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在异常人类子宫内膜中由单克隆抗体检测到的一种雌激素调节蛋白的存在。

The presence of an estrogen-regulated protein detected by monoclonal antibody in abnormal human endometrium.

作者信息

Ciocca D R, Puy L A, Edwards D P, Adams D J, McGuire W L

出版信息

J Clin Endocrinol Metab. 1985 Jan;60(1):137-43. doi: 10.1210/jcem-60-1-137.

DOI:10.1210/jcem-60-1-137
PMID:3880561
Abstract

The cellular localization of a 24,000 (24K) mol wt protein was evaluated by monoclonal antibody immunocytochemistry in atrophic and persistent proliferative endometrium as well as in various forms of hyperplastic and neoplastic human endometria. 24K was chiefly located in the cytoplasm of ciliated cells and their precursor forms, clear cells. It was absent in atrophic, resting, and regressive forms of cystic glandular hyperplasia. Persistent proliferative endometria with a low degree of proliferation has occasional 24K immunostained cells, whereas those with active proliferation contained intense 24K immunostaining. A similar pattern characterized the active forms of cystic glandular hyperplasia. The immunostaining reaction decreased in adenomatous and atypical adenomatous hyperplasia as well as in well differentiated adenocarcinomas. In poorly differentiated carcinomas, 24K protein was virtually absent. These findings suggest that 24K protein is estrogen and ciliated cell related, and endometrial ciliogenesis and 24K protein are morphological and biochemical markers, respectively, of the estrogenic endometrial response. Their increase and decrease in hyperplastic and neoplastic endometria support the concept that early hyperplasia is highly sensitive to estrogenic stimulation, whereas with increasing architectural and cytologic atypia, the estrogenic response decreases as a reflection of growing cell populations that are independent of estrogenic influence. Immunostaining with 24K is not sensitive enough to discriminate estrogen-independent cells of atypical adenomatous hyperplasia from those of early, well differentiated adenocarcinoma.

摘要

通过单克隆抗体免疫细胞化学方法,对24,000(24K)分子量蛋白在萎缩性和持续性增殖性子宫内膜以及各种增生性和肿瘤性人类子宫内膜中的细胞定位进行了评估。24K主要位于纤毛细胞及其前体形式即透明细胞的细胞质中。在萎缩性、静止性和退行性囊性腺增生中不存在。增殖程度低的持续性增殖性子宫内膜偶尔有24K免疫染色细胞,而那些有活跃增殖的则含有强烈的24K免疫染色。类似的模式也出现在囊性腺增生的活跃形式中。在腺瘤性和非典型腺瘤性增生以及高分化腺癌中,免疫染色反应减弱。在低分化癌中,几乎不存在24K蛋白。这些发现表明,24K蛋白与雌激素和纤毛细胞有关,子宫内膜纤毛发生和24K蛋白分别是雌激素对子宫内膜反应的形态学和生化标志物。它们在增生性和肿瘤性子宫内膜中的增加和减少支持了这样的概念,即早期增生对雌激素刺激高度敏感,而随着结构和细胞学异型性增加,雌激素反应减弱,这反映了与雌激素影响无关的不断增长的细胞群体。用24K进行免疫染色不足以区分非典型腺瘤性增生中不依赖雌激素的细胞和早期高分化腺癌中的细胞。

相似文献

1
The presence of an estrogen-regulated protein detected by monoclonal antibody in abnormal human endometrium.在异常人类子宫内膜中由单克隆抗体检测到的一种雌激素调节蛋白的存在。
J Clin Endocrinol Metab. 1985 Jan;60(1):137-43. doi: 10.1210/jcem-60-1-137.
2
An estrogen-regulated protein in normal and malignant endometrium.正常及恶性子宫内膜中的一种雌激素调节蛋白。
J Steroid Biochem. 1986 Jan;24(1):155-9. doi: 10.1016/0022-4731(86)90045-2.
3
Immunohistochemical estrogen receptor assessment in hyperplastic, neoplastic, and physiologic endometria.增生性、肿瘤性及生理性子宫内膜中雌激素受体的免疫组化评估
Pathol Res Pract. 1991 May;187(4):487-95. doi: 10.1016/S0344-0338(11)80012-9.
4
A new marker of maturation in the cervix: the estrogen-regulated 24K protein.
Obstet Gynecol. 1986 Dec;68(6):825-31.
5
Distribution of estrogen receptors in various cell types of normal, hyperplastic, and neoplastic human endometrial tissues.
Lab Invest. 1988 Mar;58(3):338-45.
6
Presence of an estrogen-regulated protein in endometrial cancer.子宫内膜癌中一种雌激素调节蛋白的存在。
Obstet Gynecol. 1985 Sep;66(3):423-7.
7
The cytodynamics of endometrial hyperplasia and carcinoma. A review.
Ann Pathol. 1983 Sep;3(3):189-201.
8
Malignant transformation of the human endometrium is associated with overexpression of lactoferrin messenger RNA and protein.人类子宫内膜的恶性转化与乳铁蛋白信使核糖核酸及蛋白质的过表达相关。
Cancer Res. 1995 Mar 1;55(5):1168-75.
9
Immunocytochemical study of progesterone receptors in hyperplastic and neoplastic endometrial tissues.增生性和肿瘤性子宫内膜组织中孕激素受体的免疫细胞化学研究
Cancer Res. 1988 Nov 1;48(21):6132-6.
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Microcarcinoma of the endometrium: a mapping study with special reference to cytologic atypia in the endometrium.子宫内膜微小癌:一项特别关注子宫内膜细胞非典型性的图谱研究。
Jpn J Clin Oncol. 1992 Dec;22(6):400-5.

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