Similar studies for GEO DataSets (Select 4205) - GEO DataSets

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Items: 10

Select item 42051.

Transcription factor c-JUN knockout effect on B lymphoid cells

Analysis of B lymphoid cells depleted of activating protein 1 (AP-1) transcription factor c-JUN. c-JUN is involved in BCR-ABL oncogene-induced transformation and leukemogenesis. Results provide insight into the molecular mechanisms underlying c-JUN modulation of leukemogenesis.

Organism:: Mus musculus

Type:: Expression profiling by array, transformed count, 2 genotype/variation sets

Platform:: GPL6246
Series:: GSE27028
8 Samples

Download data: CEL

DataSet

Accession:: GDS4205

ID:: 4205

Select item 2000270282.

C-JUN promotes BCR-ABL induced lymphoid leukemia by inhibiting methylation of the 5´ region of Cdk6

(Submitter supplied) The transcription factor c-JUN and its upstream kinase JNK1 have been implicated in BCR-ABL induced leukemogenesis. JNK1 has been shown to regulate BCL2 expression thereby altering leukemogenesis, but the impact of c-JUN remained unclear. In this study we show that JNK1 and c-JUN promote leukemogenesis via separate pathways, since lack of c-JUN impairs proliferation of p185BCR-ABL transformed cells without affecting viability. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Dataset:: GDS4205
Platform:: GPL6246
8 Samples

Download data: CEL

Series

Accession:: GSE27028

ID:: 200027028

Select item 2000620123.

CDK6 as key regulator of hematopoietic and leukemic stem cell activation.

(Submitter supplied) The cyclin-dependent kinases (CDK) CDK6 and CDK4 have redundant functions in regulating cell-cycle progression. We describe a novel role for CDK6 in hematopoietic and leukemic stem cells (HSCs and LSCs) that exceeds its function as cell-cycle regulator. Although hematopoiesis appears regular under steady state conditions Cdk6-/- HSCs do not efficiently repopulate upon competitive transplantation and Cdk6-deficient mice are significantly more susceptible to 5-fluorouracil (5-FU) treatment. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL10787
6 Samples

Download data: TXT

Series

Accession:: GSE62012

ID:: 200062012

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2001203374.

Genomic expression analysis of K562 cells expressing shRNA targeting lncRNA-IIRX and control cells

(Submitter supplied) LncRNA-IIRX plays critical role in Bcr-Abl-induced tumorigenesis. To discover its mechanisms underlying cellular transformation by Bcr-Abl oncogene, genome-wide mRNA expression was measured by RNA-seq in K562 cells expressing shRNA targeting lncRNA-IIRX and control cells. We identified many genes with differential expression in K562 cells after knocking down lncRNA-IIRX.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
6 Samples

Download data: TXT

Series

Accession:: GSE120337

ID:: 200120337

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 2001197705.

Identification of a novel lncRNA family that is required for efficient cellular transformation by Bcr-Abl oncogene

(Submitter supplied) Aberrantly expressed long noncoding RNAs (lncRNAs) have been described in diverse human diseases and cancer development. Chronic myeloid leukemia (CML) is a hematological malignancy induced by Bcr-Abl hybrid gene. Owing to the development of tyrosine kinase inhibitors (TKIs), especially the first-generation Imatinib, over 90% of CML patients can be cured in recent years. Here we attempt to identify Imatinib-inducible lncRNAs associated with CML by analyzing lncRNA expression profiles in K562 cells after Imatinib or control treatment. more...

Organism:: Homo sapiens

Type:: Non-coding RNA profiling by array

Platform:: GPL21096
6 Samples

Download data: TXT, XLSX

Series

Accession:: GSE119770

ID:: 200119770

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000996566.

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

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000590247.

Expression profile of BCR-ABL1-transformed, Cdk4 R24C, Cdk6 R31C cell lines

(Submitter supplied) Cdk4 and Cdk6 are two related kinases that bind D-type cyclins and regulate cell cycle progression. Due to their relevance in cancer, Cdk4/6 inhibitors are currently in advanced clinical trials in multiple tumor types. Cdk4/6 are inhibited by INK4 proteins that exert tumor suppressing functions. To test the significance of this inhibitory mechanism we have generated knock-in mice that express a Cdk6 mutant (Cdk6 R31C) insensitive to INK4-mediated inhibition. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL13912
4 Samples

Download data: TXT

Series

Accession:: GSE59024

ID:: 200059024

Select item 2001577028.

Bortezomib suppresses self-renewal and leukemogenesis of leukemia stem cell by NF-ĸB-dependent inhibition of cyclin dependent kinase 6 in MLL-rearranged myeloid leukemia

(Submitter supplied) Acute myeloid leukemia (AML) with chromosomal rearrangements involving the H3K4 methyltransferase mixed-lineage leukemia (MLL) is an aggressive subtype with low overall survival. MLL rearrangements rapidly transform hematological stem and progenitor cell (HSPC) to leukemia stem cell (LSC). Bortezomib (Velcade) is used widely in hematological malignancies. However, it is still unknown whether bortezomib possesses anti-self-renewal and anti-leukemogenesis of LSC in AML with MLL rearrangements. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL11154
2 Samples

Download data: TXT, XLSX

Series

Accession:: GSE157702

ID:: 200157702

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 2001567139.

Expression data of shDIDO1 and shCtrl HUVEC cell lines

(Submitter supplied) DIDO1(Death inducer-obliterator) gene localizes in the nucleus and cytosol, which is required in the early steps during the tumor progression and metastasis. We analyzed the GeneChip expression profiles of human umbilical vein endothelial cells transfected by RNAi lentiviral vectors, shDIDO1 cell line and shCtrl cell lines

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL15207
14 Samples

Download data: CEL

Series

Accession:: GSE156713

ID:: 200156713

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20011375210.

CDK6 antagonizes p53-induced responses during tumorigenesis

(Submitter supplied) CDK6 induces a complex transcriptional program to block p53 in hematopoietic cells. CDK6 binds to the promoters of genes including p53-antagonists. Cells lacking CDK6 kinase function are required to mutate p53 to achieve a fully transformed immortalized state.