Induction of Gene Amplification by Arsenic

Arsenic is a well-established carcinogen in humans, but there is little evidence for its carcinogenicity in animals and it is inactive as an initiator or tumor promoter in two-stage models of carcinogenicity in mice. Two arsenic salts (sodium arsenite and sodium arsenate) induced a high frequency of...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1988-07, Vol.241 (4861), p.79-81
Main Authors: Lee, Te-Chang, Tanaka, Noriho, Lamb, Patricia W., Gilmer, Tona M., Barrett, J. Carl
Format: Article
Language:English
Subjects:
Animals
Arsenates
Arsenates - pharmacology
Arsenic
Arsenic - pharmacology
Arsenites
Biological and medical sciences
Bones
Cancer
Carcinogenesis, carcinogens and anticarcinogens
Carcinogens
Cell Line
Cell lines
Cell transformation
Chemical agents
Chromosome replication
DNA - genetics
Drug Resistance
Embryonic cells
Estrogens
Gene amplification
Gene Amplification - drug effects
Genetic aspects
Humans
Medical sciences
Methotrexate
Mice
Neoplasms, Experimental - chemically induced
Neoplasms, Experimental - genetics
Nucleic Acid Hybridization
Oncogenes
Physiological aspects
Poisons & poisoning
Sodium
Sodium Compounds
Tetrahydrofolate Dehydrogenase - genetics
Tumors
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Summary:Arsenic is a well-established carcinogen in humans, but there is little evidence for its carcinogenicity in animals and it is inactive as an initiator or tumor promoter in two-stage models of carcinogenicity in mice. Two arsenic salts (sodium arsenite and sodium arsenate) induced a high frequency of methotrexate-resistant 3T6 cells, which were shown to have amplified copies of the dihydrofolate reductase gene. The ability of arsenic to induce gene amplification may relate to its carcinogenic effects in humans since amplification of oncogenes is observed in many human tumors. The inability of arsenic to induce gene mutations may relate to the negative results of arsenic in longterm animal studies and suggests that these experiments may not detect some environmental agents that act late in the carcinogenic process in humans.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.3388020