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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

Lise I. Loberg, James R. Gauger2, James L. Buthod1, William R. Engdahl and David L. McCormick3

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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