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Molecular features in arsenic-induced lung tumors

Roland Hubaux, Daiana D Becker-Santos, Katey SS Enfield, David Rowbotham, Stephen Lam, Wan L Lam and Victor D Martinez*

Author Affiliations

British Columbia Cancer Research Centre, 675 West 10th Avenue, Vancouver, BC V5Z 1L3, Canada

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Molecular Cancer 2013, 12:20  doi:10.1186/1476-4598-12-20

Published: 19 March 2013


Arsenic is a well-known human carcinogen, which potentially affects ~160 million people worldwide via exposure to unsafe levels in drinking water. Lungs are one of the main target organs for arsenic-related carcinogenesis. These tumors exhibit particular features, such as squamous cell-type specificity and high incidence among never smokers. Arsenic-induced malignant transformation is mainly related to the biotransformation process intended for the metabolic clearing of the carcinogen, which results in specific genetic and epigenetic alterations that ultimately affect key pathways in lung carcinogenesis. Based on this, lung tumors induced by arsenic exposure could be considered an additional subtype of lung cancer, especially in the case of never-smokers, where arsenic is a known etiological agent. In this article, we review the current knowledge on the various mechanisms of arsenic carcinogenicity and the specific roles of this metalloid in signaling pathways leading to lung cancer.

Arsenic; Arsenite; Lung cancer; Epigenetic; Reactive oxygen species; Epidermal growth factor receptor; Phosphatidylinositol 3-kinases; NFE2-related factor 2