Surrey researchers Sign in
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.
Journal article   Open access  Peer reviewed

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.

HM Coley, NA Safuwan, P Chivers, E Papacharalbous, T Giannopoulos, S Butler-Manuel, K Madhuri, DP Lovell and T Crook
Br J Cancer, Vol.106(3), pp.482-489
31/01/2012

Abstract

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
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.
pdf
BJC_Coley_et_al._2011237.31 kBDownloadView
TextSRIDA Open Access
url
http://dx.doi.org/10.1038/bjc.2011.566View
Published (Version of record)

Metrics

140 File views/ downloads
25 Record Views

Details

Usage Policy