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EphA2 Expression Is Associated with Aggressive Features in Ovarian Carcinoma
Purpose: EphA2 (epithelial cell kinase) is a transmembrane receptor tyrosine kinase that has been implicated in oncogenesis. There are no published data regarding the role of EphA2 in ovarian carcinoma, which is the focus of the present study. Experimental Design: Nontransformed (HIO-180) and ovaria...
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Published in: | Clinical cancer research 2004-08, Vol.10 (15), p.5145-5150 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Purpose: EphA2 (epithelial cell kinase) is a transmembrane receptor tyrosine kinase that has been implicated in oncogenesis. There
are no published data regarding the role of EphA2 in ovarian carcinoma, which is the focus of the present study.
Experimental Design: Nontransformed (HIO-180) and ovarian cancer (EG, 222, SKOV3, and A2780-PAR) cell lines were evaluated for EphA2 by Western
blot analysis. Five benign ovarian masses, 10 ovarian tumors of low malignant potential, and 79 invasive ovarian carcinomas
were also evaluated for EphA2 expression by immunohistochemistry. All samples were scored in a blinded fashion. Univariate
and multivariate analyses were used to determine significant associations between EphA2 expression and clinicopathological
variables.
Results: By Western blot analysis, EG, 222, and SKOV3 cell lines overexpressed EphA2, whereas A2780-PAR and HIO-180 had low to absent
EphA2 expression. All of the benign tumors had low or absent EphA2 expression. Among the invasive ovarian carcinomas examined
(mean age of patients was 59.2 years), 60 (75.9%) tumors overexpressed EphA2 and the other 19 tumors had negative or minimal
EphA2 expression. There was no association of EphA2 overexpression with ascites, likelihood of nodal positivity, pathological
subtype, and optimum surgical cytoreduction (residual tumor |
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ISSN: | 1078-0432 1557-3265 |
DOI: | 10.1158/1078-0432.CCR-03-0589 |