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Gene expression and copy number analysis of OVCAR-3 and CDK2 resistant sublines

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Dariush Etemadmoghadam

PROVIDER: E-GEOD-48921 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

<h4>Purpose</h4>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.<h4>Experimen ...[more]

PMID: 24004674

Similar Datasets

Copy number analysis of OVCAR-3 and CDK2 resistant sublines

Project description: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).

2013-09-01 | E-GEOD-48920 | biostudies-arrayexpress

Gene expression analysis of OVCAR-3 and CDK2 resistant sublines

Project description: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 gene expression microarrays. Arrayed samples included parental OVCAR-3 cells (n = 4 replicates) 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) and after continued passage in the absence of inhibitor (P10+).

2013-09-01 | E-GEOD-48919 | biostudies-arrayexpress

Genomic analysis of low-grade serous ovarian carcinomas

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-01 | E-GEOD-57280 | biostudies-arrayexpress

Genomic analysis of low-grade serous ovarian carcinomas [ILOEF]

Project description:Low-grade serous ovarian carcinomas are typically Ras-pathway mutated, TP53 wild-type, have limited chromosomal aberration, and are frequently associated with borderline tumors. By contrast, high-grade serous ovarian carcinoma lack Ras-pathway mutations, are invariably TP53 mutated, show widespread genomic change, and are commonly BRCA-pathway disrupted.We sought to identify differences in genomic copy number changes between co-existing borderline and invasive components of serous carcinoma. Paired co-existing borderline and invasive tumor components were sampled and profiled from formalin-fixed paraffin embedded tumors from 6 patients

2014-10-01 | E-GEOD-57276 | biostudies-arrayexpress

Genomic analysis of low-grade serous ovarian carcinomas [ILOE]

Project description:Low-grade serous ovarian carcinomas are typically Ras-pathway mutated, TP53 wild-type, have limited chromosomal aberration, and are frequently associated with borderline tumors. By contrast, high-grade serous ovarian carcinoma lack Ras-pathway mutations, are invariably TP53 mutated, show widespread genomic change, and are commonly BRCA-pathway disrupted. We sought to identify differences in genomic copy number changes in borderline and invasive components of serous carcinoma. Borderline and invasive tumor components were profiled from patients with LGSC

2014-10-01 | E-GEOD-57270 | biostudies-arrayexpress

Genomic analysis of low-grade serous ovarian carcinomas [IL610Q]

Project description:Low-grade serous ovarian carcinomas are typically Ras-pathway mutated, TP53 wild-type, have limited chromosomal aberration, and are frequently associated with borderline tumors. By contrast, high-grade serous ovarian carcinoma lack Ras-pathway mutations, are invariably TP53 mutated, show widespread genomic change, and are commonly BRCA-pathway disrupted. We sought to identify differences in genomic copy number changes between co-existing borderline and invasive components of serous carcinoma. Paired co-existing borderline and invasive tumor components of ovarian serous carcinoma were sampled and profiled from tumors from 7 patients

2014-10-01 | E-GEOD-57279 | biostudies-arrayexpress

Copy number analysis of OVCAR-3 and CDK2 resistant sublines

2013-09-01 | GSE48920 | GEO

Gene expression analysis of OVCAR-3 and CDK2 resistant sublines

2013-09-01 | GSE48919 | GEO

Genome-wide mapping of crossovers in all products of adult, single human female meioses reveals structural rearrangements of chromosomes and meiotic drive for recombinant chromatids

Project description:Meiotic recombination promotes genomic diversity by generating new combinations of alleles, while at the same time, maintaining genome stability by preventing chromosome missegregation and aneuploidy, such as Down Syndrome. We report here the first genome-wide maps of meiotic recombination in the human female meiosis. By utilizing information from all three meiotic products (oocyte, polar body 1 and polar body 2), our data reveal crossover rates that are in great excess (~40%) of recombination rate estimates from population-based studies. Recovery of all three meiotic products allowed us to identify structural defects to meiotic chromosomes that originate during meiosis, as well as true meiotic drive at meiosis II for the preferential exclusion of non-recombinant chromatids from the oocyte. Finally, we identify a novel chromosome segregation pattern reminiscent of 'inverted meiosis' that leads to chromosomally-balanced oocytes. The three products of meiosis from 13 oocytes and the gDNA from the five donors were analysed (total of 44 samples). Blank (negative) and positive (genomic DNA) control samples were provided for each DNA amplifiction run. No replicates were included as they were not available. No external references were included.

2015-03-01 | E-GEOD-53539 | biostudies-arrayexpress

DNA methylation profiles of freshly isolated CD34+ cells and upon expansion on either tissue culture plastic (TCP) or mesenchymal stromal cells (MSCs)

Project description:Hematopoietic stem and progenitor cells (HPCs) can be maintained in vitro, but the vast majority of their progeny loses M-bM-^@M-^\stemnessM-bM-^@M-^] during culture. In this study, we have analyzed DNA methylation (DNAm) profiles of freshly isolated CD34+ cells and upon expansion on either tissue culture plastic (TCP) or mesenchymal stromal cells (MSCs). DNAm profiles of expanded CD34+ versus CD34- subsets reflected hematopoietic differentiation, whereas culture on TCP or MSCs had little impact. Notably, all cultured HPCs - even those which remained CD34 positive - acquired significant DNA-hypermethylation, particularly in up-stream promoter regions, shore-regions of CpG islands, and binding sides for PU.1 and RUNX1. Our results point to a coordinated epigenetic process which needs to be controlled to enhance self-renewal of HPCs in vitro. 12 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip

2013-12-03 | E-GEOD-40799 | biostudies-arrayexpress

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