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Links from GEO DataSets

Items: 9

1.

Targeting FLT3-TAZ Signaling to Suppress Drug Resistance in Blast Crisis Chronic Myeloid Leukemia

(Submitter supplied) Although the development of tyrosine kinase inhibitors (TKIs), including BCR-ABL1 targeted therapies, rendered chronic myeloid leukemia (CML) a manageable condition, acquisition of drug resistance during blast crisis (BC) progression remains a critical challenge. Here, we elucidate the significance of FLT3 signaling in the acquisition of drug resistance in BC-CML. Mechanistically, FLT3 expression in CML cells activated FLT3-JAK-STAT3-TAZ-TEAD-CD36 pathway, which conferred resistance to wide range of tyrosine kinase inhibitors (TKIs). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: XLSX
Series
Accession:
GSE226360
ID:
200226360
2.

Effect of VDR knockdown on the gene expression of K562 cells after 10h

(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
Series
Accession:
GSE233861
ID:
200233861
3.

SHP2 Is Required for BCR-ABL1-Induced Hematologic Neoplasms

(Submitter supplied) BCR-ABL1-targeting tyrosine kinase inhibitors (TKIs) have revolutionized treatment of Philadelphia chromosome-positive (Ph+) hematologic neoplasms. Nevertheless, acquired TKI resistance remains a major problem in chronic myeloid leukemia (CML), and TKIs are less effective against Ph+ B-cell acute lymphoblastic leukemia (B-ALL). GAB2, a scaffolding adaptor that binds and activates SHP2, is essential for leukemogenesis by BCR-ABL1, and a GAB2 mutant lacking SHP2 binding cannot mediate leukemogenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
16 Samples
Download data: TXT
Series
Accession:
GSE99656
ID:
200099656
4.

H3K27 tri-methylation signature in CML CD34+ cells

(Submitter supplied) This study compares the epigenetic signatures of CD34+ cells from chronic phase chronic myeloid leukemia (CML) samples and blast phase CML samples v.s. normal CD34+ cells from cord blood and adult bone marrow samples. H3K27me3 genomic loci were detected by ChIP-seq.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL16791
20 Samples
Download data: BW
Series
Accession:
GSE188241
ID:
200188241
5.

Unraveling the molecular signature of BCR-ABLT3151 in the Drosophila melanogater CML model

(Submitter supplied) Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder resulting from a balanced translocation namely the Philadelphia chromosome. It produces the BCR-ABL1 oncogene that encodes for the BCR-ABL1 fusion protein that demonstrates increased tyrosine kinase activity. In the present study we aim to investigate the transcriptomic and molecular profiles of the wild type BCR-ABLp210 and BCR-ABLT315I mutant in attempt to examine their pathogenesis and find potential targets in chronic myeloid leukemia (CML). more...
Organism:
Drosophila melanogaster
Type:
Expression profiling by high throughput sequencing
Platform:
GPL25244
9 Samples
Download data: TXT
Series
Accession:
GSE243439
ID:
200243439
6.

Whole transcriptome sequencing for wild type and IRAIN over-expression K562 cells

(Submitter supplied) The development of tyrosine kinase inhibitors (TKIs) has revolutionarily increased the overall survival of patients with chronic myeloid leukemia (CML). However, drug resistance remains a major obstacle. Here, we demonstrated that a BCR-ABL1-independent long non-coding RNA, IRAIN, is constitutively expressed at low levels in CML, resulting in imatinib resistance. IRAIN knockdown decreased the sensitivity of CD34+ CML blasts and cell lines to imatinib, whereas IRAIN overexpression significantly increased sensitivity. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: XLSX
Series
Accession:
GSE263645
ID:
200263645
7.

Effect of Sdc1 knockout in mouse blast crisis chronic myeloid leukemia (bcCML) cells

(Submitter supplied) Here we report the genomic impact on murine bcCML by Sdc1 loss. We compare bcCML derived from a wildtype cell source to bcCML derived from a Sdc1 knockout mouse. This RNA-seq identifies a number of potential critical regulators of growth, migration, and adhesion.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: TXT
Series
Accession:
GSE159148
ID:
200159148
8.

State-transition Modeling of Blood Transcriptome Predicts Disease Evolution and Treatment Response in Chronic Myeloid Leukemia (CML)

(Submitter supplied) Chronic myeloid leukemia (CML) is initiated and initially maintained solely by the fusion gene BCR-ABL, encoding a mutant protein targeted in the clinic with tyrosine kinase inhibitors (TKIs) While TKI treatment is effective in inducing long-term remission, frequently is not curative. For these reasons, CML is an ideal disease to test our hypothesis that that transcriptome-based state-transition models accurately predict cancer evolution and treatment response. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
298 Samples
Download data: TSV
Series
Accession:
GSE244990
ID:
200244990
9.

Human SUP-B15 cells: CNV compared to reference genome.

(Submitter supplied) Copy Number Variaton (CNV) detection of human BCR-ABL positive acute lymphoblastic leukemia (ALL) cell line, SUP-B15.
Organism:
Homo sapiens
Type:
Genome variation profiling by array; Genome variation profiling by SNP array
Platform:
GPL16237
1 Sample
Download data: TXT
Series
Accession:
GSE239416
ID:
200239416
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