Gerschenson L E, Fennell R H
Pathol Res Pract. 1982 Aug;174(3):285-96. doi: 10.1016/S0344-0338(82)80071-X.
On the basis of experimental research, using rabbit uterine epithelium as a model, it is postulated that human endometrial hyperplasia or carcinoma may be due to derangement of intrinsic growth mechanisms such as cell proliferation, migration, loss and differentiation. Ovarian hormones, estrogen inhibitor or amplifying factors, prostaglandins, stroma-epithelial interactions, proteolytic activity and hormone receptors, all regulate the described intrinsic growth mechanisms, and their excess or lack could result in altered growth patterns. It is also proposed that different types of endometrial carcinoma could result from neoplastic transformation of cells at different stages of differentiation. Since cells at those stages could respond to various hormones in different ways, it would seem of therapeutic value to know the cell of origin in each type of endometrial carcinoma.
基于实验研究，以兔子宫上皮为模型，推测人类子宫内膜增生或癌可能是由于细胞增殖、迁移、丧失和分化等内在生长机制紊乱所致。卵巢激素、雌激素抑制剂或放大因子、前列腺素、基质 - 上皮相互作用、蛋白水解活性和激素受体均调节上述内在生长机制，其过多或缺乏都可能导致生长模式改变。还提出不同类型的子宫内膜癌可能源于不同分化阶段细胞的肿瘤转化。由于这些阶段的细胞对各种激素的反应方式不同，了解每种类型子宫内膜癌的起源细胞似乎具有治疗价值。
