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  • Title: Prolactin binding in ovariectomy-responsive and ovariectomy-nonresponsive rat mammary carcinoma.
    Author: Powell BL, Diamond EJ, Koprak S, Hollander VP.
    Journal: Cancer Res; 1977 May; 37(5):1328-32. PubMed ID: 15719.
    Abstract:
    Growth of the transplantable mammary tumor, MTW9, in W/Fu rats is greatly enhanced by elevated serum prolactin concentrations. This report compares the prolactin binding to tumor membranes in two mammary tumor strains derived from MTW9. Maximum binding to membranes of both tumors occurred at pH 7.6 after incubation for 30 hr at 4 degrees. The binding was inhibited only by polypeptide hormones that possess lactogenic activity. MTW9-P, an ovariectomy-responsive tumor developed in rats maintained on daily perphenazine injections, had 4-fold-higher prolactin binding than had MTW9MtT, an ovariectomy-nonresponsive tumor developed in rats bearing the mammosomatotropic pituitary tumor, MtTW10. Withdrawal of perphenazine from rats bearing MTW9-P caused a fall to normal of plasma prolactin, no tumor regression, and no significant change in prolactin binding. In contrast, resection of MtT resulted in tumor regression, a fall to normal of serum prolactin, and a nearly 3-fold increase in prolactin binding. Scatchard plots of prolactin binding data yield an apparent affinity constant, Ka, of 1.2 X 109 liters/mole for both tumors. The 4-fold-higher prolactin binding in the ovariectomy responsive variant suggests a positive correlation between ovariectomy response and the number of membrane prolactin-binding sites. No correlation between prolactin sensitivity and prolacting binding is apparent. Prolactin binding in ovariectomy-responsive and ovariectomy-nonresponsive carcinoma in the Wistar/Furth rat is compared. The time course of binding of prolactin at 4, 24, ad 37 degrees for mammary tumor (MTW9) coimplanted with MtTW10, a mammosomatotropic pituitary tumor (MTW9-MtT) or with MTW9 maintained with daily perphenazine injections (MTW9-P) was measured. Maximum binding to membranes of both tumors occurred at 4 degrees after about 30 hours incubation. The binding was inhibited by polypeptide hormones that possess lactogenic activity. Mammary tumors from animals maintained on perphenazine had a 4-fold greater binding capacity than did tumors from MtT-supported animals. When perphenazine therapy was halted the binding capacity of MTW9-P membranes was unaffected. This result held when MTW9-P animals were ovariectomized. Resection of MtT resulted in tumor regression, a fall to normal of serum prolactin, and a nearly 3-fold increase in prolactin binding. Scatchard plots of prolactin binding data yield an apparent affinity constant, K(a) of 1.2 X 10(9) liters/mole for both tumors.
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