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The cyclin-dependent kinase inhibitor p57(Kip2) is epigenetically regulated in carboplatin resistance and results in collateral sensitivity to the CDK inhibitor seliciclib in ovarian cancer.

Coley, HM, Safuwan, NA, Chivers, P, Papacharalbous, E, Giannopoulos, T, Butler-Manuel, S, Madhuri, K, Lovell, DP and Crook, T (2012) The cyclin-dependent kinase inhibitor p57(Kip2) is epigenetically regulated in carboplatin resistance and results in collateral sensitivity to the CDK inhibitor seliciclib in ovarian cancer. Br J Cancer, 106 (3). 482 - 489.

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Abstract

Carboplatin remains a first-line agent in the management of epithelial ovarian cancer (EOC). Unfortunately, platinum-resistant disease ultimately occurs in most patients. Using a novel EOC cell line with acquired resistance to carboplatin: PEO1CarbR, genome-wide micro-array profiling identified the cyclin-dependent kinase inhibitor p57(Kip2) as specifically downregulated in carboplatin resistance. Presently, we describe confirmation of these preliminary data with a variety of approaches.

Item Type: Article
Additional Information: British Journal of Cancer (2012) 106, 482 – 489 & 2012 Cancer Research UK All rights reserved 0007 – 0920/12
Uncontrolled Keywords: Antineoplastic Agents, Carboplatin, Cell Line, Tumor, Cyclin-Dependent Kinase Inhibitor p27, DNA Methylation, Dose-Response Relationship, Drug, Down-Regulation, Drug Resistance, Neoplasm, Epigenesis, Genetic, Female, Humans, Ovarian Neoplasms, Purines
Divisions: Faculty of Health and Medical Sciences > Biochemistry and Physiology
Depositing User: Symplectic Elements
Date Deposited: 29 Jun 2012 09:19
Last Modified: 23 Sep 2013 19:32
URI: http://epubs.surrey.ac.uk/id/eprint/711605

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