604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster I
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ADH5/ALDH2 Dehydrogenases and DNA Polymerase Theta Protect Hematopoietic Cells from Formaldehyde Challenge: Therapeutic Implications
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ADH5/ALDH2 Dehydrogenases and DNA Polymerase Theta Protect Hematopoietic Cells from Formaldehyde Challenge: Therapeutic Implications
AML Derived Induced Pluripotent Stem Cells Reveal a Genotype-Independent Effect of Monocytic Differentiation in Mediating Venetoclax Resistance
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AML Derived Induced Pluripotent Stem Cells Reveal a Genotype-Independent Effect of Monocytic Differentiation in Mediating Venetoclax Resistance
ATR Inhibitor Elimusertib Suppresses Drug Persister Clones in TP53-Mutated Acute Myeloid Leukemia Via CGAS-Sting-Mediated Cell Death
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ATR Inhibitor Elimusertib Suppresses Drug Persister Clones in TP53-Mutated Acute Myeloid Leukemia Via CGAS-Sting-Mediated Cell Death
Activation of Autophagy Via the SQSTM1-KEAP1-NRF2 Axis Induced By Pevonedistat Provides a Temporary Readjustment of MDS/AML Cells Leading to the Development of Resistance
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Activation of Autophagy Via the SQSTM1-KEAP1-NRF2 Axis Induced By Pevonedistat Provides a Temporary Readjustment of MDS/AML Cells Leading to the Development of Resistance
An Orally Active Pan-BCR::ABL1 Degrader Tgrx-3247 Potently Targets a Wide Spectrum of Orthosteric, Allosteric and Compound Mutations Resistant to TKI Therapies
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An Orally Active Pan-BCR::ABL1 Degrader Tgrx-3247 Potently Targets a Wide Spectrum of Orthosteric, Allosteric and Compound Mutations Resistant to TKI Therapies
Belvarafenib Inhibits the Growth of RAS-Mutant Acute Myeloid Leukemia Cell Lines in Vitro and Drives Adaptive Resistance In Vivo
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Belvarafenib Inhibits the Growth of RAS-Mutant Acute Myeloid Leukemia Cell Lines in Vitro and Drives Adaptive Resistance In Vivo
DGAT1 Inhibition Enhances Metformin-Induced Ferroptosis in AML By Targeting Lipid Metabolism
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DGAT1 Inhibition Enhances Metformin-Induced Ferroptosis in AML By Targeting Lipid Metabolism
Decitabine Activity Against TP53-Mutated Myeloid Neoplasms Is Enhanced By Combination with a Non-Cytotoxic p53/BAX-Independent Inhibitor of Pyrimidine Synthesis
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Decitabine Activity Against TP53-Mutated Myeloid Neoplasms Is Enhanced By Combination with a Non-Cytotoxic p53/BAX-Independent Inhibitor of Pyrimidine Synthesis
Decitabine-Venetoclax Treatment Reactivates Endogenous Retrovirus RNA Signaling in AML Cells and Induces T Cell Activation
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Decitabine-Venetoclax Treatment Reactivates Endogenous Retrovirus RNA Signaling in AML Cells and Induces T Cell Activation
High HDAC8 Creates Targetable Vulnerabilities in Acute Myeloid Leukemia through Dysregulation of BRCA1-Related RNA Splicing Machinery and Defective DNA Damage Repair
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High HDAC8 Creates Targetable Vulnerabilities in Acute Myeloid Leukemia through Dysregulation of BRCA1-Related RNA Splicing Machinery and Defective DNA Damage Repair
Identifying the Impact of ADAR1 Inhibition on LSC Niche Remodeling in 3D Nanobioreactors
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Identifying the Impact of ADAR1 Inhibition on LSC Niche Remodeling in 3D Nanobioreactors
Identifying ‘Druggable’ Targets and Preclinically Overcoming Non-Genetic/Adaptive Resistance to Menin Inhibitors in AML with MLL1r or mtNPM1
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Identifying ‘Druggable’ Targets and Preclinically Overcoming Non-Genetic/Adaptive Resistance to Menin Inhibitors in AML with MLL1r or mtNPM1
Loss of Cystathionine-β-Synthase Activity Results in Increased Oxidative Phosphorylation and Cytarabine Resistance in Myeloid Leukemia Associated with Down Syndrome
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Loss of Cystathionine-β-Synthase Activity Results in Increased Oxidative Phosphorylation and Cytarabine Resistance in Myeloid Leukemia Associated with Down Syndrome
PSAT1 Suppression Drives a Targetable Serine Dependence in AML
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PSAT1 Suppression Drives a Targetable Serine Dependence in AML
Potent Activity of Duocarmyin- and Mmaf-Conjugated FLT3-Directed Antibody-Drug Conjugates Towards Acute Myeloid Leukemia Stem Cells in Vitro and In Vivo
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Potent Activity of Duocarmyin- and Mmaf-Conjugated FLT3-Directed Antibody-Drug Conjugates Towards Acute Myeloid Leukemia Stem Cells in Vitro and In Vivo
Role of the Interferon Alpha Inducible Protein 6 (IFI6) in Establishing Chemoresistance in Acute Myeloid Leukemia
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Role of the Interferon Alpha Inducible Protein 6 (IFI6) in Establishing Chemoresistance in Acute Myeloid Leukemia
S227928: A Novel Anti-CD74 ADC with MCL-1 Inhibitor Payload for the Treatment of Acute Myeloid Leukemia (AML) and Other Hematologic Malignancies
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S227928: A Novel Anti-CD74 ADC with MCL-1 Inhibitor Payload for the Treatment of Acute Myeloid Leukemia (AML) and Other Hematologic Malignancies
Selinexor Depletes Ruxolitinib Refractory Myelofibrosis Hematopoietic Stem Cells By Inducing Apoptosis and Blunting the Pro-Inflammatory Milieu
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Selinexor Depletes Ruxolitinib Refractory Myelofibrosis Hematopoietic Stem Cells By Inducing Apoptosis and Blunting the Pro-Inflammatory Milieu
Synergistic Activity of BMS-986397, a First-in-Class a Cereblon (CRBN) E3 Ligase Modulator (CELMoD) Targeting Casein Kinase 1α (CK1α), in Combination with Venetoclax and/or Azacitidine in Preclinical Models of Acute Myeloid Leukemia (AML)
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Synergistic Activity of BMS-986397, a First-in-Class a Cereblon (CRBN) E3 Ligase Modulator (CELMoD) Targeting Casein Kinase 1α (CK1α), in Combination with Venetoclax and/or Azacitidine in Preclinical Models of Acute Myeloid Leukemia (AML)
The Arginine Methyltransferase PRMT5 Regulates Maintenance and TKI Resistance of Self-Renewing FLT3-ITD AML LSC
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The Arginine Methyltransferase PRMT5 Regulates Maintenance and TKI Resistance of Self-Renewing FLT3-ITD AML LSC
The Expression of BTG1 in De Novo AML Patients Regulated By Demethylation of Decitabine and Its Evaluation in the Deep Remission of Patients
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The Expression of BTG1 in De Novo AML Patients Regulated By Demethylation of Decitabine and Its Evaluation in the Deep Remission of Patients
The PTPN2/PTPN1 Inhibitor Abbv-CLS-484 Augments Immune Responses Against Leukemic Blasts and Impedes Leukemia Cell Proliferation in AML Alone and in Combination with Venetoclax
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The PTPN2/PTPN1 Inhibitor Abbv-CLS-484 Augments Immune Responses Against Leukemic Blasts and Impedes Leukemia Cell Proliferation in AML Alone and in Combination with Venetoclax