Ovarian dysplasia in prophylactic oophorectomy specimens

Deligdisch, Liane; Gil, Joan; Kerner, Hedviga; Wu, Huihui; Beck, Dan; Gershoni‐Baruch, Ruth

doi:10.1002/(sici)1097-0142(19991015)86:8<1544::aid-cncr22>3.0.co;2-i

Cited by 100 publications

(49 citation statements)

References 24 publications

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“…Several other investigators were unable to demonstrate a statistically significant increase in atypia in ovaries contralateral to ovarian tumors over control ovaries. 20,21 Deligdisch et al 22 have noted 'ovarian dysplasia' as detected by a morphometric method utilizing discriminant analysis based on nuclear area and texture in both prophylactic oophorectomy specimens and in epithelium adjacent to carcinomas.…”

Section: Morphologic Datamentioning

confidence: 99%

“…16,[19][20][21] Microscopic surface-epithelial carcinomas A very small number of microscopic or tiny gross carcinomas have been reported, usually as incidental findings at operations for other gynecologic disorders or, more recently, in prophylactic oophorectomy specimens from patients at high risk for the development of ovarian carcinoma. 6,8,9,16,22,[26][27][28] The Figure 1 Ovarian carcinoma in situ. The epithelium is thickened by stratified cells showing loss of nuclear polarity and marked nuclear pleomorphism, hyperchromasia and chromatin clumping.…”

Section: Morphologic Datamentioning

confidence: 99%

“…22,[28][29][30] One of these patients died of tumor. 29 Clearly, although the data are limited, the prognosis of patients with minute ovarian epithelial cancers is guarded.…”

Section: Morphologic Datamentioning

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: Morphologic Datamentioning

confidence: 99%

Section: Morphologic Datamentioning

confidence: 99%

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Origins and molecular pathology of ovarian cancer

2005

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“…In either model, inclusions resulting from these origins occasionally undergo neoplastic transformation, leading to a wide range of epithelial neoplasms in the ovary. 2,3 This model is most strongly supported by tumors that are indisputably ovarian in origin, including mucinous, endometrioid, and low-grade serous neoplasms. Many of these tumors are confined to the ovary when discovered and do not involve the ovarian surface.…”

Section: Introductionmentioning

confidence: 99%

“…6 Others have described dysplastic changes in the ovarian surface epithelium. 2,7 Other candidate sites of origin, including the peritoneum, have been proposed for cases with minimal ovarian involvement. The fallopian tube has been proposed as a primary site for a minority of serous carcinomas, with an estimated ovarian to fallopian tube serous cancer prevalence of 50:1.…”

Section: Introductionmentioning

confidence: 99%

A candidate precursor to pelvic serous cancer (p53 signature) and its prevalence in ovaries and fallopian tubes from women with BRCA mutations

Folkins

Jarboe

Saleemuddin

et al. 2008

Gynecologic Oncology

269

197

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Background-Early serous carcinomas (SCAs) predominate in the fimbria of BRCA+ women. An entity in non-neoplastic mucosa sharing several properties of SCA -the "p53 signature" -has been described in the distal fallopian tube and proposed as a precursor to SCA. This study compared the prevalence of p53 signatures in both ovarian cortical inclusion cysts (CICs) and fallopian tubes from BRCA+ women and explored their relationship.

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Absence of premalignant histologic, molecular, or cell biologic alterations in prophylactic oophorectomy specimens fromBRCA1 heterozygotes

Barakat

Federici

Saigo

et al. 2000

Cancer

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BACKGROUND The high mortality associated with ovarian carcinoma is largely a reflection of the inability to diagnose the disease at an early stage; the identification of a histologic lesion or molecular marker associated early stages of transformation would represent an important advance in understanding the natural history of this cancer. The existence of individuals with germline mutations in the ovarian and breast carcinoma susceptibility gene BRCA1 represents a unique opportunity to search for such premalignant alterations in ovarian tissues that are at unusually high risk for tumorigenesis. In this study, the authors addressed the hypothesis that pathologically normal ovaries removed from BRCA1 heterozygotes are likely to display premalignant histologic, molecular, and/or cell biologic alterations that may provide insight into early stages of ovarian tumorigenesis. METHODS Ovarian tissues from 18 BRCA1 heterozygotes and from 20 age‐matched controls were examined in a blinded fashion for histologic evidence of surface epithelial pseudostratification, epithelial inclusion cysts, deep cortical invaginations of surface epithelium, increased stromal cell activity, and surface papillomatosis. Immunohistochemical analyses for expression of BRCA1, p53, and ERBB‐2 and quantitation of cell proliferation (Ki‐67 expression) and apoptosis (TUNEL assay), were also performed on all specimens. RESULTS Although histologic alterations were observed, there was no difference in frequency between cases and controls. Analysis of BRCA1 expression revealed ubiquitous nuclear immunoreactivity in the surface epithelial cells of all ovaries. Similarly, no evidence was found of p53 overexpression in any ovarian tissue or of a difference in ERBB‐2 expression between cases and controls. Finally, no differences were observed in epithelial cell proliferation or apoptosis. CONCLUSIONS Clinically, normal ovaries from BRCA1 heterozygotes do not show evidence of premalignant alterations in histology, molecular markers, cell proliferation, or apoptosis, indicating that such changes are likely rare. Cancer 2000;89:383–90. © 2000 American Cancer Society.

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Ovarian dysplasia in prophylactic oophorectomy specimens

Cited by 100 publications

References 24 publications

Origins and molecular pathology of ovarian cancer

Origins and molecular pathology of ovarian cancer

A candidate precursor to pelvic serous cancer (p53 signature) and its prevalence in ovaries and fallopian tubes from women with BRCA mutations

Absence of premalignant histologic, molecular, or cell biologic alterations in prophylactic oophorectomy specimens fromBRCA1 heterozygotes

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