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Carcinogenesis Advance Access originally published online on June 29, 2005
Carcinogenesis 2006 27(1):112-116; doi:10.1093/carcin/bgi172
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Carcinogenesis vol.27 no.1 © Oxford University Press 2005; all rights reserved.

Carcinogen exposure and gene promoter hypermethylation in bladder cancer

Carmen J. Marsit 1, Margaret R. Karagas 3, Hadi Danaee 1, Mei Liu 1, Angeline Andrew 3, Alan Schned 4, Heather H. Nelson 4 and Karl T. Kelsey 1, 2, *

1 Department of Genetics and Complex Diseases and 2 Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA, 3 Department of Community and Family Medicine and 4 Department of Pathology, Dartmouth Medical School, Lebanon, NH 03756, USA

* To whom correspondence should be addressed. Tel: +1 617 432 3313; Fax: +1 617 432 0107; Email: kelsey{at}hsph.harvard.edu

Tobacco smoking, certain occupational exposures, and exposure to inorganic arsenic in drinking water have been associated with the occurrence of bladder cancer. However, in these tumors the exposure-associated pattern of somatic alterations in genes in the causal pathway for disease has been poorly characterized. In particular, the mechanism by which arsenic induces bladder cancer and the effects of lower environmental levels of exposure remain uncertain. Animal and in-vitro studies have suggested that arsenic and other exposures may act through epigenetic mechanisms. We, therefore, examined, in a population-based study of human bladder cancer, the relationship between epigenetic silencing of three tumor suppressor genes, p16INK4A, RASSF1A and PRSS3, and exposure to both tobacco and arsenic in bladder cancer. Promoter methylation of each of these genes occurred in ~30% of bladder cancers, and both RASSF1A and PRSS3 promoter methylation were associated with advanced tumor stage (P < 0.001 and P < 0.04, respectively). Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P < 0.02) and PRSS3 (P < 0.1) but not p16INK4A promoter methylation, in models adjusted for stage and other factors. Cigarette smoking was associated with a >2-fold increased risk of promoter methylation of the p16INK4A gene only, with greater risk seen in patients with exposures more recent to disease diagnosis. These results, from human bladder tumors, add to the body of animal and in vitro evidence that suggests a role in epigenetic alterations for bladder carcinogens.


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