602. Myeloid Oncogenesis: Basic: Poster III

Deciphering the Role of RAS Pathway Mutations in the Biology of Human Acute Myeloid Leukemia Using In Vivo Models

BOD1L Facilitates Chromatin Binding of SETD1A and Promotes Leukemia Cell Growth

Multiomic Characterization of Myelodysplastic Neoplasms (MDS) with Micromegakaryocytes Highlights the Role of EZH2-RUNX1 deregulation in Disease Physi

Integrative Genome and Transcriptome Sequencing Analysis Indicates Genetic and Epigenetic Dysregulation in DS-AML

Serum Amyloid A1 (SAA1) Secreted By the Stromal Microenvironment Drives Malignant Clonal Proliferation in Myelodysplastic Syndromes (MDS) and Acute My

Distinct Role of STAT3 and STAT5 Factors in MDS and AML

Phase Separation Mediates RUNX1- Mutation Leukemic Transformation

Novel Fusion Gene Aven-NUTM1 Induces Mice Myeloid Leukemia Vulnerable to HDAC Inhibitors

Rapid and Accurate Remethylation of Dnmt3a Deficient Hematopoietic Cells with Restoration of DNMT3A Activity

NUP98-Rearranged Acute Myeloid Leukemia Stem Cells Superimpose Type I Interferon Signaling with Canonical Self-Renewal Programs

Wilms’ Tumor 1 Functions As a Tumor Suppressor to Suppress FLT3-STAT Signaling and Epigenetic Remodeling in Acute Myeloid Leukemia (CALGB 8461, 9665 a

A Novel Interaction between RUNX1 and the Splicing Factor PTBP1 Is Enriched in Leukemia Cells

Signaling Pathway Mutations Cooperate with the PICALM/MLLT10 Fusion in a Knock-in AML Mouse Model

UBC9 Deficiency Accelerates AML Progression By Downregulating PARP1 Sumoylation and Subsequently Activating the NF-?B Pathway

Single-Cell Mutation Profiling and Alternative Splicing Analysis Reveals Distinct Aberrant Splicing of U2AF1S34 and U2AF1Q157 in Myeloid Malignancies

First-Hit SETBP1 Mutations Cause a Myeloproliferative Disorder with Bone Marrow Fibrosis

AML1-ETO and CCND2 Overexpression­ Cooperate to Drive AML Initiation and Progression