RU-486 can abolish glucocorticoid-induced increases in CSF-1 receptor expression in primary human breast carcinoma specimens.
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.


RESULTS
Nearly all breast carcinomas that express macrophage colony-stimulating factor-1R (CSF-1R) 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.


CONCLUSIONS
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.
Kacinski
B M
BM
Department of Therapeutic Radiol6ogy, Yale University School of Medicine, New Haven, Connecticut, USA. barry.kacinski@yale.edu
Flick
M B
MB
Sapi
E
E
D001943:Breast Neoplasms / Q000737:chemistry*; D003907:Dexamethasone / Q000494:pharmacology; D005938:Glucocorticoids / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006727:Hormone Antagonists / Q000494:pharmacology*; D006801:Humans; D007150:Immunohistochemistry; D015735:Mifepristone / Q000494:pharmacology*; D009924:Organ Culture Techniques; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000032:analysis* / Q000187:drug effects
D005938:Glucocorticoids; D006727:Hormone Antagonists; D015735:Mifepristone; D003907:Dexamethasone; D016186:Receptor, Macrophage Colony-Stimulating Factor