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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Inhibition of BCL6-dependent gene expression in Philadelphia chromosome positive acute lymphoblastic leukemia

ABSTRACT: The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. Tyrosine kinase inhibitors (TKI) are widely used to treat patients with leukemia driven by BCR-ABL1 and other oncogenic tyrosine kinases. In response to TKI-treatment, BCR-ABL1 ALL cells upregulate BCL6 protein levels by ~90-fold, i.e. to similar levels as in diffuse large B cell lymphoma (DLBCL) with BCL6 translocations. In this study, we analyzed the gene expression changes after treatment with Imatinib or Imatinib + RI-BPI. Three Ph+ ALL cell lines (BV-173, SUP-B15 and TOM-1) were treated in the presence or absence of 10 μM STI571 (Imatinib) or in the presence of both 10 μM STI571 and 20 μM RI-BPI for 24 hours.

ORGANISM(S): Homo sapiens

SUBMITTER: Markus Müschen

PROVIDER: E-GEOD-24381 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inhibition of BCL6-dependent gene expression in Philadelphia chromosome positive acute lymphoblastic leukemia

Project description:The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. Tyrosine kinase inhibitors (TKI) are widely used to treat patients with leukemia driven by BCR-ABL1 and other oncogenic tyrosine kinases. In response to TKI-treatment, BCR-ABL1 ALL cells upregulate BCL6 protein levels by ~90-fold, i.e. to similar levels as in diffuse large B cell lymphoma (DLBCL) with BCL6 translocations. In this study, we analyzed the gene expression changes after treatment with Imatinib or Imatinib + RI-BPI.

2011-03-01 | GSE24381 | GEO

Recruitment of BCL6 to target genes in Philadelphia chromosome positive acute lymphoblastic leukemia

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Project description:To identify differences in the gene regulation between BCL6+/+ and BCL6-/- CML cells a gene expression analysis has been performed. We investigated the gene expression pattern in BCL6+/+ cells in the presence or absence of Imatinib and a combination of Imatinib and RI-BPI (a novel retro-inverso BCL6 peptide inhibitor). In BCL6-/- CML cells, we investigated the gene expression pattern in the presence or absence of Imatinib. BCR-ABL1 transformed myeloid cells from BCL6+/+ mice were cultured in the presence or absence of 10µM Imatinib or 10µM Imatinib and 20µM RI-BPI for 16 hours. BCR-ABL1 transformed myeloid cells from BCL6-/- mice were cultured in the presence or absence of 10µM Imatinib. Two samples for each condition were processed.

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Effect of imatinib on philadelphia chromosome positive acute lymphoblastic leukemia

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2010-09-10 | E-GEOD-23743 | biostudies-arrayexpress

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Gene expression data of interleukin-7-dependent and BCR-ABL1-transformed pre-B cells

Project description:This analysis focused on identifying factors that protect pre-B cells against DNA double strand break (DSB)-mediated DNA damage stress during pre-B cell differentiation. Differentiation of pre-B cells including immunoglobulin light chain gene recombination were performed by withdrawal of interleukin-7 (IL-7) from IL-7-dependent murine pre-B cells or by inhibition of the BCR-ABL1 kinase activity in BCR-ABL1-transformed pre-B cells. The BCR-ABL1 kinase inhibitor STI571 (Imatinib) was used for the inhibition of BCR-ABL1. IL-7-dependent murine pre-B cells were either cultured in IL-7 (10 ng/ml) or induced to differentiate by withdrawal of IL-7. BCR-ABL1-transformed pre-B cells were either treated with 10 ÂµM STI571 (in absence or presence of 10 ng/ml IL-7) for 16 hours or cultured without STI571. Three samples for each condition were processed.

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