Transcriptomics

Dataset Information

4

Copy number analysis of OVCAR-3 and CDK2 resistant sublines


ABSTRACT: Cyclin E1 (CCNE1) is amplified in various tumor types including high-grade serous ovarian cancer where it is associated with poor clinical outcome. We have demonstrate that suppression of the Cyclin E1 partner kinase, CDK2, induces apoptosis in a CCNE1 amplicon-dependent manner. Little is known of mechanisms of resistance to CDK inhibitors. We therefore generated OVCAR-3 sublines with reduced sensitivity to CDK2 inhibitors and profiled by SNP copy number microarrays. Arrayed samples included parental OVCAR-3 cells and five independently derived sublines resistant to PHA-533533 (OVCAR3-533533-R1, -R3, -R5, -R6, -R7). The resistant cell lines were arrayed after drug selection (P5).

OTHER RELATED OMICS DATASETS IN: E-GEOD-48919

ORGANISM(S): Homo sapiens  

SUBMITTER: Dariush Etemadmoghadam   David Bowtell 

PROVIDER: E-GEOD-48920 | ArrayExpress | 2013-09-01

SECONDARY ACCESSION(S): GSE48920PRJNA212314

REPOSITORIES: GEO, ArrayExpress

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Publications

Resistance to CDK2 inhibitors is associated with selection of polyploid cells in CCNE1-amplified ovarian cancer.

Etemadmoghadam Dariush D   Au-Yeung George G   Wall Meaghan M   Mitchell Chris C   Kansara Maya M   Loehrer Elizabeth E   Batzios Crisoula C   George Joshy J   Ftouni Sarah S   Weir Barbara A BA   Carter Scott S   Gresshoff Irma I   Mileshkin Linda L   Rischin Danny D   Hahn William C WC   Waring Paul M PM   Getz Gad G   Cullinane Carleen C   Campbell Lynda J LJ   Bowtell David D DD  

Clinical cancer research : an official journal of the American Association for Cancer Research 20130904 21


PURPOSE: Amplification of cyclin E1 (CCNE1) is associated with poor outcome in breast, lung, and other solid cancers, and is the most prominent structural variant associated with primary treatment failure in high-grade serous ovarian cancer (HGSC). We have previously shown that CCNE1-amplified tumors show amplicon-dependent sensitivity to CCNE1 suppression. Here, we explore targeting CDK2 as a novel therapeutic strategy in CCNE1-amplified cancers and mechanisms of resistance. EXPERIMENTAL DESIGN  ...[more]

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