604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster II
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Therapeutic effect of menin inhibitors is reversible in AML treatment and could be enhanced by the targeting of differentiation associated chromatin complex
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Therapeutic effect of menin inhibitors is reversible in AML treatment and could be enhanced by the targeting of differentiation associated chromatin complex
LSD1 inhibition enhances venetoclax efficacy in Acute Myeloid Leukemia via metabolic rewiring
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LSD1 inhibition enhances venetoclax efficacy in Acute Myeloid Leukemia via metabolic rewiring
Synergistic targeting of KMT2A rearranged AML with combined LSD1 and menin inhibitors
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Synergistic targeting of KMT2A rearranged AML with combined LSD1 and menin inhibitors
MRC2 A tumor restricted surface antigen for immunotherapy in Acute Myeloid Leukemia
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MRC2 A tumor restricted surface antigen for immunotherapy in Acute Myeloid Leukemia
Selinexor enhances the effect of venetoclax on Acute Myeloid Leukemia stem and progenitor cells by disrupting lysosomal function
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Selinexor enhances the effect of venetoclax on Acute Myeloid Leukemia stem and progenitor cells by disrupting lysosomal function
Aberrant activation of clpp exerts multifaceted anti AML activity beyond tumor cells
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Aberrant activation of clpp exerts multifaceted anti AML activity beyond tumor cells
Sphingosine 1 phosphate receptor modulators overcome FLT3 inhibitor resistance in Acute Myeloid Leukemia with FLT3 ITD and NRAS mutations through sphingosine kinase 1 AKT pathway downregulation
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Sphingosine 1 phosphate receptor modulators overcome FLT3 inhibitor resistance in Acute Myeloid Leukemia with FLT3 ITD and NRAS mutations through sphingosine kinase 1 AKT pathway downregulation
Mechanisms of chemotherapy resistance driven by Mecom overexpression
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Mechanisms of chemotherapy resistance driven by Mecom overexpression
BT1 A CD84 targeting T cell engager for selective eradication of leukemic stem cells in Acute Myeloid Leukemia
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BT1 A CD84 targeting T cell engager for selective eradication of leukemic stem cells in Acute Myeloid Leukemia
Butyrate up regulates the expression of CDKN1A to block the cell cycle and inhibits the PI3K AKT signaling pathway to promote apoptosis to play an anti Acute Myeloid Leukemia role
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Butyrate up regulates the expression of CDKN1A to block the cell cycle and inhibits the PI3K AKT signaling pathway to promote apoptosis to play an anti Acute Myeloid Leukemia role
Targeting metabolic vulnerabilities in Acute Myeloid Leukemia Therapeutic potential of l asparaginase and synergy with venetoclax
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Targeting metabolic vulnerabilities in Acute Myeloid Leukemia Therapeutic potential of l asparaginase and synergy with venetoclax
PARP inhibition by talazoparib results in leukemia cell death via induction of myeloid differentiation
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PARP inhibition by talazoparib results in leukemia cell death via induction of myeloid differentiation
Unleashing intrinsic inflammation in AML using therapeutic cytokines overcomes pro survival pathways and induces deep and durable remission In Vivo
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Unleashing intrinsic inflammation in AML using therapeutic cytokines overcomes pro survival pathways and induces deep and durable remission In Vivo
Extracellular arginine deprivation enhances venetoclax sensitivity in acute myeloidleukemia via mitochondrial fission impairment and apoptotic priming
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Extracellular arginine deprivation enhances venetoclax sensitivity in acute myeloidleukemia via mitochondrial fission impairment and apoptotic priming
Synergistic efficacy of EZH2 inhibitor combined with new flavonoid derivatives in AML patient derived xenograft mouse models
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Synergistic efficacy of EZH2 inhibitor combined with new flavonoid derivatives in AML patient derived xenograft mouse models
CSF1R CSF1 axis blockade with axatilimab effectively targets leukemia stem cells and monocytes in AML resistant to BH3 mimetics
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CSF1R CSF1 axis blockade with axatilimab effectively targets leukemia stem cells and monocytes in AML resistant to BH3 mimetics
INCB160058 selectively targets JAK2V617F driven hematopoiesis in diverse and drug resistant models of myeloproliferative neoplasms
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INCB160058 selectively targets JAK2V617F driven hematopoiesis in diverse and drug resistant models of myeloproliferative neoplasms
ZBTB7A modulates response to BCL 2 inhibition by venetoclax in acute myeloid leukemia AML
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ZBTB7A modulates response to BCL 2 inhibition by venetoclax in acute myeloid leukemia AML
Overcoming midostaurin resistance via dual MYC and GSPT1 degradation by the protac GT19715 in FLT3 amplified AML cells
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Overcoming midostaurin resistance via dual MYC and GSPT1 degradation by the protac GT19715 in FLT3 amplified AML cells
Cytoplasmic localization of qki mediates therapeutic resistance and immune evasion
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Cytoplasmic localization of qki mediates therapeutic resistance and immune evasion
Identifying epigenetic vulnerabilities for treatment of HMA refractory myeloid leukemia
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Identifying epigenetic vulnerabilities for treatment of HMA refractory myeloid leukemia
PTEN loss reprograms lipid metabolism to modulate venetoclax resistance in acute myeloid leukemia
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PTEN loss reprograms lipid metabolism to modulate venetoclax resistance in acute myeloid leukemia
Cardio safe degrader CT 03p degrades MCL 1 and overcomes venetoclax resistance in AML
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Cardio safe degrader CT 03p degrades MCL 1 and overcomes venetoclax resistance in AML
Temporal multiomic profiling reveals intrinsic resistance mechanisms to ERK inhibition in relapsed Acute Myeloid Leukemia
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Temporal multiomic profiling reveals intrinsic resistance mechanisms to ERK inhibition in relapsed Acute Myeloid Leukemia