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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression data of BCR-ABL1 transformed B cell precursors from BCL6 wild-type and BCL6 knockout mice

ABSTRACT: To elucidate the mechanism of BCL6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed BCL6+/+ and BCL6-/- B cell precursors. Pharmacological inhibition of BCR-ABL1 was performed with the BCR-ABL1 kinase inhibitor STI571 (Imatinib). BCR-ABL1 transformed B cell precursors of BCL6 wildtype and BCL6 knockout mice were either treated with 10ÂµM STI571 (Imatinib) for 16 hours or cultured in absence of STI571. Three samples for each condition were processed.

ORGANISM(S): Mus musculus

SUBMITTER: Jose Polo

PROVIDER: E-GEOD-20987 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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BCL6-mediated repression of p53 is critical for leukemia stem cell survival in chronic myeloid leukemia.

Hurtz Christian C Hatzi Katerina K Cerchietti Leandro L Braig Melanie M Park Eugene E Kim Yong-mi YM Herzog Sebastian S Ramezani-Rad Parham P Jumaa Hassan H Müller Martin C MC Hofmann Wolf-Karsten WK Hochhaus Andreas A Ye B Hilda BH Agarwal Anupriya A Druker Brian J BJ Shah Neil P NP Melnick Ari M AM Müschen Markus M

The Journal of experimental medicine 20110912 11

Chronic myeloid leukemia (CML) is induced by the oncogenic BCR-ABL1 tyrosine kinase and can be effectively treated for many years with tyrosine kinase inhibitors (TKIs). However, unless CML patients receive life-long TKI treatment, leukemia will eventually recur; this is attributed to the failure of TKI treatment to eradicate leukemia-initiating cells (LICs). Recent work demonstrated that FoxO factors are critical for maintenance of CML-initiating cells; however, the mechanism of FoxO-dependent ...[more]

PMID: 21911423

Publication: 1/5

Similar Datasets

Gene expression data of BCR-ABL1 transformed B cell precursors from BCL6 wild-type and BCL6 knockout mice

Project description:To elucidate the mechanism of BCL6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed BCL6+/+ and BCL6-/- B cell precursors. Pharmacological inhibition of BCR-ABL1 was performed with the BCR-ABL1 kinase inhibitor STI571 (Imatinib).

2010-05-10 | GSE20987 | GEO

Gene expression data of BCR-ABL1 transformed myeloid cells from BCL6 wild-type and BCL6 knockout mice treated with and without Imatinib and RI-BPI

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.

2011-08-23 | E-GEOD-24813 | biostudies-arrayexpress

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.

2010-05-27 | E-GEOD-21664 | biostudies-arrayexpress

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. 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.

2011-03-01 | E-GEOD-24381 | biostudies-arrayexpress

Recruitment of BCL6 to target genes 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 used genome tiling arrays to identify BCL6 target genes with specific recruitment of BCL6. Three Ph+ ALL cell lines (BV-173, NALM-1 and TOM-1) in duplicate were either treated with 10µM STI571 (Imatinib) for 24 hours or cultured in absence of STI571.

2011-02-15 | E-GEOD-24404 | biostudies-arrayexpress

Effect of Bach2 overexpression in BCL6+/+ and -/- BCR-ABL1 transformed pre-B cells

Project description:The aim was to investigate how BCL6 genotype affects Bach2 dependent gene expression changes. We compared gene expression profiles of BCL6+/+ and BCL6-/- BCR-ABL1 transformed pre-B cells after inducible overexpression of Bach2.

2013-07-11 | E-GEOD-41042 | biostudies-arrayexpress

Gene expression data of BCR-ABL1 transformed B cell precursors from Dusp6 wild-type and Dusp6 knockout mice

Project description:To elucidate the mechanism of Dusp6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed Dusp6+/+ and Dusp6-/- B cell precursors. BCR-ABL1 transformed B cell precursors of Dusp6 wildtype and Dusp6 knockout mice were subjected to RNA isolation

2013-06-03 | E-GEOD-34832 | biostudies-arrayexpress

Gene expression data of BCR-ABL1 transformed B cell precursors from ETV5 wild-type and ETV5 knockout mice

Project description:To elucidate the mechanism of ETV5-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed ETV5+/+ and ETV5-/- B cell precursors. BCR-ABL1 transformed B cell precursors of ETV5wild-type and ETV5 knockout mice were subjected to RNA isolation

2013-06-03 | E-GEOD-34833 | biostudies-arrayexpress

Transcription profiling of human BCR-ABL1-transformed acute lymphoblastic leukemia cells reveals Activation-induced cytidine deaminase acts as a mutator

Project description:The Philadelphia chromosome (Ph) encoding the oncogenic BCR-ABL1 kinase defines a subset of ALL with a particularly unfavorable prognosis. Acute lymphoblastic leukemia (ALL) cells are derived from B cell precursors in most cases and typically carry rearranged immunglobulin heavy chain (IGH) variable (V) region genes devoid of somatic mutations. Somatic hypermutation is restricted to mature germinal center B cells and depends on activation-induced cytidine deaminase (AID). Studying AID expression in 108 cases of ALL, we detected AID mRNA in 24 of 28 Ph-positive ALLs as compared to 6 of 80 Ph-negative ALLs. Forced expression of BCR-ABL1 in Ph-negative ALL cells and inhibition of the BCR-ABL1-kinase showed that aberrant expression of AID depends on BCR-ABL1 kinase activity. Consistent with aberrant AID expression in Ph-positive ALL, IGH V region genes and BCL6 were mutated in many Ph-positive but unmutated in most Ph-negative cases. In addition, AID introduced DNA-single-strand breaks within the tumor suppressor gene CDKN2B in Ph-positive ALL cells, which was sensitive to BCR-ABL1 kinase inhibition and silencing of AID expression by RNA interference. These findings identify AID as a BCR-ABL1-induced mutator in Ph-positive ALL cells, which may be relevant with respect to the particularly unfavorable prognosis of this leukemia subset. Experiment Overall Design: To study the gene expression profile of two Ph-positive ALL cell lines (BV173 and SUP-B15) in the presence or absence of 10 Î¼mol/l STI571 for 16 hours

2008-06-15 | E-GEOD-7182 | biostudies-arrayexpress

Effect of imatinib on 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. In this study, the tyrosine kinase inhibitor imatinib was used for pharmacological inhibition of BCR-ABL1. Gene expression profiles of Ph+ ALL cell lines were analyzed in response to imatinib treatment. Four Ph+ ALL cell lines (BV-173, NALM-1, SUP-B15, and TOM1) were either treated with 10µM STI571 (Imatinib) for 16 hours or cultured in absence of STI571.

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

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