Histological Features of the Contralateral Ovary in Patients with Unilateral Ovarian Cancer: A Case Control Study

Tresserra, F.; Grases, Pedro; Labastida, R; Ubeda, Alicia

doi:10.1006/gyno.1998.5185

Cited by 41 publications

(32 citation statements)

References 14 publications

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“…A few such studies have shown an increase in the number of inclusion cysts in prophylactic oophorectomy specimens 15 and in ovaries contralateral to ovarian carcinoma, 25 others have failed to confirm these findings. 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.…”

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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“…26 For clinical applications, the ability to view the surface of the epithelial layer and a layer 50 to 100 μm below the surface can provide clinicians important information of tissue abnormalities. Therefore, the system is optimized, so the image of the tissue surface and depth takes up half the aperture of the camera and determines the maximum field of view (FOV) of the system when one camera is used.…”

Section: Ovary Imaging Requirementsmentioning

confidence: 99%

Volume holographic imaging endoscopic design and construction techniques

et al. 2017

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Abstract. A reflectance volume holographic imaging (VHI) endoscope has been designed for simultaneous in vivo imaging of surface and subsurface tissue structures. Prior utilization of VHI systems has been limited to ex vivo tissue imaging. The VHI system presented in this work is designed for laparoscopic use. It consists of a probe section that relays light from the tissue sample to a handheld unit that contains the VHI microscope. The probe section is constructed from gradient index (GRIN) lenses that form a 1:1 relay for image collection. The probe has an outer diameter of 3.8 mm and is capable of achieving 228.1 lp∕mm resolution with 660-nm Kohler illumination. The handheld optical section operates with a magnification of 13.9 and a field of view of 390 μm × 244 μm. System performance is assessed through imaging of 1951 USAF resolution targets and soft tissue samples. The system has also passed sterilization procedures required for surgical use and has been used in two laparoscopic surgical procedures.

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“…Notre définition d'atypies ovariennes se base sur les précé-dentes études de dysplasie ovarienne, à savoir, la dysplasie décrite dans les ovaires à risque génétique (ovariectomie prophylactique pour mutation BRCA 1 ou 2) [4][5][6], dans les zones « saines » adjacentes à un cancer de l'ovaire [7,8], dans l'ovaire controlatéral « d'allure saine » à un cancer de l'ovaire unilatéral [9,10] et dans les ovaires stimulés [11]. Afin que la méthodologie soit reproductible, nous avons retenu 11 critères histopathologiques évalués lors de précé-dentes études, à la fois sur les ovaires à risque génétique et les ovaires stimulés [12,13] :…”

Section: Critères Histopathologiquesunclassified