Comparative immunohistochemical studies of <i>bcl</i>‐2 and p53 proteins in benign and malignant ovarian endometriotic cysts

Nezhat, Farr; Cohen, Carmel J.; Rahaman, Jamal; Gretz, Herbert; Cole, B S Patrick; Kalir, Tamara

doi:10.1002/cncr.10566

Cited by 85 publications

(53 citation statements)

References 17 publications

(20 reference statements)

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“…[124][125][126][127][128][129][130][131] They have shown that most benign-appearing ovarian endometriotic cysts are monoclonal. 124,125,129,130,131 Jiang et al 124,132 have shown loss of heterozygosity at several loci on chromosomes 9q, 11q and 22q in less than 20% of ovarian endometriotic cysts and Sato et al 126 found a higher frequency of LOH of 56% at 10q23.3.…”

Section: Molecular Genetic Datamentioning

confidence: 99%

“…PTEN mutations have been noted in 21% of endometriotic cysts. 126 Several studies have failed to demonstrate either mutations or overexpression of p53 127,128,133 or KRAS mutations 128 in benign endometriotic cysts.…”

Section: Molecular Genetic Datamentioning

confidence: 99%

“…[126][127][128][129][130][131][132][133][134][135][136][137][138][139][140][141][142][143] Mutations of CTNNB1, the gene that encodes b-catenin have been reported in 16-54% of cases. [134][135][136][137][138][139][140] Tumors associated with such mutations are more frequently low-grade and stage and have a favorable prognosis.…”

Section: Endometrioid Carcinomamentioning

confidence: 99%

“…126,128 TP53 mutations or overexpression or both have been reported in 42-63% of ovarian endometrioid adenocarcinomas. 127,128 Microsatellite instability has been reported in 12-19% of ovarian endometrioid adenocarcinomas. 140,141 A small number of studies have examined ovarian endometrioid adenocarcinomas and adjacent synchronous endometriosis for common genetic events.…”

Section: Endometrioid Carcinomamentioning

confidence: 99%

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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: Molecular Genetic Datamentioning

confidence: 99%

Section: Molecular Genetic Datamentioning

confidence: 99%

Section: Endometrioid Carcinomamentioning

confidence: 99%

Section: Endometrioid Carcinomamentioning

confidence: 99%

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Origins and molecular pathology of ovarian cancer

2005

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“…Alterations in the P53 gene (by mutation analysis) have been found in 42% of serous and 42-65% of endometrioid ovarian adenocarcinomas. 43,44 Staining is infrequent in benign tumours. 44,45 The P53 gene probably plays an important role in malignant transformation of ovarian endometriosis.…”

Section: Specific Genetic Alterations In Endometriosis and Ovarian Camentioning

confidence: 99%

Ovarian endometriosis as a premalignant condition: epidemiological, histological and molecular evidence

Dreyer

2012

Southern African Journal of Gynaecological Oncology

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Endometriosis is a common monoclonal benign proliferative disorder that may give rise to pelvic malignancy. Epithelial ovarian carcinoma is responsible for a large proportion of gynaecological cancer-associated deaths. Early diagnosis is difficult and screening is generally unsuccessful. Knowledge of the risk factors for the development of endometriosis and progression to malignancy may assist in identifying women at risk of developing endometriosis-related neoplasia. The associations between infertility, endometriosis and the development of cancer are reviewed in this article. Proliferative growth, metaplasia, hyperplasia and atypia are identified as proliferative disorders in endometriosis and atypia is considered a premalignant lesion. Several endometriosis-related pelvic malignancies have been described, and these all develop from the multipotent Müllerian cell differentiating into epithelial and/or stromal components. The probable histological type depends on the site of the endometriotic lesion and the population group. Cytogenetic and specific gene alterations that are involved in the carcinogenetic process are described briefly and these may help to predict risk of malignancy or to confirm histological subtype. The importance of endometriosis as a precursor of ovarian and related malignancies was probably seriously underestimated in the past. Advances in molecular testing, histology and our understanding of oncogenesis may empower us to help prevent these devastating diseases.Peer reviewed.

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