Overexpression of p34 cdc2 Protein Kinase in Epithelial Ovarian Carcinoma

To investigate the role of expression of p34cdc2 protein kinase in normal, benign, and malignant ovarian epithelium. Tissue sections from 24 patients with epithelial ovarian carcinoma (EOC) along with 6 normal ovarian specimens and 12 benign cystadenomas were incubated with mouse IgG monoclonal anti...

Full description

Saved in:
Bibliographic Details
Published inMayo Clinic proceedings Vol. 72; no. 10; pp. 925 - 929
Main Authors Barrette, Brigitte A., Srivatsa, Preeti J., Cliby, William A., Keeney, Gary L., Suman, Vera J., Podratz, Karl C., Roche, Patrick C.
Format Journal Article
LanguageEnglish
Published Elsevier Inc 01.10.1997
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:To investigate the role of expression of p34cdc2 protein kinase in normal, benign, and malignant ovarian epithelium. Tissue sections from 24 patients with epithelial ovarian carcinoma (EOC) along with 6 normal ovarian specimens and 12 benign cystadenomas were incubated with mouse IgG monoclonal antibody to human p34cdc2 protein kinase, followed by detection with use of a standard peroxidase labeled streptavidin-biotin technique. Immunohistochemical staining was graded and compared. Clinical data were also reviewed. Normal surface epithelium and 10 of 12 benign cystadenomas failed to stain for p34cdc2 protein kinase. Of the 24 EOC specimens, however, 19 (79%) stained positively. The staining pattern or intensity was not associated with the histologic grade or surgical stage. Expression of p34cdc2 protein kinase is strongly up-regulated in most cases of EOC but not in normal epithelial ovarian tissue or in most cases of benign epithelial tumors evaluated. Therefore, it may be associated with early events in careinogenesis. Redundant overexpression of cyclin-dependent kinases such as p34cdc2 may contribute to deranged cell cycle progression and proliferation of EOC. Observation of overexpression of p34cdc2 protein kinase in other malignant lesions suggests a common mechanism.
ISSN:0025-6196
1942-5546
DOI:10.4065/72.10.925