Ovarian dysplasia. A Study of identical twins

Gusberg, S.B.; Deligdisch, Liane

doi:10.1002/1097-0142(19840701)54:1<1::aid-cncr2820540102>3.0.co;2-9

Cited by 70 publications

(29 citation statements)

References 10 publications

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“…[5][6][7][8][9][10][11] These lesions are characterized by stratification of cells lining the ovarian surface or epithelial inclusion glands with loss of nuclear polarity and marked nuclear pleomorphism, hyperchromasia and chromatin clumping ( Figure 1). In their study of cul-desac aspirates obtained for ovarian cancer screening, Graham et al 9 identified these changes adjacent to a microscopic serous carcinoma in one patient and in the surface epithelium of 20 additional patients with malignant cells in their aspirates.…”

Section: Morphologic Datamentioning

confidence: 99%

Origins and molecular pathology of ovarian cancer

2005

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Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. Current data indicate that each of these histologic subtypes is associated with distinct morphologic and molecular genetic alterations: high-grade serous and possibly endometrioid carcinomas most probably arise from surface epithelial inclusion glands with TP53 mutations and dysfunction of BRCA1 and/or BRCA2; low-grade serous carcinomas probably arise in a stepwise fashion in an adenoma-borderline tumor-carcinoma sequence from typical to micropapillary borderline tumors to low-grade invasive serous carcinoma via activation of the RAS-RAF signaling pathway secondary to mutations in KRAS and BRAF; mucinous carcinomas arise via an adenoma-borderline tumor-carcinoma sequence with mutations in KRAS; low-grade endometrioid carcinomas arise from endometriosis via mutations in CTNNB1 (the gene encoding b-catenin) and PTEN. Although the morphologic data strongly support an origin of clear cell carcinoma from endometriosis, there is limited data on the genetic alterations in these uncommon tumors. Thus it is likely that most low-grade, relatively indolent ovarian carcinomas of serous, mucinous and endometrioid type arise from pre-existing cystadenomas or endometriosis whereas most high-grade serous carcinomas arise without an easily identifiable precursor lesion. Modern Pathology (2005) 18, S19-S32. doi:10.1038/modpathol.3800306Keywords: ovarian cancer; ovarian borderline tumors; histogenesis; molecular pathology Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. 1,2 Two types of ovarian surface epithelial lesions have been described as possible precursors of these carcinomas: lesions that appear in situ in surface epithelium or surface epithelial inclusion glands (SEIG); and preexisting benign epithelial ovarian tumors and endometriosis. The morphologic and genetic data implicating each as a precursor lesion of the major histologic subtypes of ovarian carcinoma are discussed. Surface epithelium and surface epithelial inclusion glands as precursor lesions Morphologic DataTwo types of morphologic data are available regarding the malignant potential of ovarian surface epithelium and inclusion glands, alterations in these structures and studies on microscopic ovarian carcinoma.Surface epithelium and surface epithelial inclusion glands Despite the widespread acceptance of the origin of surface epithelial cancers from the ovarian surface epithelium and its inclusion glands, only rarely have putative precursor lesions been described at these sites. Two...

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Section: Morphologic Datamentioning

confidence: 99%

Origins and molecular pathology of ovarian cancer

2005

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“…1,2 Moreover, results from several observational studies support the hypothesis that dysplasia or hyperplasia arising within these epithelial inclusion cysts may represent a histological precursor to ovarian carcinoma. [7][8][9][10] Together, these morphological observations suggest that the OSE normally undergoes a physical relocation from the surface into the ovarian cortex through processes related to ovulation and aging. Once entrapped in the cortex, a conversion from the flat cuboidal mesothelial cells to stratified Müllerian epithelial cells can occur, perhaps under the influence of stromal hormones.…”

Section: Andmentioning

confidence: 99%

Expression of candidate tumor markers in ovarian carcinoma and benign ovary: Evidence for a link between epithelial phenotype and neoplasia

2004

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“…L'analyse microscopique des pièces d'annexectomie prophylactique de jumelles monozygotes dont l'une était porteuse d'un cancer de l'ovaire a révélé des anomalies cytologiques et architecturales (papillomatose de surface, kystes d'inclusion, pléiomorphisme nucléaire, pseudostratification épithéliale et invaginations épithéliales) [3]. Par analogie aux lésions pré-invasives cervicales, le terme générique de « dysplasie » a été proposé (Fig.…”

Section: Discussionunclassified

“…Bien que l'aspect macroscopique des pièces d'ovariectomies prophylactiques soit bien souvent normal, l'examen anatomopathologique attentif de l'ensemble de l'ovaire est susceptible de mettre en évidence ces modifications cytologiques et architecturales fines dénommées « dysplasie ovarienne » [3].…”

Section: Introductionunclassified