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Patient-derived secondary AML cells were treated with 100 nM of SY-5609 for 24 hours, 100 nM of FHD-286 for 48 hours, or 20 µM of Tasquinimod for 48 hours to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and lethal effects of treatment with...
ORGANISM(S): Homo sapiens (Human) 
2025-04-28 | PXD053548 | Pride
Treatment with Menin inhibitor (MI) disrupts interaction between Menin and MLL1 or MLL1-fusion protein (FP), inhibits HOXA9/MEIS1, induces differentiation and loss of survival of AML harboring MLL1 re-arrangement (r) and FP, or expressing mutant (mt)-NPM1. Following MI treatment, although clinical r...
ORGANISM(S): Homo sapiens 
2022-03-12 | GSE190719 | GEO
AML MV4-11, OCI-AML3 and Menin inhibitor tolerant resistant MV4-11-MITR, and OCI-AML3-MITR cells were treated with 500 nM of SNDX-50469 for 48 hours to determine the global protein expression alterations that correlate with the tolerant/resistant phenotype compared to parental controls as well as th...
ORGANISM(S): Homo sapiens (Human) 
2026-09-03 | PXD053575 | Pride
Menin inhibitors (MI) disrupt the binding of Menin to MLL1 leading to repression of MLL1 or MLL1-fusion protein (FP) target genes, including reduced levels of HOXA9 and MEIS1 in AML with mtNPM1 or MLL1-r. While MIs are relatively well-tolerated and induce clinical remissions, these are often short-l...
ORGANISM(S): Homo sapiens 
2026-03-03 | GSE315339 | GEO
Menin inhibitors (MI) disrupt the binding of Menin to MLL1 leading to repression of MLL1 or MLL1-fusion protein (FP) target genes, including reduced levels of HOXA9 and MEIS1 in AML with mtNPM1 or MLL1-r. While MIs are relatively well-tolerated and induce clinical remissions, these are often short-l...
ORGANISM(S): Homo sapiens 
2026-03-03 | GSE315341 | GEO
Genomics
AML cells with acquired resistance to menin inhibition
Effective Menin inhibitor-based combinations against AML with MLL rearrangement or NPM1 mutation (NPM1c)
Overcoming Menin inhibitor resistance in AML cells with combinations including BET proteins and dual BRG1/BRM inhibitor [ChIP-seq]
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