A survey of epithelial inclusions in the ovarian cortex of 470 patients

Mulligan, R. M.

doi:10.1002/jso.2930080110

Cited by 11 publications

(3 citation statements)

References 18 publications

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“…One difference is the apparent broader range of p73 immunostaining, which can be seen in cells without conspicuous cilia, a feature more commonly encountered in the SBTs. This mixed phenotype is also characteristic of Müllerian inclusions in the ovarian cortex, which were also present in the cases immunostained and presumably give rise to SBTs (5,12,14,21). Whether this benign ovarian “precursor” condition is derived from the fallopian tube or via mesothelial-to-Müllerian trans-differentiation of the ovarian surface lining is controversial (1).…”

Section: Discussionmentioning

confidence: 70%

Fallopian Tube Correlates of Ovarian Serous Borderline Tumors

Laury

Ning

Quick

et al. 2011

American Journal of Surgical Pathology

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Ovarian serous borderline tumors (SBTs) are presumed to originate in the ovarian cortex or peritoneal surface. The pathogenetic role of the fallopian tube (FT) is unclear but recently, secretory cell outgrowths (SCOUTs) lacking PAX2 expression have been described in benign FTs. This study addressed 1) the differentiation characteristics of SBTs, 2) the frequency of SCOUTs lacking PAX2 expression in the fallopian tubes of patients with SBTs, and compared 3) SCOUT morphology and 4) PAX2 expression with SBTs. SBTs and FT epithelium shared both ciliated (p73) and secretory (HMFG2) differentiation. PAX2-null SCOUT frequency in FT cross sections from patients with SBTs was 0.27 (110/398) versus 0.09 in benign hysterectomies and nearly zero in pediatric and post partum sterilization specimens. (p=<0.001). When adjusted for age, the differences narrowed but remained significant (p = 0.010). SCOUTs were heterogenous, some displaying ciliated differentiation and papillary architecture. Two cases of discrete multi-focal papillary SCOUTs in the fallopian tube were associated with SBTs. All SBTs had heterogeneous PAX2 staining with areas of PAX2 loss. This study shows for the first time that PAX2-null SCOUTs are more common in the oviducts of women with SBTs and that loss of PAX2 expression occurs in most SBTs. These discoveries link both morphologic and functional gene (PAX2) alterations in the oviduct to SBTs, similar to that reported in high grade serous carcinoma. Further study is warranted to clarify the relationship of the oviduct to serous neoplasia.

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Section: Discussionmentioning

confidence: 70%

Fallopian Tube Correlates of Ovarian Serous Borderline Tumors

Laury

Ning

Quick

et al. 2011

American Journal of Surgical Pathology

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“…Limited literature exists regarding the possible features of a precursor lesion for ovarian carcinoma. Histologically, ovarian surface epithelial cells occasionally may be seen trapped within stromal cells of the ovarian cortex, probably resulting from the process of ovulatory repair; related phenomena of epithelial‐lined clefts and inclusion cysts in the ovarian cortex are more commonly seen and likely result from postovulation wound repair and, possibly, changes in the ovarian contour associated with pregnancy or aging 4–6. Results from several observational studies have led to the hypothesis that dysplasia or hyperplasia arising within these epithelial inclusion cysts may represent a histologic precursor to ovarian carcinoma 7–10.…”

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confidence: 99%

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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“…( v ) (vi) Difficulties caused by the tendency of proliferating mucinous epithelium to develop an enteroid change with argentaffin cells (Fenoglio, Ferenczy & Richart 1975, 1976 and occasionally Paneth cells (Michelany 1948) rather than the hormonesensitive cervical-type reserve cells, and by the current view that Brenner tumours are composed of urothelium (Roth 1974), which is neither Mullerian nor coelomic in origin, need not be elaborated, as the present article throws no direct light on them.…”

Section: Introductionmentioning

confidence: 99%

Benign endometrioid tumours of the ovary and the Müllerian concept of ovarian epithelial tumours

Hughesdon

1984

Histopathology

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The difficulties of a consistent Müllerian interpretation of the epithelial ovarian tumours include their inconstant hormonal responsiveness, the doubtful nature of the clear cell tumour and the apparent rarity of benign endometrioid forms. The reported frequency figures for the different types of endometrioid tumour suggest that their nature is made evident by proliferation. The appearance of indolent forms is explored by a study of inactive neoplastic areas associated with endometrioid carcinomas, or with proliferating endometrioid tumours or arising in endometriosis. These jointly suggest that most such tumours are identical with inactive ‘serous’ adenofibromas of glandular pattern and have senile endometrium as their prototype. Increasing proliferation develops more overt endometrioid forms which, if luxuriant, may be associated with corpus carcinoma. The endometrium of pregnancy is probably the prototype of the clear cell tumour, with a corresponding range of cell types. There is tenuous evidence that tumours may respond to steroid hormones if they arise in endometriosis and a difficulty of deducing such an origin is noted. The term ‘serous’ may be generic and comprise several different tissue types.

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A survey of epithelial inclusions in the ovarian cortex of 470 patients

Cited by 11 publications

References 18 publications

Fallopian Tube Correlates of Ovarian Serous Borderline Tumors

Fallopian Tube Correlates of Ovarian Serous Borderline Tumors

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

Benign endometrioid tumours of the ovary and the Müllerian concept of ovarian epithelial tumours

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