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Published on: October 30, 2013
Molecular pathogenesis of non muscle-invasive bladder cancer: implications for novel targeted therapies
I Zachos1, V Tzortzis, P A Konstantinopoulos
1Department of Urology, University of Thessalia, Larissa, Greece.
Abstract:
Approximately 70% to 80% of patients with urothelial carcinomas of the bladder are initially diagnosed with non-muscle invasive disease. Superficial, non-muscle invasive bladder cancers (NMIBCs) are managed with cystoscopic transurethral resection of all visible lesions followed by intravesical chemotherapy and/or immunotherapy. Despite this treatment, up to 70% of these tumors will recur within five years and 15% will ultimately progress to muscle-invasive disease, suggesting that novel therapeutic strategies are necessary. Recent studies have greatly advanced our understanding of urothelial carcinogenesis and have highlighted the distinct molecular pathogenesis of NMIBCs versus muscle-invasive bladder tumors. It is now clear that diverse genetic and epigenetic events are driving the oncogenesis of NMIBCs, thereby attesting to their potential as therapeutic targets for these tumors. This article reviews the molecular pathogenesis of NMIBCs, discusses recently completed and ongoing clinical trials and anticipates the future direction of molecular targeted agents in this disease.
Insights
Non-muscle invasive bladder cancer (NMIBC) often recurs or progresses despite treatment. Understanding NMIBC
Area of Science:
- Uro-oncology
- Molecular pathogenesis
- Cancer therapeutics
Background:
- Non-muscle invasive bladder cancer (NMIBC) accounts for 70-80% of initial diagnoses.
- Current treatments include transurethral resection and intravesical therapies.
- High recurrence (70%) and progression (15%) rates necessitate novel strategies.
Purpose of the Study:
- To review the molecular pathogenesis of NMIBC.
- To discuss current and future clinical trials for NMIBC.
- To explore molecular targeted agents for NMIBC treatment.
Main Methods:
- Review of recent scientific literature on NMIBC molecular pathogenesis.
- Analysis of completed and ongoing clinical trials.
- Discussion of emerging targeted therapies.
Main Results:
- NMIBC pathogenesis differs significantly from muscle-invasive bladder tumors.
- Diverse genetic and epigenetic events drive NMIBC oncogenesis.
- These molecular events represent potential therapeutic targets.
Conclusions:
- Novel therapeutic strategies targeting molecular pathways are needed for NMIBC.
- Molecularly targeted agents show promise for NMIBC treatment.
- Future research should focus on developing and testing these agents.
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