Immunohistochemical study of the expression of adhesion molecules in ovarian serous neoplasms

Cho, Eun Yoon; Choi, Yoon‐La; Chae, Seoung Wan; Sohn, Jin Hee; Ahn, Geung Hwan

doi:10.1111/j.1440-1827.2006.01925.x

Cited by 81 publications

(77 citation statements)

References 39 publications

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“…Increased CD56 expression has been associated with a more aggressive form of solid tumors, such as lung, ovarian, and renal cell, and in hematopoietic malignancies-lymphoblastic and myeloid leukemias (37,(43)(44)(45). CD56 over expression in ES may contribute to the aggressiveness of this childhood tumor.…”

Section: Discussionmentioning

confidence: 99%

Excellent Prognosis in a Subset of Patients with Ewing Sarcoma Identified at Diagnosis by CD56 Using Flow Cytometry

Ash

Luria

Cohen

et al. 2011

Clinical Cancer Research

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Purpose: Ewing sarcoma (ES) is considered a systemic disease with the majority of patients harboring micrometastases at diagnosis. Multiparameter flow cytometry (MPFC) was used to detect ES cells in bone marrow (BM) of ES patients at diagnosis and to evaluate the prognostic significance of CD56 expression in BM samples.Experimental Design: BM samples from 46 ES patients, 6 tumor aspirates, 2 ES cell lines, and 10 control BM samples were analyzed by MPFC. ES cells were identified by the combination of CD45À/CD90þ/ CD99þ. CD56 was evaluated on these cells by a cutoff of 22%.Results: BM samples obtained from all patients at diagnosis were found to be positive for micrometastatic tumor cells assessed by CD99þ/CD90þ/CD45À expression. A total of 60% of the BM samples harbored high CD56 expression. There was a highly significant correlation between CD56 expression and progression-free survival (PFS; 69% in low/negative expression versus 30% in high expression groups, P ¼ 0.024). In patients with localized nonpelvic disease, those expressing low/negative CD56 had 100% PFS versus 40% in the high expressing group (P ¼ 0.02).

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Section: Discussionmentioning

confidence: 99%

Excellent Prognosis in a Subset of Patients with Ewing Sarcoma Identified at Diagnosis by CD56 Using Flow Cytometry

Ash

Luria

Cohen

et al. 2011

Clinical Cancer Research

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“…In more advanced, poorly differentiated carcinomas, both absent and persistent E-cadherin expression have been reported [16,18,51,59]. While complete loss of E-cadherin expression is uncommon, reduced E-cadherin staining is often detected in late stage carcinomas and in ascites-derived tumor cells [59,62,63]. Correspondingly, ascites cells may be more invasive than paired solid tumor cells from the same patient [60].…”

Section: B Cadherin Expression In Eocmentioning

confidence: 99%

Phenotypic plasticity of neoplastic ovarian epithelium: unique cadherin profiles in tumor progression

Hudson

Zeineldin

Stack

2008

Clin Exp Metastasis

165

172

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The mesodermally derived normal ovarian surface epithelium (OSE) displays both epithelial and mesenchymal characteristics and exhibits remarkable phenotypic plasticity during post-ovulatory repair. The majority of epithelial ovarian carcinomas (EOC) are derived from the OSE and represent the most lethal of all gynecological malignancies, as most patients (~70%) present at diagnosis with disseminated intra-abdominal metastasis. The predominant pattern of EOC metastasis involves pelvic dissemination rather than lymphatic or hematologic spread, distinguishing EOC from other solid tumors. Acquisition of the metastatic phenotype involves a complex series of interrelated cellular events leading to dissociation (shedding) and dispersal of malignant cells. A key event in this process is disruption of cell-cell contacts via modulation of intercellular junctional components. In contrast to most carcinomas that downregulate E-cadherin expression during tumor progression, an unique feature of primary well-differentiated ovarian cancers is a gain of epithelial features, characterized by an increase in expression of E-cadherin. Subsequent reacquisition of mesenchymal features is observed in more advanced tumors with concomitant loss of E-cadherin expression and/ or function during progression to metastasis. The functional consequences of this remarkable phenotypic plasticity are not fully understood, but may play a role in modulation of cell survival in suspension (ascites), chemoresistance, and intraperitoneal anchoring of metastatic lesions. Keywords ovarian cancer; epithelium; cadherin; keratin; vimentin; epithelial-mesenchymal transition; plasticity Ovarian Cancer-OverviewTumors arising from the ovarian epithelium account for ~90% of ovarian malignancies and epithelial ovarian carcinoma (EOC) is the leading cause of death from gynecologic malignancy, resulting in approximately 15,280 deaths in the United States alone in 2006 [1]. These distressing statistics are largely due to the low detection rate of disease confined to the ovary (stage 1) when 5-year survival is >90%. Approximately 75% of women are initially diagnosed with disseminated intra-abdominal disease (stage III-IV) and have a 5-year survival of <20%.Ovarian tumors are pathologically heterogeneous with four major histotypes: serous, endometroid, clear cell and mucinous. These classifications are histogenetically based on The early steps of EOC metastasis involve shedding of the cells from the primary tumor to form free floating cells or multi-cellular aggregates (MCAs) in ascites [ Fig. 1]. Cell-cell and cell-matrix adhesion molecules mediate interaction of metastasizing tumor cells with mesothelial cells lining the inner surface of the peritoneal cavity and the sub-mesothelial extracellular matrix (ECM). Localized proteolytic degradation of sub-mesothelial ECM components facilitates migration of tumor cells and anchoring of secondary lesions on adjacent pelvic organs, and at later stages, metastasis to distant organs [9,10]. However, the majority of wo...

