GEO DataSets

(Submitter supplied) Autophagy is associated with both survival and cell death in myeloid malignancies. Therefore, deciphering its role in different genetically defined subtypes of acute myeloid leukemia (AML) is critical. Activating mutations of the KIT receptor tyrosine kinase are frequently detected in core-binding factor AML and are associated with a greater risk of relapse. Herein, we report that basal autophagy was significantly increased by the KITD816V mutation in AML cells and contributed to support their cell proliferation and survival. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL16686

6 Samples

Download data: CEL

(Submitter supplied) Long-term treatment of Kasumi-1 cells at clinically attained doses of dasatinib led to decreased drug-sensitivity by means of IC50 values (relative to treatment-naive cells). Changes were paralled by profound alterations in c-KIT expression and cell signaling signatures. Upon brief discontinuation of dasatinib treatment, these alterations reversed and drug sensitivity was restored. We used gene expression profiling to examine reversal of dasatinib-resistance at the molecular/expression level.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5600

Platform:

GPL6244

9 Samples

Download data: CEL

Analysis of dasatinib-sensitive, KITmut t(8;21) AML cell line Kasumi-1 treated with dasatinib for 12 wks giving rise to R48 cells. After 1 wk of dasatinib cessation, R48 cells give rise to PR48 cells. Results provide insight into molecular effects of long-term dasatinib treatment on t(8;21) AML.

Organism:

Homo sapiens

Type:

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

Platform:

GPL6244

Series:

GSE39073

9 Samples

Download data: CEL

(Submitter supplied) Many cases of acute myeloid leukemia (AML) are associated with mutational activation of RTKs such as FLT3. However, RTK inhibitors have limited clinical efficacy as single agents, indicating that AML is driven by concomitant activation of different signaling molecules. We used a functional genomic approach to identify RET, encoding an RTK not previously implicated in AML, as essential gene in different AML subtypes, and observed that RET-dependent AML cells show activation of RET signaling via ARTN/GFRA3 and NRTN/GFRA2 ligand/co-receptor complexes.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

260 Samples

Download data: CEL