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TranscriptomicsRNA-seq of AML cells with MPI KO and FLT3 tyrosine kinase inhibition
Molm13 AML cell line both control and MPI KO, treated with AC220 (quizartinib) and mannose at 24 and 72 hours after drug treatment. 2 reads and 2 repeats for each condition, 2 timepoints, 48 total files.
ORGANISM(S): Homo sapiens 
2023-02-27 | E-MTAB-11750 | biostudies-arrayexpress
UnknownA Genome-Wide CRISPR Screen Identifies Genes Critical for Resistance to FLT3 Inhibitor AC220.
Not available
S-EPMC5559306 | biostudies-literature
OtherA genome-wide CRISPR screen identifies genes critical for resistance to FLT3 inhibitor AC220
To understand the mechanisms of drug resistance to AC220, we undertook an unbiased approach with a novel CRISPR pooled library to screen new genes whose loss of function confers resistance to AC220. In our screen, we identified SPRY3, an intracellular inhibitor of FGF signaling, and GSK3, a canonica...
ORGANISM(S): Homo sapiens 
2017-05-06 | GSE98612 | GEO
GenomicsDifferential expression analysis of primary AML cells treated with AC220 vs DMSO in endothelial cell co-culture.
Differential expression analysis of primary AML cells treated with AC220 vs DMSO in endothelial cell co-culture.
PRJNA575538 | ENA
UnknownThe Combined Treatment With the FLT3-Inhibitor AC220 and the Complex I Inhibitor IACS-010759 Synergistically Depletes Wt- and FLT3-Mutated Acute Myeloid Leukemia Cells.
Not available
S-EPMC8417744 | biostudies-literature
UnknownCrystal structure of the FLT3 kinase domain bound to the inhibitor Quizartinib (AC220).
Not available
S-EPMC4383440 | biostudies-literature
UnknownInternal Tandem Duplication in FLT3 Attenuates Proliferation and Regulates Resistance to the FLT3 Inhibitor AC220 by Modulating p21Cdkn1a and Pbx1 in Hematopoietic Cells.
Not available
S-EPMC4936702 | biostudies-literature
ProteomicsGlobal phosphoproteome analysis of human bone marrow reveals predictive phosphorylation markers for the treatment of acute myeloid leukemia with quizartinib
Treatment with inhibitors of the receptor tyrosine kinase FLT3 are currently studied as promising therapies in acute myeloid leukemia (AML). However, only a subset of patients benefit from these treatments and the presence of activating mutations within FLT3 can predict response to a certain extent ...
ORGANISM(S): Homo sapiens (Human) 
2017-05-10 | PXD006475 | Pride
Biomarker  classification  aml  ac220  quizartinib  phosphoproteomics  response prediction 
GenomicsHomo sapiens
A genome-wide CRISPR screen identifies genes critical for resistance to FLT3 inhibitor AC220
PRJNA385668 | ENA
ProteomicsMZH29 is a novel potent FLT3 tyrosine kinase inhibitor with activity of overcoming drug resistant mutations in AML
In this study, we screened a group of newly synthesized tyrosine kinase inhibitors, and discovered MZH29 was a potent FLT3 inhibitor. Remarkably, MZH29 is well tolerated and effective in the clinically known FLT3 mutants in the constructed BaF3 model cells. MZH29 could also lead to complete tumor re...
ORGANISM(S): Homo sapiens (Human) Apis mellifera (Honeybee) 
2016-12-12 | PXD004278 | Pride
Tyrosine kinases inhibitor  aml  drug resistance  mv4-11 
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