Reproductive Sciences

 

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Reproductive Sciences, Vol. 8, No. 2, 114-116 (2001)
DOI: 10.1177/107155760100800209

RU-486 Can Abolish Glucocorticoid-Induced Increases in CSF-1 Receptor Expression in Primary Human Breast Carcinoma Specimens

Barry M. Kacinski, MD, PhD

Departments of Therapeutic Radiology and Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut; Hunter Radiation Therapy Center, Room 132, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8040; barry.kacinski{at}yale.edu

Maryann B. Flick, PhD

Eva Sapi, PhD

Departments of Therapeutic Radiology and Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut

OBJECTIVE: We present the results of the application of organ culture techniques previously described in this journal to the study of steroid hormone responsiveness of primary breast carcinoma specimens.

METHODS AND RESULTS: Nearly all breast carcinomas that express macrophage colony-stimulating factor-1R (CSF-IR) at tissue harvest (15 of 18) had levels of CSF-1R expression lowered after incubation in steroid-free media. The decrease in CSF-1R expression was reversed by treatment with glucocorticoids; this glucocorticoid-induced increase in CSF-1R expression can be blocked by mifepristone (RU-486), a competitive inhibitor of glucocorticoid action.

CONCLUSION: These results demonstrate that steroid hormone responsiveness of primary breast carcinomas can be assayed in vitro, a result which can not only be employed to better predict the responsiveness of breast carcinomas to therapies with steroid hormone agonists and antagonists, but also suggests that the therapeutic utility of mifepristone in breast cancer deserves further study.

Key Words: Breast carcinoma • organ culture • CSF-1R • c-fms • mifepristone


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