GEO DataSets

(Submitter supplied) Lin-CD34+CD38+ and Lin-CD34-CD38- cells were isolated from 5 CML patients at diagnosis and 4 healthy donors.

Organism:

Homo sapiens

Type:

Expression profiling by RT-PCR

Platform:

GPL19066

18 Samples

Download data: TXT

(Submitter supplied) 33 miRNAs significantly decreased and 75 miRNAs significantly increased in BCR-ABL+ LSK compared with BCR-ABL- LSK cells, suggesting distinct BCR-ABL-dependent mechanisms of microRNA regulation.

Organism:

Mus musculus

Type:

Non-coding RNA profiling by high throughput sequencing

Platform:

GPL17021

4 Samples

Download data: TXT

(Submitter supplied) Tyrosine kinase inhibitors (TKI) are highly effective in treatment of chronic myeloid leukemia (CML) but do not eliminate leukemia stem cells (LSC), which remain a potential source of relapse. TKI treatment effectively inhibits BCR-ABL kinase activity in CML LSC, suggesting that additional kinase-independent mechanisms contribute to LSC preservation. We investigated whether signals from the bone marrow (BM) microenvironment protect CML LSC from TKI treatment. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4756

Platform:

GPL6244

12 Samples

Download data: CEL

Analysis of CML cells treated with tyrosine kinase inhibitor (TKI) imatinib and BM mesenchymal stromal cells (MSCs). Coculture with MSCs protects the CML cells from TKI-mediated cell death and depletion. Results provide insight into microenvironmental protection of CML cells from TKI treatment.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 4 protocol, 2 tissue sets

Platform:

GPL6244

Series:

GSE43225

12 Samples

Download data: CEL

(Submitter supplied) The biology of chronic myeloid leukemia (CML)-stem cells is still incompletely understood. Therefore, we previously developed an inducible transgenic mouse model in which stem cell targeted induction of BCR-ABL expression leads to chronic phase CML-like disease. Here, we now demonstrate that the disease is transplantable using BCR-ABL positive LSK cells (lin-Sca-1+c-kit+). Interestingly, the phenotype is enhanced when unfractionated bone marrow (BM) cells are transplanted. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: DAT

(Submitter supplied) To determine the specific gene expression of imatinib in CML cells with or without miR-342-5P expression, gene array analysis was performed.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL21282

8 Samples

Download data: GPR

(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) 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) In chronic myeloid leukemia (CML) neoplastic stem cells (NCS) represent a critical target of therapy. However, little is known about markers and targets expressed in CML NSC. 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, 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:

GPL16686

2 Samples

Download data: CEL

(Submitter supplied) To understand gene expression signatures of CML stem cells underlying imatinib-resistance, we compared transcriptomes of CML stem and progenitor cells from vehicle and imatinib-treated CML mice, respectively.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

12 Samples

Download data: TXT

(Submitter supplied) The family of signal transduction adapter proteins (STAPs) has been reported to be involved in a variety of intracellular signaling and transcriptional molecules. We originally cloned STAP-2 as a c-fms interacting protein and found the effects on chronic myeloid leukemia (CML) leukemogenesis. STAP-2 binds to BCR-ABL, up-regulates BCR-ABL phosphorylation and activates its downstream molecules. In this study, we evaluated the role of STAP-1, another member of the family, in CML pathogenesis. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

2 Samples

Download data: TXT

(Submitter supplied) Aberrant long noncoding RNA (lncRNA) expression has been described in many human malignancies, including leukemia. Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) is a stem cell disease induced by Bcr-Abl hybrid gene. Here we attempt to identify lncRNAs associated with CML by analyzing lncRNA expression profiles in K562 cells when Bcr-Abl gene silenced. LncRNA microarray analysis revealed a group of lncRNAs that exhibit Bcr-Abl-dependent expression. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL14715

6 Samples

Download data: CALLS, PAIR

(Submitter supplied) AF1q/MLLT11 expression was significantly upregulated in CML patients and elevated AF1q expression was associated with disease progression. Enforced AF1q expression promoted cell survival, protected CML cells from IM treatment and increased engraftment of CML cells in vivo. We used microarrays in AF1q-overexpressing K562 cells and negative control cells to profile differentially expressed genes that might be involved in AF1q regulation.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

6 Samples

Download data: CEL

(Submitter supplied) Leukemic stem cells (LSCs) can acquire non-mutational resistance following drug treatment leading to therapeutic failure and relapse. However, oncogene-independent mechanisms of drug persistence in LSCs are incompletely understood, which is the primary focus of this study. We integrated proteomics, transcriptomics, and metabolomics to determine the contribution of STAT3 in promoting metabolic changes in tyrosine kinase inhibitor (TKI) persistent chronic myeloid leukemia (CML) cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

11 Samples

Download data: BW, TXT

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

Organism:

Homo sapiens; Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL19057 GPL18573

23 Samples

Download data: BW

(Submitter supplied) Leukemic stem cells (LSCs) can acquire non-mutational resistance following drug treatment leading to therapeutic failure and relapse. However, oncogene-independent mechanisms of drug persistence in LSCs are incompletely understood, which is the primary focus of this study. We integrated proteomics, transcriptomics, and metabolomics to determine the contribution of STAT3 in promoting metabolic changes in tyrosine kinase inhibitor (TKI) persistent chronic myeloid leukemia (CML) cells. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: TXT

(Submitter supplied) Leukemic stem cells (LSCs) can acquire non-mutational resistance following drug treatment leading to therapeutic failure and relapse. However, oncogene-independent mechanisms of drug persistence in LSCs are incompletely understood, which is the primary focus of this study. We integrated proteomics, transcriptomics, and metabolomics to determine the contribution of STAT3 in promoting metabolic changes in tyrosine kinase inhibitor (TKI) persistent chronic myeloid leukemia (CML) cells. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

4 Samples

Download data: BW, XLSX

(Submitter supplied) To investigate the effect of VDR in the regulation of K562 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: XLSX

(Submitter supplied) Total RNA was extracted from Lin-Sca-1+c-Kit+ (LSK) cells sorted from the BM of Spred1HSCΔ/ΔSCLtTA/BCR-ABL (HSC KO) and Spred1HSCwt/wtSCLtTA/BCR-ABL (HSC wt) (n=5 mice per group, both group given 7 doses of 250μg poly(I:C), ip, every two days, to activate Mx1-cre), Spred1ECΔ/ΔSCLtTA/BCR-ABL (EC KO) and Spred1ECwt/wtSCLtTA/BCR-ABL (EC wt) (n=5 mice per group) mice using the miRNeasy micro Kit (Qiagen, Valencia, CA). more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

26 Samples

Download data: TXT

(Submitter supplied) Tyrosine kinase inhibitors (TKIs) have revolutionized chronic myelogenous leukemia (CML) management. Disease eradication, however, is hampered by innate resistance of leukemia initiating cells (LICs) to TKI-induced killing, which also provides the basis for subsequent emergence of TKI-resistant mutants. We report that EZH2, the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), is overexpressed in CML LICs, required for colony formation, and survival and cell cycle progression of CML cell lines. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8321

8 Samples

Download data: CEL