Scully R E
Department of Pathology, Harvard Medical School, Massachusetts General Hospital, Boston 02114, USA.
J Cell Biochem Suppl. 1995;23:208-18. doi: 10.1002/jcb.240590928.
Ninety percent of ovarian cancers in the Western world are epithelial cancers derived from the surface epithelium of the ovary and its inclusion cysts. The so-called surface epithelium is mesothelium that comes to resemble epithelium as it is reflected over the surfaces of the ovaries. At various ages, but particularly in women in the reproductive, menopausal, and postmenopausal age groups, this epithelium migrates into the ovarian stroma to form inclusion cysts. These cysts probably results from a dynamic interplay of surface epithelium and underlying ovarian stroma, but can also develop as a result of periovarian adhesions. There is abundant evidence that their formation is not related to repair of ovulation. It is generally accepted that benign and malignant ovarian epithelial tumors arise from surface epithelium and its cystic derivatives because they both, but particularly the latter, have a potential to differentiate into epithelia similar to those of normal müllerian derivation (tubal, endometrial, and endocervical epithelia) and their tumors resemble those of the fallopian tube, endometrium, and endocervix. Also, both intraepithelial carcinomas and precarcinomatous lesions can be observed in the surface epithelium and its cystic derivatives. These carcinomas may arise de novo or as a transformation of pre-existing benign tumors and non-neoplastic lesions of similar derivation. Surface epithelial inclusion cysts have a greater propensity to undergo neoplasia than does the surface epithelium itself. This difference has been recognized for many years most epithelial ovarian tumors are intraparenchymal, rather than being located on the ovarian surface. More recent evidence includes the immunohistochemical demonstration of various ovarian carcinoma antigens far more frequently in inclusion cyst epithelium than in surface epithelium; and the much more frequent presence of tubal metaplasia in the cyst epithelium than in the surface epithelium. Tubal metaplasia is encountered in non-neoplastic ovaries contralateral to ovarian carcinomas two to three times as frequently as in control ovaries, suggesting that the metaplastic epithelium is more prone to the development of carcinoma that non-metaplastic epithelium. Carcinoma precursors occur in the ovary, as in the cervix and endometrium, but have been reported only rarely because they are easily overlooked and have not been searched for by pathologists.
在西方世界，90%的卵巢癌是上皮性癌，起源于卵巢表面上皮及其包涵囊肿。所谓的表面上皮是间皮，当它覆盖在卵巢表面时类似上皮。在不同年龄段，尤其是生殖期、围绝经期和绝经后期的女性，这种上皮会迁移到卵巢间质中形成包涵囊肿。这些囊肿可能是表面上皮与下方卵巢间质动态相互作用的结果，但也可能因卵巢周围粘连而形成。有充分证据表明其形成与排卵修复无关。一般认为，良性和恶性卵巢上皮性肿瘤起源于表面上皮及其囊性衍生物，因为它们都有，尤其是后者，有分化为类似于正常苗勒管来源（输卵管、子宫内膜和宫颈内膜上皮）上皮的潜能，并且它们的肿瘤类似于输卵管、子宫内膜和宫颈的肿瘤。此外，在表面上皮及其囊性衍生物中可观察到上皮内癌和癌前病变。这些癌可能是新发的，也可能是由先前存在的良性肿瘤和类似来源的非肿瘤性病变转化而来。表面上皮包涵囊肿比表面上皮本身更易发生肿瘤形成。这种差异已被认识多年，大多数上皮性卵巢肿瘤位于实质内，而非位于卵巢表面。最近的证据包括免疫组化显示，各种卵巢癌抗原在包涵囊肿上皮中出现的频率远高于表面上皮；以及囊肿上皮中输卵管化生比表面上皮中更常见。在与卵巢癌对侧的非肿瘤性卵巢中，输卵管化生的发生率是对照卵巢的两到三倍，这表明化生上皮比未化生上皮更易发生癌变。癌前病变在卵巢中也会出现，如同在宫颈和子宫内膜中一样，但报道很少，因为它们很容易被忽视，而且病理学家也没有对其进行查找。
