Pre-Cancerous Changes in Bladder Epithelium

Schade, R. O. K.; Swinney, John

doi:10.1016/s0140-6736(68)91169-0

Cited by 121 publications

(19 citation statements)

References 4 publications

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“…The fieldcancerization theory, which has been shown to be important in the development of multicentric squamous cell carcinomas of the head and neck (53 -55), suggests that multifocal urothelial carcinomas arise secondary to numerous independent mutational events at different sites within the urothelial tract as a consequence of external cancer-causing influences. In support of the field effect theory is the frequent finding in patients with bladder cancer of genetic instability in normal-appearing bladder mucosa (56) and of abnormalities in the surrounding urothelium, such as dysplasia or carcinoma in situ (57). In addition, the application of the carcinogen N -butyl-N -(4-hydroxybutyl)nitrosamine to the bladders of chimeric C3H/HeN-BALB/c mice resulted in the formation of multiple urothelial tumors of oligoclonal origin in 30% of cases (58).…”

Section: Discussionmentioning

confidence: 94%

Molecular Evidence Supporting Field Effect in Urothelial Carcinogenesis

Jones¹,

Wang²,

Eble³

et al. 2005

Clinical Cancer Research

166

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Purpose: Human urothelial carcinoma is thought to arise from a field change that affects the entire urothelium. Multifocality of urothelial carcinoma is a common finding at endoscopy and surgery. Whether these coexisting tumors arise independently or are derived from the same tumor clone is uncertain. Molecular analysis of microsatellite alterations and X-chromosome inactivation status in the cells from each coexisting tumor may further our understanding of urothelial carcinogenesis. Experimental Design: We examined 58 tumors from 21patients who underwent surgical excision for urothelial carcinoma. All patients had multiple separate foci of urothelial carcinoma (two to four) within the urinary tract. Genomic DNA samples were prepared from formalin-fixed, paraffinembedded tissue sections using laser-capture microdissection. Loss of heterozygosity (LOH) assays for three microsatellite polymorphic markers on chromosome 9p21 (IFNA and D9S171), regions of putative tumor suppressor gene p16, and on chromosome17p13 (TP53), the p53 tumor suppressor gene locus, were done. X-chromosome inactivation analysis was done on the urothelial tumors from 11female patients. Results: Seventeen of 21 (81%) cases showed allelic loss in one or more of the urothelial tumors in at least one of the three polymorphic markers analyzed. Concordant allelic loss patterns between each coexisting urothelial tumor were seen in only 3 of 21 (14%) cases. A concordant pattern of nonrandom X-chromosome inactivation in the multiple coexisting urothelial tumors was seen in only 3 of 11 female patients; of these 3 cases, only one displayed an identical allelic loss pattern in all of the tumors on LOH analysis. Conclusion: LOH and X-chromosome inactivation assays show that the coexisting tumors in many cases of multifocal urothelial carcinoma have a unique clonal origin and arise from independently transformed progenitor urothelial cells, supporting the ''field effect'' theory for urothelial carcinogenesis.

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Section: Discussionmentioning

confidence: 94%

Molecular Evidence Supporting Field Effect in Urothelial Carcinogenesis

Jones¹,

Wang²,

Eble³

et al. 2005

Clinical Cancer Research

166

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“…The risk of tumor recurrence after local resection of superficial transitional cell carcinoma of the bladder is around 70% [1,2], One of the hypotheses proposed for this high rate of recurrence is that bladder cancer is a gross manifestation of a field change disease of the urothelium, and that most bladder tumor recurrences are, in fact, new tumor occurrences [3][4][5][6].…”

Section: Methodsmentioning

confidence: 99%

Multiple Mucosal Biopsies and Postoperative Urinary Cytology in Patients with Bladder Cancer

Gil-Salom

Sánchez²,

Chuan³

et al. 1990

Eur Urol

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“…The reason for this could be the continuous exposure of the bladder wall to urinary carcinogens, dissemination due to tumor implanta tion during TUR. incomplete resection or the presence of areas of dysplasia or carcinoma in situ which progress at a later stage and/or a disturbance in host-cell-mediated immunosurveillance mechanisms [9]. The chance to progress to muscle invasive disease varies between 5 and 15%.…”

Section: Which Agent Should Be Used?mentioning

confidence: 99%

Current Insights in the Treatment of Superficial Transitional Cell Carcinoma of the Bladder

Reijke¹,

Kurth²,

Boer³

et al. 1996

Oncol Res Treat

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Patients with superficial transitional cell carcinoma of the bladder (Ta, Tl, Tis) can nowadays be subdivided in different risk groups for tumor recurrence and progression, based on prognostic factors, which have been obtained from the results of clinical Phase III trials. For adjuvant therapy a choice can be made between intravesical instillations with chemotherapeutic or immunotherapeutic agents. The optimal treatment schedule and time to start intravesical therapy is not known. None of the investigated chemotherapeutic agents turned out to be superior in delaying tumor recurrence. Intravesical immunotherapy, using bacillus Calmette Guérin (BCG), seems to be as effective and maybe superior in high-risk groups in delaying tumor recurrence compared to chemotherapeutic agents. The side effects, however, are a disadvantage. The exact working mechanism of BCG and its antitumor effect is not known. In the field of recognizing patients at risk for recurrence or progressive disease, biological markers have been identified. In daily practice these markers cannot be used yet. Using all these different treatment options, it is important to obtain information on the impact of these treatment schedules on the quality of life, especially if the treatment results do not differ. A start has been made to imply questionnaires in superficial bladder cancer studies.

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Pre-Cancerous Changes in Bladder Epithelium

Cited by 121 publications

References 4 publications

Molecular Evidence Supporting Field Effect in Urothelial Carcinogenesis

Molecular Evidence Supporting Field Effect in Urothelial Carcinogenesis

Multiple Mucosal Biopsies and Postoperative Urinary Cytology in Patients with Bladder Cancer

Current Insights in the Treatment of Superficial Transitional Cell Carcinoma of the Bladder

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