Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Arsenic

  • Ann M. Bode
  • Zigang Dong
Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_403-2

Definition

Arsenic is a “trace element” that is found naturally in the environment. A “trace element” refers to chemical elements present or required in minute quantities. Arsenic (As) is considered to be an important factor in human health. Humans are exposed to arsenic through the air, drinking water, and food. No documented evidence exists that would support a beneficial biological function or documented clinical deficiency in humans. Arsenic has been associated with cancer as far back as 1887, and current evidence suggests a positive correlation between arsenic exposure and increased risk for developing various cancers, especially skin cancer.

Characteristics

Arsenic is a metalloid that is found in various oxidation states, depending on the pH and the presence of oxidizing and reducing substances. Arsenite (As3+) and arsenate (As5+) forms are the main forms of arsenic found in drinking water.

Arsenic compounds are classified as inorganic or organic arsenic. Inorganic arsenic is...

Keywords

Epidermal Growth Factor Receptor Acute Promyelocytic Leukemia Arsenic Exposure Arsenic Trioxide Arsenic Compound 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

  1. Bode AM, Dong Z (2002) The paradox of arsenic: molecular mechanisms of cell transformation and chemotherapeutic effects. Crit Rev Oncol Hematol 42:5–24CrossRefPubMedGoogle Scholar
  2. Kitchin KT (2001) Recent advances in arsenic carcinogenesis: modes of action, animal model systems, and methylated arsenic metabolites. Toxicol Appl Pharmacol 172:249–261CrossRefPubMedGoogle Scholar
  3. Rossman TG (2003) Mechanism of arsenic carcinogenesis: an integrated approach. Mutat Res 533:37–65CrossRefPubMedGoogle Scholar
  4. Tapio S, Grosche B (2006) Arsenic in the aetiology of cancer. Mutat Res 612:215–246CrossRefPubMedGoogle Scholar

See Also

  1. (2012) Carcinogen. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 644. doi:10.1007/978-3-642-16483-5_839Google Scholar
  2. (2012) Cellular transformation assay. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 743. doi:10.1007/978-3-642-16483-5_1020Google Scholar
  3. (2012) Glioblastoma. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1554. doi:10.1007/978-3-642-16483-5_2421Google Scholar
  4. (2012) Liver cancer. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 2063. doi:10.1007/978-3-642-16483-5_3393Google Scholar
  5. (2012) Renal cancer. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, pp 3225–3226. doi:10.1007/978-3-642-16483-5_6575Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.The Hormel Institute, University of MinnesotaAustinUSA