Oncogenomic disruptions in arsenic-induced carcinogenesis

Adam P. Sage, Brenda C. Minatel, Kevin W. Ng, Greg L. Stewart, Trevor J.B. Dummer, Wan L. Lam and Victor D. Martinez _

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Oncotarget. 2017; 8:25736-25755. https://doi.org/10.18632/oncotarget.15106

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Adam P. Sage1,*, Brenda C. Minatel1,*, Kevin W. Ng1, Greg L. Stewart1, Trevor J.B. Dummer2, Wan L. Lam1 and Victor D. Martinez1

1 Department of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada

2 Centre of Excellence in Cancer Prevention, School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada

* These authors have contributed equally to this work

Correspondence to:

Victor D. Martinez, email:

Keywords: arsenic, cancer, genetics, epigenetics, non-coding RNA

Received: November 30, 2016 Accepted: January 24, 2017 Published: February 05, 2017


Chronic exposure to arsenic affects more than 200 million people worldwide, and has been associated with many adverse health effects, including cancer in several organs. There is accumulating evidence that arsenic biotransformation, a step in the elimination of arsenic from the human body, can induce changes at a genetic and epigenetic level, leading to carcinogenesis. At the genetic level, arsenic interferes with key cellular processes such as DNA damage-repair and chromosomal structure, leading to genomic instability. At the epigenetic level, arsenic places a high demand on the cellular methyl pool, leading to global hypomethylation and hypermethylation of specific gene promoters. These arsenic-associated DNA alterations result in the deregulation of both oncogenic and tumour-suppressive genes. Furthermore, recent reports have implicated aberrant expression of non-coding RNAs and the consequential disruption of signaling pathways in the context of arsenic-induced carcinogenesis. This article provides an overview of the oncogenomic anomalies associated with arsenic exposure and conveys the importance of non-coding RNAs in the arsenic-induced carcinogenic process.

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