Manni A, Trujillo J E, Pearson O H
Cancer Res. 1977 Apr;37(4):1216-9.
The effect of prolactin in supporting the growth of 7, 12-dimethylbenz(a)anthracene-induced mammary tumor in adult female Sprague-Dawley rats was investigated when estrogen receptors were blocked by the nonsteroidal antiestrogen, Tamoxifen, ICI 46,474. Following an oophorectomy-induced remission, perphenazine, which stimulates endogenous prolactin release, was able to restore tumor growth whether or not Tamoxifen was added. A second course of perphenazine treatment, instituted after the tumors were allowed to shrink, was again effective in stimulating tumor growth. After a regression in tumor size induced by oophorectomy and daily administration of Tamoxifen, perphenazine was able to restore original tumor size despite continued treatment with Tamoxifen. In intact rats, after regression was obtained by daily administration of Tamoxifen and the prolactin inhibitor, lergotrile mesylate, perphenazine induced tumor growth when the latter was discontinued, even though Tamoxifen was continued for 50 days. Estrogen receptors measured at the time of maximum stimulation by perphenazine were undetectable. On the other hand, estradiol did not stimulate tumor growth when serum prolactin was depressed to undetectable levels by lergotrile. These results indicate that prolactin supports the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor and that estrogen receptors are not required under these conditions.
当雌激素受体被非甾体类抗雌激素他莫昔芬（Tamoxifen）、ICI 46,474阻断时，研究了催乳素对成年雌性斯普拉格 - 道利（Sprague-Dawley）大鼠中7,12 - 二甲基苯并(a)蒽诱导的乳腺肿瘤生长的影响。在卵巢切除诱导的缓解后，刺激内源性催乳素释放的奋乃静，无论是否添加他莫昔芬，都能够恢复肿瘤生长。在肿瘤缩小后进行的第二个疗程的奋乃静治疗，再次有效地刺激了肿瘤生长。在卵巢切除和每日给予他莫昔芬诱导肿瘤大小消退后，尽管继续用他莫昔芬治疗，奋乃静仍能够恢复肿瘤的原始大小。在完整大鼠中，通过每日给予他莫昔芬和催乳素抑制剂甲磺酸麦角腈获得消退后，当停用后者时，尽管继续给予他莫昔芬50天，奋乃静仍诱导肿瘤生长。在奋乃静最大刺激时测量的雌激素受体无法检测到。另一方面，当血清催乳素被麦角腈抑制到无法检测的水平时，雌二醇不会刺激肿瘤生长。这些结果表明，催乳素支持7,12 - 二甲基苯并(a)蒽诱导的大鼠乳腺肿瘤的生长，并且在这些条件下不需要雌激素受体。
