Therapeutic targeting of preleukemia cells in a mouse model of NPM1 mutant acute myeloid leukemia is a research paper published in Science (2020). On theSindex it has a DataRank of 0. It has been cited 275 times.
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National Institutes of Health
Grant: CA176745
National Institutes of Health
Grant: CA204639
National Institutes of Health
Grant: CA066996
National Institutes of Health
Grant: CA206963
German research Foundation
Grant: SFB 1074, project B3
NCI NIH HHS
Grant: P50 CA206963
NCI NIH HHS
Grant: R01 CA176745
NCI NIH HHS
Grant: R35 CA197594
Medical Research Council
Grant: MC_PC_17230
NCI NIH HHS
Grant: R01 CA204639
Cancer Research UK
Grant: 23015
NCI NIH HHS
Grant: P01 CA066996
NIH HHS
Grant: U54 OD020355
NCI NIH HHS
Grant: P30 CA008748
NCI NIH HHS
Grant: R01 CA092660
Medical Research Council
Grant: MC_PC_12009
FWCI
17.15
Citation Percentile
1.0%
Citation Trend
Fields of Study
MeSH Terms
Keywords
Sustainable Development Goals
Additional file 1 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 1 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 2 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 2 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 3 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 3 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 4 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 4 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 6 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 6 of Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity
Additional file 1 of A novel Menin-MLL1 inhibitor, DS-1594a, prevents the progression of acute leukemia with rearranged MLL1 or mutated NPM1
Additional file 1 of A novel Menin-MLL1 inhibitor, DS-1594a, prevents the progression of acute leukemia with rearranged MLL1 or mutated NPM1
Additional file 1 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML
Additional file 1 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML
Additional file 2 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML
Additional file 2 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML
Additional file 3 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML
Additional file 3 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML
Additional file 4 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML
Additional file 4 of Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML