article and Find Full Text PDFNat Genet
January 2025
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Members of the KMT2C/D-KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and Kmt2c/d knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation.
View Article and Find Full Text PDFiScience
January 2025
Department of Biology, University of Copenhagen, 2100 Copenhagen, Denmark.
Chromothripsis, a hallmark of cancer, is characterized by extensive and localized DNA rearrangements involving one or a few chromosomes. However, its genome-wide frequency and characteristics in urothelial carcinoma (UC) remain largely unknown. Here, by analyzing single-regional and multi-regional whole-genome sequencing (WGS), we present the chromothripsis blueprint in 488 UC patients.
View Article and Find Full Text PDFJ Clin Med
December 2024
Institute of Medical Sciences, University of Rzeszow, 35-310 Rzeszow, Poland.
The majority of patients with bladder cancer suffer from tumour recurrence. Identifying prognostic factors for tumour recurrence is crucial for treatment and follow-up in affected patients. The study aimed to assess the impact of somatic mutations in bladder cancer on patient outcomes and tumour recurrence.
View Article and Find Full Text PDFInt J Environ Res Public Health
December 2024
Department of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
The objective of this study is to investigate the potential mutagenic effects of the exposure of mice to aerosols produced from the component liquids of an electronic nicotine delivery system (ENDS). The use of electronic cigarettes (e-cigs) and ENDSs has increased tremendously over the past two decades. From what we know to date, ENDSs contain much lower levels of known carcinogens than tobacco smoke.
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