604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster III

AML Blasts Intrinsic Interferon Production Causes Resistance to Venetoclax in Human Acute Myeloid Leukemia Via Upregulation of MCL1, BCL2A1 and BCL-XL

APG-2449, a Novel Focal Adhesion Kinase (FAK) Inhibitor, Exhibits Antileukemic Activity and Enhances Lisaftoclax (APG-2575)-Induced Apoptosis in Acute Myeloid Leukemia (AML)

BMS-986397, a First-in-Class Molecular Glue Degrader of Casein Kinase 1α (CK1α) for the Treatment of Acute Myeloid Leukemia (AML) and High-Risk Myelodysplastic Syndrome (HR-MDS) Harboring Functional TP53

CD74 Antibody Conjugated to an MCL1 Inhibitor (S227928) Combines Synergistically with Venetoclax to Enhance Killing of Acute Myeloid Leukemia

Characterizing Secondary-Site Mutations in Isocitrate-Dehydrogenase-1 (IDH1)

Effects of Magrolimab Therapy in Conjunction with Conventional Chemotherapeutics in Pediatric Acute Myeloid Leukemia Patient Derived Xenograft Models

Integrated Stress Response Activation Induced By Usnic Acid Alleviates BCL-2 Inhibitor ABT-199 Resistance in Acute Myeloid Leukemia

Interferon Synergizes with Inhibition of Pro-Apoptotic Proteins to Reduce Leukemia Burden in PDX Models of ML-DS

Loss of TET2 Creates a Distinct Immunopeptidome in Acute Myeloid Leukemia

Loss of TET2 Increases MHC Class I Expression in Acute Myeloid Leukemia

Pharmacodynamic Analysis of Mcl-1 and RNA Pol IISer2 Phosphorylation in Blasts from Patients with Relapsed or Refractory Acute Myeloid Leukemia Treated on a Phase 1 Study of Venetoclax Plus Voruciclib

Pharmacological Evaluation of a First-in-Class Hemoglobin Elevating Agent (HbEA) AND017 in a Mouse MDS Model of an Inducible Mutant c-Myc Knock-in

RGT-61159, Best-in-Class Small Molecule Inhibitor of MYB Via Selective RNA Splicing Alteration, Showed Robust Anti-Tumor Activity across AML Tumor Models Harboring Common Genetic Lesions

Reactivation of p53 in TP53-Y220C Mutant AML: Mechanism of Action and Mechanism-Based Drug Combinations

Specific Bone Marrow Niche Components Determine Degree of Protection from Gilteritinib Induced Differentiation Response in FLT3-ITD AML

Statins Kill Acute Myeloid Leukemia Cells through Low-Density Lipoprotein Receptor-Mediated Unfolded Protein Response Activation

Synergistic Effect of EZH2 Inhibitor Dznep and Flavonoid GL-V9 in AML through Inhibition Hells and Induction of DNA Damage

Targeting Chronic Myeloid Leukemia with Potent and Specific BCR::ABL1 Degraders

Targeting PERK Arm of Unfolded Protein Response Helps to Eliminate Therapy-Induced Residual Senescent-like Acute Myeloid Leukemia Cells

Targeting the IRE1α-XBP1s Pathway to Enhance Venetoclax Effectiveness in AML

The Hyperbolic NAMPT Inhibitor RPT1G Synergizes with BCL-2 Family Inhibitors and Helps Overcome Venetoclax Resistance in Acute Myeloid Leukemia Cells

Type 2 Diabetes Leads to the Senescence of the Bone Marrow Microenvironment, and the Increase in DNA Damage Repair Function of AML Cells Mediates Anthracycline Resistance through Sasp

Using Structure-Based Modeling to Identify Effective Drug Combinations in RAS-Mutant Acute Myeloid Leukemia