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Estrogen Action following Irradiation of Human Breast Cancer Cells¹

Department of Medicine [R. E. B., D. T. Z., W. L. M.] and Radiology [J. G. M., R. D.], The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284

Estrogen responsiveness of human breast cancer cells after radiotherapy was examined with the use of the MCF-7 breast cancer cell line (derived at the Michigan Cancer Foundation from a aetastatic human breast adenocarcinoma). Estrogen receptor binding characteristics were unaltered in MCF-7 cells, which survived highly destructive doses of -radiation. Biological responses to estrogen were also normal in surviving postirradiated cells.

Initial experiments demonstrated that cytosol preparations from MCF-7 cells could be directly irradiated with 20,000 rads of Co⁶⁰ -rays (single dose) without any net alterations of the binding capacity of estrogen receptor for ligand. Subsequent studies with the use of postirradiated whole cells showed that MCF-7 cell proliferation was inhibited in a radiation dose-dependent fashion. A small percentage of the cell population survived nearlethal doses of radiation. Cells surviving a single dose of 1000 rads were grown to confluence, subcultured, and studied further; they were designated MCF-7R. Both the binding affinity and capacity of MCF-7R cytosol and nuclear estrogen receptors were unchanged from nonirradiated cells. The population doubling time of MCF-7R cells was 43 hr even after 4 months of culture, whereas that of MCF-7 control cells was still 34 hr. MCF-7R cells treated with 10 nM 17ß-estradiol responded normally with a 2-fold elevation in lactic dehydrogenase activity compared to untreated controls. Furthermore, inhibition of MCF-7R cell growth by the antiestrogen nafoxidine could be rescued rapidly by subsequent treatment with estrogen.

These experiments provide evidence at the cellular level that irradiated tissues can be used for receptor assays and that breast cancer patients may still be amenable to endocrine therapy of recurrent and/or metastatic lesions following extensive local radiation therapy.

¹ Supported in part by Grants CB-23862, CA 11378, and CA 09042 from The National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 3/20/78. Accepted 6/ 6/78.