Carcinogenesis, Vol. 20, No. 8, 1633-1636,
August 1999
© 1999 Oxford University Press
Short Communications |
Gene expression in human breast epithelial cells exposed to 60 Hz magnetic fields
Experimental Toxicology and Carcinogenesis Division,
1 Microbiology and Immunology Division and
2 Electronics and Electromagnetics Section, IIT Research Institute, Chicago, IL 60616, USA
Epidemiology suggests a possible relationship between exposure to power frequency magnetic fields (EMF) and breast cancer. One mechanism through which EMF could stimulate breast cancer induction is via altered expression of oncogenes and/or tumor suppressor genes that regulate normal and neoplastic growth. To evaluate the hypothesis that EMF action in the breast is mediated by alterations in gene expression, transcript levels of c-myc and a battery of other cancer-associated genes were quantitated in human breast epithelial cells exposed to pure, linearly polarized 60 Hz EMF with low harmonic distortion. HBL-100 cells and normal (non-transformed) human mammary epithelial cells were exposed to EMF flux densities of 0.1, 1.0 and 10.0 Gauss (G) for periods ranging from 20 min to 24 h; concurrent sham controls were exposed to ambient fields (<0.001 G) only. Gene expression was quantitated using ribonuclease protection assays. EMF exposure had no statistically significant effect on basal levels of c-myc transcripts in either human breast cell model, and had no effect on alterations in c-myc expression induced by 12-O-tetradecanoylphorbol-13-acetate. Transcript levels of c-erbB-2, p53, p21, GADD45, bax, bcl-x, mcl-1, and c-fos were also unaffected by EMF exposure. These results suggest that EMF is unlikely to influence breast cancer induction through a mechanism involving altered expression of these genes.
Abbreviations: EMF, 60 Hz magnetic field; G, Gauss; GADPH, glyceraldehyde-6-phosphate dehydrogenase gene; mG, milliGauss; HME cells, human mammary epithelial cells; RPA, ribonuclease protection assay; TPA, 12-O-tetradecanoylphorbol-13-acetate.
3 To whom correspondence should be addressed Email: dmccormick{at}iitri.org
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