Abstract
The hormone-dependent nature of some human breast cancers has been appreciated since the pioneering work of Beatson more than 75 years ago.
1
Since then, a variety of ablative and additive therapies have been used to induce clinically important palliations in patients with metastatic breast cancer. Such tumor regressions have also been duplicated in several animal-model systems — notably, in rats with dimethylbenz(a)anthracene-induced mammary cancer.
2
Nonetheless, the data accumulated in clinical and animal studies have failed to define the mechanisms whereby adrenalectomy, hypophysectomy or treatment with androgens, estrogens, progestins or glucocorticoids leads to tumor regression in some patients. In vivo studies . . .
