Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 255, Issue 1-2, Pages 57-66Publisher
SPRINGER
DOI: 10.1023/B:MCBI.0000007261.04684.78
Keywords
arsenic; carcinogenesis; gene expression; reactive oxygen species; genetic toxicity; signal transduction; kinase; methylation
Categories
Funding
- NCI NIH HHS [CA103180, CA094964] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA094964, R01CA103180] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Arsenic is a metalloid compound that is widely distributed in the environment. Human exposure of this compound has been associated with increased cancer incidence. Although the exact mechanisms remain to be investigated, numerous carcinogenic pathways have been proposed. Potential carcinogenic actions for arsenic include oxidative stress, genotoxic damage, DNA repair inhibition, epigenetic events, and activation of certain signal transduction pathways leading to abberrant gene expression. In this article, we summarize current knowledge on the molecular mechanisms of arsenic carcinogenesis with an emphasis on ROS and signal transduction pathways.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available