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• W2912462203 abstract "2215 Over 60,000 new cases of bladder cancer will be diagnosed this year in the United States. Tobacco use, occupational exposures (particularly to aromatic amines), and exposure to arsenic are all etiologically related to bladder cancer, although the pattern of somatic alterations attributable to these exposures remains unclear. Our lab and others have observed associations between tobacco-smoke exposure and epigenetic silencing of specific tumor suppressors, through promoter hypermethylation, in lung cancer. Associations between carcinogenic exposures and epigenetic silencing of tumor suppressor genes may yield critical understanding of the mechanistic roles of these exposures in carcinogenesis. To identify the relationship of promoter hypermethylation of specific tumor suppressor genes to known etiologic risk factors of the disease, we investigated a series study of bladder cancer derived from a case-control study of bladder cancer in New Hampshire. This study is unique due to its population-based approach, thereby reducing bias in the sampling of tumors. In 360 cases, promoter hypermethylation of CDKN2A, DAPK, RARB, RASSF1A, CDH1, and CDH13 were determined utilizing methylation-specific PCR. The prevalence of hypermethylation for each gene was: RASSF1A 33%, CDKN2A 31%, CDH13 18%, RARB 15%, DAPK 9%, and CDH1 3%. Controlling for age and sex, hypermethylation of CDKN2A occurred more than twice as often in ever-smokers compared to non-smokers (O.R. 2.55 95% C.I. 1.19-5.47) and was associated with invasive tumors (O.R.1.69, 95% C.I. 1.03-2.78). Hypermethylation of RASSF1A, controlling for age and sex, was positively associated with invasive tumors (O.R. 2.86, 95% C.I. 1.54-5.31), TP53 alterations (O.R 2.03, 95% C.I. 1.06-3.87), and arsenic exposure, measured by toenail arsenic (O.R. 3.30, 95% C.I. 1.14-9.54). Both RASSF1A and CDKN2A strongly related to bladder cancer invasiveness making these candidates for determining patient prognosis. The relationship between smoking and CDKN2A methylation provides additional evidence that tobacco carcinogens induce epigenetic silencing or act to select silenced cells which produce altered clonal fields. Finally, the association between RASSF1A methylation and high level arsenic exposure suggests a novel mechanism of carcinogenicity for this non-mutagenic metal. Additional analyses will define relationships between these various epigenetic alterations. Specifically, we will investigate if there is evidence, in bladder cancer, for a CpG island methylator phenotype, similar to that described in other tumor types." @default.
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• W2912462203 date "2005-05-01" @default.
• W2912462203 modified "2023-09-26" @default.
• W2912462203 title "Tobacco smoking and arsenic exposure are associated with tumor suppressor gene hypermethylation in bladder cancer" @default.
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