Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse 32Dcl3 cell lines expressing oncogenic tyrosine kinases or cells treated with small molecule inhibitors


ABSTRACT: Oncogenic tyrosine kinases, such as BCR-ABL, TEL-ABL, TEL-PDGF-beta-R and FLT3-ITD, play a major role in the development of hematopoietic malignancy. They activate many of the same signal transduction pathways. To identify the critical target genes required for transformation in hematopoietic cells, we used a comparative gene expression strategy in which selective small molecules were applied to 32Dcl3 cells that had been transformed to factor-independent growth by these respective oncogenic alleles. Experiment Overall Design: In our microarray study, we have total 22 samples from four different cell lines expressing BCR-ABL, TEL-ABL, FLT3-ITD or TEL-PDGF-betaR. Each cell line was treated with specific small molecule inhibitors for 4 hours, then RNA was extracted and cRNA was hybridized to Affymetrix U74 oligonucleotide arrays. Untreated cells or cells treated with unrelated inhibitors were used as controls or references. We have three replicates and six references obtained from three independent experiments for cells expressing BCR-ABL or FLT3-ITD. We have one treated and one untreated sample for each cell line expressing TEL-ABL or TEL-PDGF-beta-R.

ORGANISM(S): Mus musculus

SUBMITTER: Winnie Tam 

PROVIDER: E-GEOD-11794 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells.

Tam Winnie F WF   Gu Ting-Lei TL   Chen Jing J   Lee Benjamin H BH   Bullinger Lars L   Fröhling Stefan S   Wang Andrew A   Monti Stefano S   Golub Todd R TR   Gilliland D Gary DG  

Blood 20080617 5


Oncogenic tyrosine kinases, such as BCR-ABL, TEL-ABL, TEL-PDGFbetaR, and FLT3-ITD, play a major role in the development of hematopoietic malignancy. They activate many of the same signal transduction pathways. To identify the critical target genes required for transformation in hematopoietic cells, we used a comparative gene expression strategy in which selective small molecules were applied to 32Dcl3 cells that had been transformed to factor-independent growth by these respective oncogenic alle  ...[more]

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