Gene expression in human breast epithelial cells exposed to 60 Hz magnetic fields

Carcinogenesis. 1999 Aug;20(8):1633-6. doi: 10.1093/carcin/20.8.1633.


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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Breast / radiation effects*
  • Carcinogens
  • Cell Line
  • Electromagnetic Fields / adverse effects*
  • Epithelial Cells / radiation effects
  • Female
  • Gene Expression*
  • Genes, Tumor Suppressor*
  • Genes, myc / radiation effects*
  • Humans
  • Proto-Oncogene Proteins c-myc / metabolism
  • Radiation Dosage
  • Receptor, ErbB-2 / metabolism
  • Tetradecanoylphorbol Acetate
  • Time Factors


  • Carcinogens
  • Proto-Oncogene Proteins c-myc
  • Receptor, ErbB-2
  • Tetradecanoylphorbol Acetate