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The Requirement for Cyclin D Function in Tumor Maintenance

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE40512: Gene expression profile of human T-ALL cell line KOPTK1 treated with vehicle or PD 0332991 GSE40513: Gene expression profile of mouse breast cancer V720 cells treated with vehicle or PD 0332991 Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Takaomi Sanda

PROVIDER: E-GEOD-40514 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profile of mouse breast cancer V720 cells treated with vehicle or PD 0332991

Project description:D-cyclins represent components of cell cycle machinery. To test the efficacy of targeting D-cyclins in cancer treatment, we engineered mouse strains which allow acute and global ablation of individual D-cyclins in a living animal. Ubiquitous shutdown of cyclin D1 or inhibition of cyclin D associated kinase activity in mice bearing ErbB2-driven mammary carcinomas halted cancer progression and triggered tumor-specific senescence, without compromising the animals' health. Ablation of cyclin D3 in mice bearing T-cell acute lymphoblastic leukemias (T-ALL) triggered tumorspecific apoptosis. Such selective killing of leukemic cells can be also achieved by inhibiting cyclin D associated kinase activity in mouse and human T-ALL models. Hence, contrary to what one might expect from ablation of a cell cycle protein, acute shutdown of a D-cyclin leads not only to cell cycle arrest, but it also triggers tumor cell senescence or apoptosis, and it affects different tumor types through distinct cellular mechanisms. Inhibiting cyclin D-activity represents a highly-selective anticancer strategy which specifically targets cancer cells without significantly affecting normal tissues. Mouse breast cancer V720 cells were cultured in the presence of the CDK4/6 inhibitor PD 0332991 (PD; 1 microM) or vehicle (VO) for 24 hrs. Experiment was done in biological triplicate. A total of 6 RNA samples (3 vehicle treated and 3 PD 0332991 treated samples) were used for microarray expression analysis.

2012-10-16 | E-GEOD-40513 | biostudies-arrayexpress

Gene expression profile of human T-ALL cell line KOPTK1 treated with vehicle or PD 0332991

Project description:D-cyclins represent components of cell cycle machinery. To test the efficacy of targeting D-cyclins in cancer treatment, we engineered mouse strains which allow acute and global ablation of individual D-cyclins in a living animal. Ubiquitous shutdown of cyclin D1 or inhibition of cyclin D associated kinase activity in mice bearing ErbB2-driven mammary carcinomas halted cancer progression and triggered tumor-specific senescence, without compromising the animals' health. Ablation of cyclin D3 in mice bearing T-cell acute lymphoblastic leukemias (T-ALL) triggered tumorspecific apoptosis. Such selective killing of leukemic cells can be also achieved by inhibiting cyclin D associated kinase activity in mouse and human T-ALL models. Hence, contrary to what one might expect from ablation of a cell cycle protein, acute shutdown of a D-cyclin leads not only to cell cycle arrest, but it also triggers tumor cell senescence or apoptosis, and it affects different tumor types through distinct cellular mechanisms. Inhibiting cyclin D-activity represents a highly-selective anticancer strategy which specifically targets cancer cells without significantly affecting normal tissues. A human T-ALL cell line KOPTK1 cells were cultured in the presence of the CDK4/6 inhibitor PD 0332991 (PD; 1 microM) or vehicle (VO) for 48 hrs. Experiment was done in biological triplicate. A total of 6 RNA samples (3 vehicle treated and 3 PD 0332991 treated samples) were used for microarray expression analysis.

2012-10-16 | E-GEOD-40512 | biostudies-arrayexpress

Expression data from vehicle or PD-0332991 treated human T-ALL lines

Project description:Cyclin D3 is critical hematopoiesis and loss of cyclin D3 leads to resistance to transformation of bone marrow progenitors by Notch1-IC. We used a small molecule targeting cyclin D3:CDK4/6 activity to study whether its inhibition is an effective therapeutic strategy. We analyzed T-ALL lines in vitro with PD-0332991 or vehicle control to determine genes affected by the drug. CEM, Jurkat, DND41, and CUTL-1 cell lines were treated with 1 uM PD-0332991 or DMSO for 15 hours prior to RNA extraction and hybridization to Human Genome U133 Plus 2.0 Affymetrix arrays.

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Metabolic re-programming of pancreatic cancer mediated by CDK4/6 inhibition elicits unique vulnerabilities

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CDK4/6 inhibitors in ER positive breast cancers

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2016-08-01 | E-GEOD-80987 | biostudies-arrayexpress

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Single-cell chromatin accessibility data using scATAC-seq

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2015-06-17 | E-GEOD-65360 | biostudies-arrayexpress

PD-1 interacting proteins in Jurkat cells stimulated with Raji cells and SEE - Part3

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PD-1 interacting proteins in SILAC labelled Jurkat cells stimulated with Raji cells - Part4

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