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Analysis of cyclin E and CDK2 in ovarian cancer: Gene amplification and RNA overexpression
Author(s) -
Marone Maria,
Scambia Giovanni,
Giannitelli Cecilia,
Ferrandina Gabriella,
Masciullo Valeria,
Bellacosa Alfonso,
BenedettiPanici Pierluigi,
Mancuso Salvatore
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19980105)75:1<34::aid-ijc6>3.0.co;2-2
Subject(s) - cyclin dependent kinase 2 , cyclin e , cyclin dependent kinase , cyclin d , cancer research , cyclin a2 , biology , cyclin a , cyclin , cyclin e1 , ovarian cancer , cyclin b , cell cycle , microbiology and biotechnology , cancer , genetics
Cyclins and their associated kinases (cdks) play a key role in controlling the cell cycle, a process whose disregulation can potentially lead to uncontrolled cell growth and hence to cancer. We have studied the role of both cyclin E and its associated kinase cdk2 in ovarian cancer. Primary, metastatic, recurrent and benign ovarian tumors were screened for cyclin E and cdk 2 gene amplification. Cyclin E was shown to be amplified in 21% and cdk 2 in 6.4% of the cases analyzed. Cyclin E and cdk2 RNA expression levels were determined by semi‐quantitative RT‐PCR analysis in a partially overlapping series of samples and compared to the expression levels of normal ovarian surface epithelial cells. Cyclin E RNA was overexpressed in 29.5% and cdk2 in 6.5% of ovarian tumors tested. We determined that in most cases gene amplification leads to higher RNA levels for cyclin E and that the overall levels of cyclin E and cdk2 RNA were correlated. We hypothesize that cyclin E and cdk2 are, in part co‐regulated and that they may concur to ovarian tumor development. Int. J. Cancer 75:34–39, 1998.© 1998 Wiley‐Liss, Inc.