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子宫内膜异位症中的卵巢癌:一项免疫组织化学和比较基因组杂交研究。

Ovarian carcinomas in endometriosis: an immunohistochemical and comparative genomic hybridization study.

作者信息

Mhawech Paulette, Kinkel Karen, Vlastos Georges, Pelte Marie-Françoise

机构信息

Department of Pathology, Geneva University Hospital, Switzerland.

出版信息

Int J Gynecol Pathol. 2002 Oct;21(4):401-6. doi: 10.1097/00004347-200210000-00010.

DOI:10.1097/00004347-200210000-00010
PMID:12352189
Abstract

Malignant transformation of endometriosis, an uncommon phenomenon, can occur in gonadal and extragonadal sites and results in a wide histological range of tumors. Published series reporting malignant transformation of endometriosis have largely been confined to clinical and histopathological discussions with no studies reporting oncoprotein expression and genetic alterations. We report three cases of carcinomas arising in ovarian endometriosis: a serous cystadenocarcinoma, an endometrioid carcinoma with squamous differentiation, and a pure squamous cell carcinoma. Each tumor was analyzed immunohistochemically to compare oncoprotein expression (p53, bcl2, cyclin D1, and c-erb B2) between the tumors and the endometriotic tissue as well as with comparative genomic hybridization (CGH) to compare genetic alterations. All three tumors expressed nuclear p53, in contrast to the endometriotic tissue in which no p53 expression was found. Both endometrial and tumor tissue expressed bcl-2. No expression of cyclin D1 or c-erb B2 was detected in endometriotic or tumoral tissues. The CGH analysis revealed one or two chromosomal aberrations in each of the three tumors with gains on chromosomes 1q, 8q, and 13q, and losses on chromosome 10p. The endometriotic tissue, as expected, showed a normal genetic profile. These results suggest that p53 protein abnormalities and chromosomal aberrations may be involved in malignant transformation of endometriosis in the ovary. However, our results are limited by the number of cases examined and a definite conclusion on the pathogenesis of this process should be followed by future studies with a larger number of cases.

摘要

子宫内膜异位症的恶变是一种罕见现象,可发生于性腺和性腺外部位,并导致多种组织学类型的肿瘤。已发表的关于子宫内膜异位症恶变的系列报道主要局限于临床和组织病理学讨论,尚无研究报道癌蛋白表达和基因改变情况。我们报告3例卵巢子宫内膜异位症恶变的病例:1例浆液性囊腺癌、1例伴鳞状分化的子宫内膜样癌和1例纯鳞状细胞癌。对每例肿瘤进行免疫组化分析,以比较肿瘤与异位内膜组织之间的癌蛋白表达(p53、bcl2、细胞周期蛋白D1和c-erb B2),并采用比较基因组杂交(CGH)技术比较基因改变情况。所有3例肿瘤均表达核p53,而异位内膜组织未发现p53表达。子宫内膜组织和肿瘤组织均表达bcl-2。在异位内膜组织或肿瘤组织中均未检测到细胞周期蛋白D1或c-erb B2的表达。CGH分析显示,3例肿瘤各有1或2个染色体畸变,1q、8q和13q染色体获得,10p染色体缺失。正如预期的那样,异位内膜组织显示正常的基因图谱。这些结果提示,p53蛋白异常和染色体畸变可能参与卵巢子宫内膜异位症的恶变过程。然而,我们的结果受病例数量的限制,关于这一过程发病机制的确切结论有待未来更多病例的研究得出。

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