Shafie S M, Hilf R
Cancer Res. 1978 Mar;38(3):759-64.
Insulin and estrogen binding have been determined in 7,12-dimethylbenz(a)anthracene-induced mammary tumors of rats in various endocrine states. Hormonal therapy, such as diabetes and ovariectomy, resulted in differential effects on growth patterns and hormone binding of tumors coexisting in the same host or in different hosts. It was observed that tumors that continued to grow after the host was made diabetic (insulin independent) or started to regress after ovariectomy (ovarian dependent) demonstrated decreased insulin binding. Tumors that regressed in diabetic hosts (insulin dependent) or continued to grow in ovariectomized animals (ovarian independent) showed an increased insulin-binding capacity. No significant change in insulin binding was observed in tumors that remained static after ovariectomy or induction of diabetes. Estrogen binding in tumor cells from diabetic rats paralleled the pattern of tumor growth response to diabetes; insulin-independent tumors demonstrated a significant increase in binding compared to tumors from intact hosts, and insulin-dependent tumors showed decreased estrogen receptor levels. From these results, we conclude that (a) insulin plays a positive role in regulating estrogen-binding capacity, (b) ovarian hormones may play a role in regulating insulin-binding capacity, and (c) a relationship between insulin and ovarian hormones and the growth of 7,12-dimethylbenz(a)anthracene-induced tumors is strongly suggested and may have therapeutic implications.
已对处于各种内分泌状态的7,12-二甲基苯并(a)蒽诱导的大鼠乳腺肿瘤中的胰岛素和雌激素结合情况进行了测定。激素疗法，如糖尿病和卵巢切除术，对同一宿主或不同宿主中并存的肿瘤的生长模式和激素结合产生了不同的影响。观察到，在宿主患糖尿病后仍继续生长的肿瘤（胰岛素非依赖性）或在卵巢切除术后开始消退的肿瘤（卵巢依赖性）表现出胰岛素结合减少。在糖尿病宿主中消退的肿瘤（胰岛素依赖性）或在去卵巢动物中继续生长的肿瘤（卵巢非依赖性）显示胰岛素结合能力增加。在卵巢切除或诱导糖尿病后保持静止的肿瘤中未观察到胰岛素结合有显著变化。糖尿病大鼠肿瘤细胞中的雌激素结合与肿瘤对糖尿病的生长反应模式相似；与完整宿主的肿瘤相比，胰岛素非依赖性肿瘤的结合显著增加，而胰岛素依赖性肿瘤的雌激素受体水平降低。从这些结果中，我们得出结论：(a)胰岛素在调节雌激素结合能力方面起积极作用；(b)卵巢激素可能在调节胰岛素结合能力方面起作用；(c)强烈提示胰岛素和卵巢激素与7,12-二甲基苯并(a)蒽诱导的肿瘤生长之间存在关联，且可能具有治疗意义。
