The pathological assessment of ovarian neoplasms. i: introduction to the common ‘epithelial’ tumours and analysis of benign ‘epithelial’ tumours

Russell, Peter

doi:10.3109/00313027909063533

Cited by 140 publications

(51 citation statements)

References 30 publications

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“…Although isolated examples of serous and mucinous carcinoma have been reported to originate in endometriosis, the association of these tumors in general with that disorder is not significant. Russell 104 found only a 2.5% frequency of pelvic endometriosis in 163 cases of serous carcinoma and a 6% frequency in 17 cases of mucinous carcinoma; and Aure et al 99 detected no ovarian endometriosis in 283 cases of serous carcinoma and only an 0.8% frequency, in 203 cases of mucinous carcinoma. Rutgers and Scully, 109 however, reported the finding of ovarian endometriosis in 30% of cases of mucinous borderline tumors of endocervical-like (Mü llerian) type, which accounted for 15% of the mucinous borderline tumors in their series; in contrast, there was no significant association of ovarian endometriosis and the more common mucinous borderline tumor of intestinal type.…”

Section: Morphologic Datamentioning

confidence: 96%

“…Ipsilateral ovarian endometriosis has been detected in 11-31%, ovarian endometriosis of unspecified laterality in 9-20%, and pelvic endometriosis in 11-28% of cases of ovarian endometrioid carcinoma. 96,[99][100][101][102][103][104][105][106][107] Well-differentiated or low-grade endometrioid ovarian carcinomas are associated with an especially high frequency of associated endometriosis (63%) or endometrioid adenofibromas (47%). 108 Russell 104 reported a 47% frequency of pelvic endometriosis in 30 cases of clear cell carcinoma of the ovary, and Aure et al 99 demonstrated a 24% frequency of ovarian endometriosis in 59 cases of the same type of tumor; both of those figures were surprisingly higher than the figures given by the same authors for the association of endometriosis with endometrioid carcinoma (28 and 9%, respectively).…”

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: 96%

Section: Morphologic Datamentioning

confidence: 99%

Origins and molecular pathology of ovarian cancer

2005

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“…Histopathologic diagnoses were based on WHO criteria; 25 tumor grades were based on GOG criteria (see introduction); and disease stages were assessed according to the FIGO system. [26][27][28][29][30] Diseasespecific survival rates were calculated as the percentage of subjects who survived with the disease for a defined period (reported as time since diagnosis), and only deaths from the disease were counted. Time to progression (disease-free survival) was defined as the interval from the date of treatment initiation until the disease progression was clinically evidenced by a 25% or greater increase in tumor size, appearance of new lesions, or a rise of serum CA 125 level to more than twice the upper limit of normal.…”

Section: Patient Selectionmentioning

confidence: 99%

Low membranous expression of β-catenin and high mitotic count predict poor prognosis in endometrioid carcinoma of the ovary

et al. 2010

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Mutations in the b-catenin gene are common in ovarian endometrioid carcinoma. Few studies have addressed the association of b-catenin expression with tumor characteristics and patient outcome, yielding controversial results. The purpose of this study was to retrospectively assess the expression of b-catenin in ovarian endometrioid carcinoma and correlate its expression with the Gynecologic Oncology Group's (GOG) grading system, clinicopathological characteristics, and patient survival. A total of 49 patients with primary ovarian endometrioid carcinoma were included in this study. A four-tier score grading system was used for the membranous staining (negative, weak, moderate, and strong) and the percentage of positive cells for the nuclear staining of b-catenin. The status of five morphometric parameters, nuclear morphology (uniform or pleomorphic), mitotic count, glandular pattern, degree of squamous differentiation, and status of papillary pattern, was assessed. We found that a low membranous expression of b-catenin and a high mitotic count (415 per 10 high-power fields) were significantly associated with poor prognosis and early recurrence of ovarian endometrioid carcinoma. In addition, cases with nuclear expression of b-catenin showed an intermediate overall survival risk and late disease recurrence. Young age at the time of diagnosis, advanced disease stage, and suboptimal debulking were among the clinical factors predicting poor survival and early disease recurrence. The presence of squamous differentiation, a papillary pattern or nuclear pleomorphism did not show any correlation with overall survival or disease-free survival. Low membranous expression of b-catenin and high mitotic count are poor prognostic indicators in patients with ovarian endometrioid carcinoma, whereas the GOG grading system showed no prognostic value. Our data suggest that there is a need to define a better grading system for ovarian endometrioid carcinoma. Molecular markers such as b-catenin and mitotic count could aid in defining this grading system.

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“…Samples used in this study were from patients with primary epithelial ovarian cancers who had undergone initial surgery at [20][21][22][23][24] Diseasespecific survival rates were calculated as the percentage of patients who survived with disease for a defined period, reported as time since diagnosis or treatment, and only deaths from the disease were counted.…”

Section: Patient Samplesmentioning

confidence: 99%

Insulin-like growth factor-binding protein 2 and 5 are differentially regulated in ovarian cancer of different histologic types

et al. 2006

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The family of insulin-like growth factor-binding proteins (IGFBPs) comprises six members, which bind and regulate the functions of insulin-like growth factors. Overexpression of IGFBP2 and IGFBP5 contributes to the invasiveness and progression of several human cancers, but their role and clinical significance in ovarian cancer has not been investigated in detail. We examined IGFBP2 and IGFBP5 expression levels using two tissue microarrays, one containing six normal surface epithelium, six benign serous cysts, 10 serous borderline tumors, eight low-grade, and 20 high-grade serous carcinomas. The other comprising 441 ovarian cancers of different histologic types linked to a clinicopathologic database. Each tumor was sampled in duplicate with a 1.0-mm punch core needle. Immunohistochemical staining was performed using antibodies against IGFBP2 or IGFBP5. The staining intensity was scored semiquantitatively as negative (0), weak (1-10%), moderate (10-50%), or strong (50-100%) using computerized image analysis. Statistical analyses used Fisher's exact test and Kaplan-Meier method. IGFBP2 and IGFBP5 were overexpressed in high-grade serous carcinomas compared to normal surface epithelium, benign serous cysts, serous borderline tumors, or low-grade serous carcinoma. They were differentially expressed in different types of ovarian carcinomas, being more often expressed at high levels in high-grade serous carcinoma, malignant mixed mullerian tumors and undifferentiated carcinoma, and more often expressed at low levels or not at all in clear cell and mucinous carcinomas. We concluded that IGFBP2 and IGFBP5 might play a role in the development of high-grade ovarian serous carcinoma, but not in mucinous or clear cell ovarian carcinomas.

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The pathological assessment of ovarian neoplasms. i: introduction to the common ‘epithelial’ tumours and analysis of benign ‘epithelial’ tumours

Cited by 140 publications

References 30 publications

Origins and molecular pathology of ovarian cancer

Origins and molecular pathology of ovarian cancer

Low membranous expression of β-catenin and high mitotic count predict poor prognosis in endometrioid carcinoma of the ovary

Insulin-like growth factor-binding protein 2 and 5 are differentially regulated in ovarian cancer of different histologic types

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