On the mechanism of hormone action in 7, 12 dimethylbenz(A) anthracene-induced mammary tumor. I. Prolactin and progesterone effects on estrogen receptor in vitro

✍ Scribed by Gordon H. Sasaki; Dr. Benjamin S. Leung

• Publisher: John Wiley and Sons
• Year: 1975
• Tongue: English
• Weight: 552 KB
• Volume: 35
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/1097-0142(197503)35:3<645::aid-cncr2820350316>3.0.co;2-t

✦ Synopsis

The presence of ER in DMBA-tumors was demonstrated by the use of dextrancharcoal assay, sephadex chromatography, sucrose gradient sedimentation, and organ culture techniques. It was found that tumors have binding sites ranging from 10-" to 10-l' moles/mg protein, and a dissociation constant of ER 10-' to lo-'' M. In experiments with tumor explants, prolactin-insulin significantly stimulated ER binding capacity, as compared with control without prolactin. This stimulation was tissue-specific and inhibited by progesterone. Insulin had a synergistic effect on prolactin stimulation of ER. Our results present a plausible explanation for tumor responses to these hormones in vivo. This interaction of prolactin, estrogen, and progesterone may be a common phenomenon for all estrogen-responsive tissues.

b w 35:645-651, 1975.

LTHOUGH THE INFLUENCE OF OVARIAN AND

A pituitary hormones on growth patterns of 7,12 dimethylbenz(a)anthracene-induced mammary tumors (DlMBA-tumors) in Sprague-Dawley rats is well the exact hormonal requirement at the tumor site is unclear. In animal studies, an increase in prolactin or estrogen levels stimulates tumor growth. Recently, Pearson et a1.I' and Nagasawa and Yanai" demonstrated that tumors which regressed following ovariectomy and adrenalectomy resumed their growth when high doses of ovine prolactin were injected daily. Estrogen, on the contrary, failed to stimulate tumor growth of hypophysectomized rats bearing DLMBAtumors. These investigators suggest that pro-