Shiohara S, Shiozawa T, Shimizu M, Toki T, Ishii K, Nikaido T, Fujii S
Department of Obstetrics and Gynecology, School of Medicine, Shinshu University, Asahi, Matsumoto, Japan.
Cancer. 1997 Sep 1;80(5):908-16.
Mucinous tumors of the ovary have been thought to originate in two ways: by müllerian-type metaplasia of surface epithelium, and as monodermal teratomas. To gain a better understanding of their pathogenesis, the authors analyzed these tumors for their expression of estrogen receptors (ER) and progesterone receptors (PR) as markers of müllerian-type differentiation and for their content of gastric-type mucin as a marker of gastric differentiation.
The histochemical expression of ER, PR, and gastric-type mucin was studied in 10 specimens of the cervix with normal endocervical glands (as a representative of müllerian-derived mucin-containing cells), 3 ovary specimens with surface epithelial inclusion cysts that contained endocervical-like mucin-containing cells (representing müllerian-type metaplasia), and 47 mucinous tumors of the ovary (29 benign, 8 with low malignant potential, and 10 malignant).
Normal endocervical glands expressed ER and PR and rarely expressed gastric-type mucin. Ovarian inclusion cysts showed strong expression of ER and PR in the cuboidal cells and drastically reduced expression in the endocervical-like mucin-containing cells. The cuboidal cells were negative for gastric-type mucin, but the endocervical-like mucin-containing cells expressed gastric-type mucin. Endocervical-like mucinous cells in benign and borderline mucinous tumors showed expression of PR and/or gastric-type mucin in all cases.
The staining results for the inclusion cysts support the thesis that the endocervical-like mucinous cells encountered in the ones that express ER and PR weakly or not at all and have histochemical properties of normal gastric epithelium have their origin in metaplasia of müllerian-type epithelium. Application of the same staining methods to benign ovarian tumors and those with low malignant potential suggests strongly that similar müllerian-type metaplasia is a major pathway in their pathogenesis.
卵巢黏液性肿瘤被认为有两种起源方式：通过表面上皮的苗勒氏型化生，以及作为单胚层畸胎瘤。为了更好地理解其发病机制，作者分析了这些肿瘤中雌激素受体（ER）和孕激素受体（PR）的表达，作为苗勒氏型分化的标志物，并分析了胃型黏液的含量，作为胃分化的标志物。
研究了10例宫颈内有正常宫颈腺的标本（作为含有苗勒氏来源黏液细胞的代表）、3例卵巢表面上皮包涵囊肿标本（其中含有类似宫颈黏液的细胞，代表苗勒氏型化生）以及47例卵巢黏液性肿瘤（29例良性、8例低恶性潜能和10例恶性）中ER、PR和胃型黏液的组织化学表达。
正常宫颈腺表达ER和PR，很少表达胃型黏液。卵巢包涵囊肿在立方体细胞中显示ER和PR的强表达，而在类似宫颈黏液的细胞中表达急剧降低。立方体细胞胃型黏液呈阴性，但类似宫颈黏液的细胞表达胃型黏液。良性和交界性黏液性肿瘤中的类似宫颈黏液的细胞在所有病例中均显示PR和/或胃型黏液的表达。
包涵囊肿的染色结果支持这样的论点，即那些ER和PR表达弱或不表达且具有正常胃上皮组织化学特性的包涵囊肿中遇到的类似宫颈黏液的细胞起源于苗勒氏型上皮化生。将相同的染色方法应用于良性卵巢肿瘤和低恶性潜能肿瘤强烈提示，类似的苗勒氏型化生是其发病机制中的主要途径。
