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

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This study analyzed three ovarian carcinomas arising from endometriosis, finding that p53 abnormalities and specific chromosomal aberrations distinguish the malignant tumors from their benign endometriotic precursors.

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This study investigated the molecular mechanisms underlying malignant transformation in ovarian endometriosis by analyzing three specific carcinoma cases using immunohistochemistry and comparative genomic hybridization. The researchers compared oncoprotein expression and genetic profiles between the tumors and their associated endometriotic tissues, finding that all carcinomas exhibited nuclear p53 expression and distinct chromosomal aberrations absent in the benign tissue. While bcl-2 was present in both tissue types, cyclin D1 and c-erb B2 were not detected, leading to the conclusion that p53 abnormalities and specific genetic changes likely drive this rare progression. This paper is centrally about endometriosis — specifically examining the histological and genetic features of its malignant transformation into ovarian carcinomas.

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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.
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Ovarian Carcinomas in Endometriosis: An Immunohistochemical and Comparative Genomic Hybridization Study - Paulette Mhawech - Karen Kinkel - Georges Vlastos - Marie-Françoise Pelte Summary: 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.

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Condition tags

endometriosis

MeSH descriptors

Cell Transformation, Neoplastic Endometriosis Endometriosis Ovarian Neoplasms Ovarian Neoplasms Adult Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Squamous Cell Carcinoma, Squamous Cell Carcinoma, Squamous Cell Carcinoma, Squamous Cell Carcinoma, Squamous Cell Cell Transformation, Neoplastic Chromosome Aberrations Cyclin D1 Cyclin D1

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europepmc
last seen: 2026-09-12T06:55:35.949492+00:00
pubmed
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