GEO DataSets

(Submitter supplied) We identified the BCL6 protooncogene as a critical downstream effector of FoxO3A in self-renewal signaling of CML-initiating cells. BCL6 represses Arf and p53 in CML cells and is required for leukemia stem cell maintenance, colony formation and initiation of leukemia in transplant recipients. Importantly, peptide inhibition of BCL6 in human CML cells compromises colony formation and leukemia-initiation in xenotransplanted mouse recipients. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL10999

2 Samples

Download data: BED, TXT, WIG

(Submitter supplied) In order to investigate the function of STAT5 in ALL, we isolated bone marrow cells from STAT5 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-GFP or empty vector control (GFP) and subjected to gene expression analysis.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

6 Samples

Download data: CEL

(Submitter supplied) 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. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

10 Samples

Download data: CEL

(Submitter supplied) The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which is present in almost every patient with chronic myeloid leukemia. In this study, the tyrosine kinase inhibitor Imatinib was used for pharmacological inhibition of BCR-ABL1. Gene expression profiles of CML cell lines were analyzed in response to Imatinib treatment.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4177

Platform:

GPL570

6 Samples

Download data: CEL

(Submitter supplied) 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).

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

12 Samples

Download data: CEL

Analysis of CML cell lines (KU-812, KCL-22, and JURL-MK1) treated with tyrosine kinase inhibitor imatinib. Imatinib inhibits oncogenic BCR-ABL1, a tyrosine kinase present in most CML patients. Results provide insight into molecular mechanisms underlying imatinib inhibition of CML.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 agent, 3 cell line sets

Platform:

GPL570

Series:

GSE24493

6 Samples

Download data: CEL

(Submitter supplied) We used microarrays to assess differential gene expression between treatment arms.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL571

36 Samples

Download data: CEL

(Submitter supplied) ABL1 kinase inhibitors such as imatinib mesylate (IM) are effective in managing chronic myelogenous leukemia (CML) but incapable of eliminating leukemia stem cells (LSCs), suggesting that kinase−independent pathways support LSC survival. Given that the bone marrow hypoxic microenvironment supports hematopoietic stem cells, we investigated if hypoxia similarly contributes to LSC persistence. Importantly, we found that while BCR−ABL1 kinase remained effectively inhibited by IM under hypoxia, apoptosis became partially suppressed. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

24 Samples

Download data: TXT

(Submitter supplied) BACKGROUND: BCR-ABL1+ chronic myeloid leukemia (CML) is characterized by abnormal production of leukemic stem (LSC) and progenitor cells and their spread from the bone marrow into the blood resulting in extramedullary myeloproliferation. So far, little is known about specific markers and functions of LSC in CML. METHODS: We examined the phenotype and function of CD34+/CD38─/Lin─ CML LSC by a multi-parameter screen approach employing antibody-phenotyping, mRNA expression profiling, and functional studies, including LSC repopulation experiments in irradiated NOD-SCID-IL-2Rgamma-/- (NSG) mice, followed by marker-validation using diverse control-cohorts and follow-up samples of CML patients treated with imatinib. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL15207

10 Samples

Download data: CEL

(Submitter supplied) We show the molecular and functional characterization of a novel population of lineage-negative CD34-negative (Lin- CD34-) hematopoietic stem cells (HSCs) from chronic myelogenous leukemia (CML) patients at diagnosis. Molecular caryotyping and quantitative analysis of BCR/ABL transcript demonstrated that about one third of CD34- was leukemic. CML CD34- cells showed kinetic quiescence and limited clonogenic capacity. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL8300

6 Samples

Download data: CEL, CHP

(Submitter supplied) A comparison of global gene expression between rigorously defined stem and progenitor cells from patients with chronic myeloid leukaemia (CML) in chronic (CP), accelerated (AP) and blastic (BC) phase and similar populations isolated from normal volunteers.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

67 Samples

Download data: CEL

(Submitter supplied) In comparing gene expression of normal and CML CD34+ quiescent (G0) and proliferating (G1/S/G2/M) cells, 292 genes were down-regulated and 192 genes were up-regulated in the CML G0 cells. The differentially expressed genes were grouped according to their reported functions and correlations were sought with biological differences previously observed between the same groups. The most apparent correlations include: i) Normal and CML G0 cells are more primitive than G1/S/G2/M cells; ii) CML G0 cells are in a more advanced stage of development and more poised to begin proliferating than normal G0 cells; iii) When CML G0 cells are stimulated to proliferate, they undergo further differentiation and maturation more rapidly than normal G0 cells, but both granulopoiesis and erythropoiesis are less efficient than normal; iv) Whereas normal G0 cells form only granulocyte/monocyte (GM) colonies when stimulated by cytokines, CML G0 cells consistently form a combination of GM and erythroid clusters and colonies; and v) Prominin-1 (CD133) is the gene most down-regulated in CML G0 cells and its down-regulation appears to be associated with the spontaneous formation of erythroid colonies by CML progenitors without EPO. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

24 Samples

Download data: CEL

(Submitter supplied) Newly diagnosed chronic phase chronic myeloid leukemia (CML) patients with a major cytogenetic response (MCyR) after 12 months of imatinib therapy have an excellent long-term outcome, while patients without MCyR have a high progression risk. Since patients with primary cytogenetic resistance may benefit from more intensive therapy up-front, we sought to identify biomarkers to predict MCyR. Keywords: Two group comparison to identify trasncriptomic signature that predicts response to therapy

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

59 Samples

Download data: CEL

(Submitter supplied) Chronic myelogenous leukaemia (CML) is a malignant disorder of the hematopoietic stem cell, which is characterized by the reciprocal translocation between chromosomes 9 and 22 (t(9;22)(q34;q11)) The translocation results in the formation of the BCR-ABL fusion oncogene encoding a protein with constitutive activated tyrosine kinase activity which plays a central role in the pathogenesis of the disease. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS2342

Platform:

GPL201

17 Samples

Download data

Analysis of CD34+ hematopoietic stem and progenitor cells from the bone marrow of untreated patients with chronic myelogenous leukemia (CML) in first chronic phase. Results provide insight into the pathogenesis of chronic phase CML.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 disease state sets

Platform:

GPL201

Series:

GSE5550

17 Samples

Download data

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Genome binding/occupancy profiling by genome tiling array

Platforms:

GPL8275 GPL6480

21 Samples

Download data: PAIR, TXT

(Submitter supplied) 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. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by genome tiling array

Platform:

GPL8275

12 Samples

Download data: PAIR

(Submitter supplied) This comparative genomic hybridization (CGH) study investigated the effect of BCL6 on clonal evolution in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). The frequencies of copy number alterations in BCR-ABL1-transformed BCL6+/+ and BCL6-/- leukemias were determined.

Organism:

Mus musculus

Type:

Genome variation profiling by genome tiling array

Platform:

GPL10989

6 Samples

Download data: PAIR, TXT

(Submitter supplied) 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. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6480

9 Samples

Download data: TXT

(Submitter supplied) 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.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4175

Platform:

GPL571

8 Samples

Download data: CEL