Prolactin and murine mammary tumorigenesis: a review.
Prolactin and murine mammary tumorigenesis: a review.
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催乳素和小鼠乳腺肿瘤发生：综述。
作者：
C. Welsch;H. Nagasawa
毫无疑问，催乳素在小鼠乳腺肿瘤的发生过程中是一种有影响的激素。Berenblum假说(7)是一个著名的肿瘤发生理论模型，它将这一致癌过程描述为一个两步机制，即启动和促进，这是一个概念性的方案，其中催乳素在乳腺肿瘤发生中的作用可以被理解。根据这一概念模型，催乳素参与了乳腺肿瘤发生的启动和促进步骤，在启动阶段，催乳素分泌的变化似乎会影响乳腺上皮细胞的代谢，从而使上皮细胞对启动剂(如化学致癌物、物理致癌物、致癌病毒等)更容易接受或更难接受。即，允许的动作。在促进期，催乳素可以作为“转化的”乳腺上皮的启动子或反启动子。在促进过程中，激素可能直接或间接(通过卵巢)刺激“转化”的上皮细胞的有丝分裂活动。在抗促进作用中，激素在必要的激素(如糖皮质激素)存在的情况下，可协同诱导“转化”的上皮分化(如哺乳)。肿瘤会导致前者(促进)，但不会导致后者(反促进)。催乳素是否对人类乳腺肿瘤的发生有重大影响仍有待确定。这是一个极其重要的研究领域，理所当然地受到越来越多的关注。因为如果能够证明催乳素对人类乳腺上皮的影响与其对啮齿动物乳腺组织的影响类似，那么通过适当的药物介导的催乳素抑制，预防和/或化疗控制人类乳腺肿瘤的发生可能是可行的。
It is unequivocal that prolactin is an influential hormone in murine mammary tumorigenesis. The Berenblum hypothesis (7), a well-known theoretical model of tumorigenesis that depicts this oncogenic process as a two-step mechanism, i.e., initiation and promotion, is a conceptual scheme in which the action of prolactin in mammary tumorigenesis may be understood. According to this conceptual model, prolactin would participate in both the initiation and promotion steps of mammary tumorigenesis, In the initiation phase, variations in prolactin secretion appear to influence the metabolism of the mammary epithelium, so that the epithelium would be either more receptive to or refractory to an initiating agent (e.g., chemical carcinogen, physical carcinogens, oncogenic viruses, ets.) i.e., a permissive action. In the promotion phase, prolactin may act as either a promoter or an antipromoter of the "transformed" mammary epithelium. In promotion, the hormone may either directly or indirectly (via the ovary) stimulate mitotic activity of the "transformed" epithelium. In antipromotion the hormone, in the presence of requisite hormones (e.g., glucocorticoids), may synergistically induce differentiation (e.g., lactation) in the "transformed" epithelium. A tumor would result in the former (promotion) but not in the latter (antipromotion) case. Whether or not prolactin is significantly influential in human breast tumorigenesis remains to be determined. This is an extremely important area of research which is justifiably receiving increased attention. For if prolactin can be shown to influence human breast epithelium in a manner similar to its effect on rodent mammary tissue, then prophylactic and/of chemotherapeutic control of human breast tumorigenesis may be feasible by appropriate drug-mediated prolactin suppression.