604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster I
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Azacitidine panobinostat activates NF kb signaling in the bone marrow microenvironment to chemosensitize KMT2A rearranged pediatric AML
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Azacitidine panobinostat activates NF kb signaling in the bone marrow microenvironment to chemosensitize KMT2A rearranged pediatric AML
Optimizing establishment of high need pediatric Acute Myeloid Leukemia AML patient derived xenograft PDX models
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Optimizing establishment of high need pediatric Acute Myeloid Leukemia AML patient derived xenograft PDX models
Negative feedback regulation of nfkb MAPK and JAK STAT drives adaptive resistance to gilteritinib in AML
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Negative feedback regulation of nfkb MAPK and JAK STAT drives adaptive resistance to gilteritinib in AML
Mechanistic approach exploring combination agents to potentiate anti leukemia activity of Hu8F4 a clinical stage T cell receptor mimic antibody
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Mechanistic approach exploring combination agents to potentiate anti leukemia activity of Hu8F4 a clinical stage T cell receptor mimic antibody
Mechanism of acquired resistance to histone deacetylase inhibitor romidepsin in myeloid leukemia associated with down syndrome
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Mechanism of acquired resistance to histone deacetylase inhibitor romidepsin in myeloid leukemia associated with down syndrome
Protein degradation of MYC GSPT1 combined with menin inhibition overcomes resistance to menin inhibition in KMT2A rearranged Acute Myeloid Leukemia
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Protein degradation of MYC GSPT1 combined with menin inhibition overcomes resistance to menin inhibition in KMT2A rearranged Acute Myeloid Leukemia
CⅡTA mediated up regulation of MHC reverses immune evasion of leukemia stem cells in refractory relapsed AML
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CⅡTA mediated up regulation of MHC reverses immune evasion of leukemia stem cells in refractory relapsed AML
Disrupting monocytic AML and monocytic leukemia stem cells with a novel cladribine regimen From bench to bedside
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Disrupting monocytic AML and monocytic leukemia stem cells with a novel cladribine regimen From bench to bedside
PPM1D mutations confer resistance to venetoclax in pre leukemic and AML populations
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PPM1D mutations confer resistance to venetoclax in pre leukemic and AML populations
Pharmacokinetics and cardiac impact of arsenic trioxide ATO oral solution SDK001 under fasting fed and calcium carbonate co administration conditions compared with intravenous ATO in patients with acute promyelocytic leukemia
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Pharmacokinetics and cardiac impact of arsenic trioxide ATO oral solution SDK001 under fasting fed and calcium carbonate co administration conditions compared with intravenous ATO in patients with acute promyelocytic leukemia
Targeting nucleotide metabolism to enhance ara c sensitivity in myeloid leukemia associated with down syndrome
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Targeting nucleotide metabolism to enhance ara c sensitivity in myeloid leukemia associated with down syndrome
Investigating KAT2A protac therapy for targeting leukemic blast differentiation in acute myeloid leukaemia
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Investigating KAT2A protac therapy for targeting leukemic blast differentiation in acute myeloid leukaemia
Nonclinical evaluation of APL 4098 a novel GCN2 kinase inhibitor reveals potent anti leukemic effects through mitochondrial stress induction and synergy with venetoclax targeting AML blasts and LSCs
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Nonclinical evaluation of APL 4098 a novel GCN2 kinase inhibitor reveals potent anti leukemic effects through mitochondrial stress induction and synergy with venetoclax targeting AML blasts and LSCs
The fanconi anemia pathway restrains MLL rearranged leukemogenesis through suppressing NHEJ mediated genomic instability
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The fanconi anemia pathway restrains MLL rearranged leukemogenesis through suppressing NHEJ mediated genomic instability
Novel BCR ABL1 fusion alongside T315I reveals mechanism for dual ponatinib asciminib resistance and proves sensitive to addition of axitinib
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Novel BCR ABL1 fusion alongside T315I reveals mechanism for dual ponatinib asciminib resistance and proves sensitive to addition of axitinib
Identifying novel ‘druggable targets via Npm1A turboid fusion and mass spectrometry to overcome genetic or adaptive resistance to menin inhibitors in mtNPM1 AML
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Identifying novel ‘druggable targets via Npm1A turboid fusion and mass spectrometry to overcome genetic or adaptive resistance to menin inhibitors in mtNPM1 AML
Single cell insights into acute myeloid leukemia treated with venetoclax based therapy
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Single cell insights into acute myeloid leukemia treated with venetoclax based therapy
Targeting DNA repair vulnerabilities to eradicate TP53 mutated AML
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Targeting DNA repair vulnerabilities to eradicate TP53 mutated AML
Preclinical activity of investigational menin inhibitor DSP 5336 Enzomenib based combinations against MLL1 rearranged MLL r or mutant NPM1 AML models
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Preclinical activity of investigational menin inhibitor DSP 5336 Enzomenib based combinations against MLL1 rearranged MLL r or mutant NPM1 AML models
Chidamide reprograms AML associated macrophages via HDAC3 inhibition to boost CD8 T cell immunity
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Chidamide reprograms AML associated macrophages via HDAC3 inhibition to boost CD8 T cell immunity
Liposomal melatonin targets mutant hematopoiesis and bone marrow remodeling in MPN
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Liposomal melatonin targets mutant hematopoiesis and bone marrow remodeling in MPN
TP53 activation by the natural quassinoid brusatol enhances venetoclax efficacy and overcomes resistance in myeloid leukemias
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TP53 activation by the natural quassinoid brusatol enhances venetoclax efficacy and overcomes resistance in myeloid leukemias
Pharmacological targeting of CTPS1 elicits macrophage mediated anti leukemia immunity
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Pharmacological targeting of CTPS1 elicits macrophage mediated anti leukemia immunity
Amx 883 a potent and selective degrader of BRD9 drives differentiation in acute myeloid leukaemia and shows synergistic efficacy in combination with venetoclax In Vivo and prevents the emergence of resistance to venetoclax in vitro
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Amx 883 a potent and selective degrader of BRD9 drives differentiation in acute myeloid leukaemia and shows synergistic efficacy in combination with venetoclax In Vivo and prevents the emergence of resistance to venetoclax in vitro
Combined FLT3 and EZH1 2 inhibition reduces LSCs and promotes myeloid differentiation in PDX models of AML
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Combined FLT3 and EZH1 2 inhibition reduces LSCs and promotes myeloid differentiation in PDX models of AML
Ferroptosis escape in AML stem cells uncovered by single cell profiling and reversed by STAT3 NRF2 inhibition
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Ferroptosis escape in AML stem cells uncovered by single cell profiling and reversed by STAT3 NRF2 inhibition