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“…Repression of E-cadherin has been described in a high percentage of borderline ovarian tumors and carcinomas when compared with benign tumors. Moreover, ascites cells with low E-cadherin expression were found to be more invasive than solid tumor cells (23). This initial shift towards a more differentiated phenotype early in tumor progression appears to be followed by reacquisition of mesenchymal features in more advanced ovarian tumors, involving a secondary loss of E-cadherin (24).…”

Section: Introductionmentioning

confidence: 96%

Alteration of epithelial-mesenchymal transition markers in human normal ovaries and neoplastic ovarian cancers

Kim

et al. 2014

International Journal of Oncology

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Abstract. Most ovarian cancers originate in the ovarian surface epithelium (OSE). Ovarian cancers might undergo epithelial-mesenchymal transition (EMT) in response to various mediators or regulators such as EMT-inducing factors. In this study, ovarian tumor specimens from patients were analyzed to demonstrate alteration of EMT-related markers according to benign and malignant types of ovarian cancers. In the three ovarian cancer cell lines, OVCAR-3, SKOV-3, and BG-1, the expression of epithelial (E-cadherin) and mesenchymal (vimentin) cell markers was identified by RNA and protein analysis. OVCAR-3 and BG-1 cells strongly expressed E-cadherin as well as morphological features such as epithelial cells, but vimentin was not observed. In contrast to these cancer cells, SKOV-3 showed a typical phenotype of mesenchymal cells. Alteration of EMT markers and EMT-related transcriptional factors were confirmed in clinical ovarian tissue samples obtained from 74 patients. E-cadherin was expressed in 57.1% of benign tumors, while vimentin was expressed in 83.3% of normal ovaries by western blot analysis in the tissue specimens. Evaluation of the EMT-associated transcriptional factors Snail, Slug, and Twist revealed that Snail was overexpressed by 7.1-fold in malignant ovarian cancer compared to normal ovaries or benign tumors. Although expression levels of other factors were higher in benign and malignant ovarian tumors, they were not closely correlated with the aforementioned ovarian cancer types. Overall, Snail may affect the EMT process in ovarian cancer development and upregulation of Snail expression followed by the downregulation of E-cadherin enhances the invasiveness of ovarian cancer. IntroductionEpithelial-mesenchymal transition (EMT) is a critical process in cell differentiation, morphogenesis, growth and change of function (1). EMT is a cellular mechanism recognized as a central feature of normal physiological development such as organogenesis during embryonic development and wound healing (2). Several developmental milestones, including gastrulation, neural crest formation, and heart morphogenesis, rely on the plastic transition between epithelial cells and mesenchymal cells (3). However, dysregulated EMT appears to occur in cancer progression and metastasis, as well as the pathogenesis of chronic degenerative fibrotic disorders in several organs (4). Epithelial and mesenchymal cells differ in function and characteristics. Epithelial cells are closely adjoined by specialized membrane structures such as desmosomes, as well as tight, adherent, and gap junctions, and have apical-basolateral polarization (5). Conversely, mesenchymal cells do not form an organized cell layer, nor do they have the same apical-basolateral organization, polarization of the cell surface molecules (6). In culture, epithelial cells grow in clusters, whereas mesenchymal cells have a spindle shaped and fibroblast-like morphology (7). During the EMT process, epithelial cells are removed of cellular polarity and epithelial cell-cell as well a...

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Immunohistochemical study of the expression of adhesion molecules in ovarian serous neoplasms

Cited by 81 publications

References 39 publications

Excellent Prognosis in a Subset of Patients with Ewing Sarcoma Identified at Diagnosis by CD56 Using Flow Cytometry

Excellent Prognosis in a Subset of Patients with Ewing Sarcoma Identified at Diagnosis by CD56 Using Flow Cytometry

Phenotypic plasticity of neoplastic ovarian epithelium: unique cadherin profiles in tumor progression

Alteration of epithelial-mesenchymal transition markers in human normal ovaries and neoplastic ovarian cancers

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