GEO DataSets

(Submitter supplied) Internal tandem duplications (ITD) of FLT3 predict poor prognosis in acute myeloid leukemia (AML) and often co-exist with inactivating DNMT3A mutations. In a genetically modified mouse model harboring these genetic aberrations, we analyzed the role of the adaptor protein Gab2 in this disease. We observed Gab2 to be essential for the development of Flt3-ITD driven AML in vivo, which was corroborated by RNA sequencing data of whole murine bone marrow with different Gab2 genotypes

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

8 Samples

Download data: TXT

(Submitter supplied) RNA-seq was used to demonstrate the differential expression genes in MOLM14 and MV4-11 cells after FLT3 inhibition.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL18573 GPL24676

24 Samples

Download data: CSV

(Submitter supplied) Fms-like tyrosine kinase 3 (FLT3) is a critical receptor for functional dendritic cell (DC) development. Mutations associated with FLT3 are commonly observed in acute myeloid leukemia (AML) patients. Internal tandem duplication (FLT3-ITD) results in ligand-independent constitutive signaling and promotes tumor survival. Basic characterization of dendritic cells in the context of AML is lacking, therefore we investigated how FLT3-ITD impacts DC homeostasis and what downstream affects on the immune system may be. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

16 Samples

Download data: MTX, TSV

(Submitter supplied) Internal tandem duplication (ITD) mutations within the FMS-like receptor tyrosine kinase-3 (FLT3) can be found in up to 25~30% of acute myeloid leukemia (AML) patients and confer a poor prognosis. Although FLT3 tyrosine kinase inhibitors (TKIs) have shown clinical responses, the overall outcome of FLT3-ITD+ AML patients remains poor, and most of them would relapse very shortly. TKIs can not eliminate primitive FLT3-ITD+ AML cells, which are potential sources of relapse. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

6 Samples

Download data: TXT

(Submitter supplied) we observed synergistic cytotoxic effects, preferentially reducing cell proliferation and inducing apoptosis in FLT3/ITD+ AML cell lines and in primary AML cells. Furthermore, the combination of FLT3-TKI and GSI eradicated leukemic cells and prolonged survival in a FLT3/ITD+ patient derived xenograft (PDX) AML model. Mechanistically, decreased expression of CXCR3 that lead to down-regulated ERK signaling was partially responsible for the observed synergy. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL23227

16 Samples

Download data: TXT

(Submitter supplied) Gene expression in control and Flt3-ITD, Stat5 and Runx1 mutant HSCs and HPCs from different developmental stages.

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL21163 GPL10787

117 Samples

Download data: TXT

(Submitter supplied) FLT3/ITD-SmoM2 mice developed rapidly fatal myeloid leukemia compared to FLT3/ITD only mice, suggesting that overactivation of the Hedgehog signaling pathway via SmoM2 can drive myeloid disease progression We used the Affymetrix Mouse 430_2.0 microarray to detail global gene expression responsible for disease progression in sorted bone marrow cells and found that the Hedgehog signaling pathway contributes to disease progression by enhancing FLT3 signaling

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5806

Platform:

GPL1261

6 Samples

Download data: CEL, CHP

Analysis of KSL and GMP cells isolated from bone marrow of Flt3/ITD-SmoM2 transgenics at around 3 months of age when they developed leukemia. Wild-type and FLT3/ITD littermates of the FLT3/ITD-SmoM2 animals were also examined. Results provide insight into the role of SmoM2 in leukemic progression.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 cell type, 3 genotype/variation sets

Platform:

GPL1261

Series:

GSE67134

6 Samples

Download data: CEL, CHP

(Submitter supplied) CircMYBL2 is more highly expressed in AML patients with FLT3-ITD mutations than in those without the FLT3-ITD mutation. We found that circMYBL2 knockdown specifically inhibits proliferation and promotes the differentiation of FLT3-ITD AML cells in vitro and in vivo. We used the ribosome profiling and RNA-seq libraries sequenced with Illumina HiSeq 2500 to identify the mRNA that circMYBL2 targeted. Interestingly, we found that circMYBL2 significantly influences the protein level of mutant FLT3 kinase, which contributes to the activation of FLT3-ITD-dependent signaling pathways. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Other

Platform:

GPL24676

8 Samples

Download data: CSV, TXT

(Submitter supplied) Oncogenic addiction to FLT3 kinase signaling is a hallmark of FLT3-ITD+ acute myeloid leukemia (AML). While FLT3 inhibitors like sorafenib show initial therapeutic efficacy, resistance rapidly develops through mechanisms that are incompletely understood. Here, utilizing RNA-Seq based analysis of patient leukemic cells, we found significant up-regulation of the Tec-family kinase BMX during sorafenib resistance. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

8 Samples

Download data: TXT

(Submitter supplied) Diagnostic samples of peripheral blood form acute myeloid leukemia were analysed for gene expression differences MLL Munich Leukemia Laboratory

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

325 Samples

Download data: CEL, PDF