651. Multiple Myeloma and Plasma Cell Dyscrasias: Basic and Translational: Poster I

Targeting Distinct Epitopes of FCRL5 Using CAR-T Generated with Sequences Derived from Newly Identified FCRL5 Humanized Antibodies Resulted in Potent

IRF4-BLOC1S5, the First Genomic Fusion Gene Identified in the TEMPI Syndrome

Translation Inhibition through eIF4A1 Targeting in Multiple Myeloma Is a Promising Therapeutic Strategy

Intracytoplasmatic BCMA Point Mutation and Teclistamab Resistance: Genomic Assessment of a Multidrug-Resistant Multiple Myeloma Patient

Circulating Exosomal miRNA Signature As a Potential Risk Factor for DNA Virus Infection in Patients with Multiple Myeloma

IRF2 Regulates De Novo Active Chromatin Regions and Participates in the Development and Pathogenesis of Multiple Myeloma

IGF2BP1 Promotes Multiple Myeloma with Chromosome 1q Gain Via Increasing CDC5L Expression in an m6A-Dependent Manner

CREB1 Promotes Immune Escape of Multiple Myeloma Cells By Inducing HLA-E

Global Proteomics Identifies CDK11A/B As Integral to Myeloma Proliferation and High-Risk Disease

Mechanisms of Resistance and Relapse with Talquetamab in Patients with Relapsed/Refractory Multiple Myeloma from the Phase 1/2 MonumenTAL-1 Study

BCMA-Targeted Bortezomib Nanotherapy (BCMA-BTZ-Nps) Targets Tumor, Enhances Therapeutic Efficacy, Triggers Immunogenic Cell Death, Overcomes Drug Resi

Preclinical In Vivo Imaging of Multiple Myeloma with [18f]Fluorohomoleucine (FHL) PET/CT

CD70/CD27 Signaling Promotes Expansion of Clonal Plasma Cells in Multiple Myeloma and Is a Promising Therapeutic Target in Advanced Disease

Development of First in Class DNA-Zip Code Drug Conjugate (ZDC) in Multiple Myeloma

The Impact of Treatment-Free Intervals on T-Cell Exhaustion and Clonotypic Diversity in Myeloma Patients Treated with BCMA Bispecific Antibodies

Transcriptional Co-Activator P300 Promotes Extra-Medullary Disease Formation and Myeloma Disease Progression

Baseline CD57+ and CD16+ NK-Cells Predict Treatment Outcome in Non-Transplant Eligible Newly Diagnosed Multiple Myeloma Patients Treated with Daratumu

A High-Risk Subgroup Multiple Myeloma Classification Based on the Detection of PR Minor Subclones

Stable MGUS and SMM Are Characterized By Distinct Senescent Features in the Pre-Malignant Plasma Cells and the Proximate Bone Microenvironment

Immune and Genome Profiling of Myeloma Patients Treated with Sequential Immunotherapies Reveal Differential Non-Overlapping Mechanisms of Resistance

Novel Isoforms Identified By Isoseq Analysis Drive Expression Differences in Key Genes That Delineate the Subtypes of Waldenstrom’s Macroglobulinemia

A Functional Genomic Screen to Identify Novel Genes Involved in Multiple Myeloma Tumour Development

Co-Expression of GPRC5D, FcRH5 and BCMA Suggests That Targeting More Than One Cell Surface Marker May be a Viable Strategy in Relapsed/Refractory Mult

Characterization of a New Metabolic Score Correlated with CD38 Cell-Surface Expression and Response to Daratumumab Treatment in Multiple Myeloma

Inhibiting FOXM1 Sensitizes Myeloma Cells to BCL2 Inhibitor Venetoclax By Repressing MYC Pathway

Higher CD56 Expression on Multiple Myeloma Cells Increases CD38 Expression, Reduces Intracellular NAD+ Levels, and Enhances the Efficacy of Daratumuma

Early Subclones Showing Aberrant Co-Expression of Stem Cell, T Cell and Myeloid Genes Can be Detected By Flow Cytometry in MYD88 Mutated Waldenström’s

A CD38/CD28xCD3 Trispecific T-Cell Engager (TCE) As a Potentially Active Agent in Multiple Myeloma Patients Relapsed and/or Refractory (RRMM) to Anti-