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MapleLMS Implementation
Conferences and Meetings 602. Myeloid Oncogenesis: Basic: Poster II

602. Myeloid Oncogenesis: Basic: Poster II

Short name: 602. Myeloid Oncogenesis: Basic: Poster II
Course start date: 11/09/2025

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AML Cells Have Increased Mitochondrial RNA Degradation and Inhibiting This Degradation Promotes Cell Differentiation, Decreases Viability, and Increases Sensitivity to Immune-Mediated Killing
CBL Loss or Mutations Reduces MHCII Expression through Downregulating ERG in Myeloid Malignancies
CRISPR-Cas9 Screening Identifies Therapeutic Targets for AML1-ETO Positive Leukemia
Chromatin-Based Cellular Dependency of HOXA9/MEIS1-Driven Acute Myeloid Leukemia
Codon-Specific Differences in RAS Mutations in AML and Differential Response to Therapeutic Agents
DNMT3A Mutations Deregulate the DNA Demethylation Pathway in Acute Myeloid Leukemia
ETV6 Contributes to Maintenance of Leukemia Stem Cells in Acute Myeloid Leukemia with High EVI1 Expression
FLT3-ITD Signaling Continuously Degrades p53 By the Ubiquitin-Proteosome Pathway Explaining Chemo-Resistance
Imatinib-Sensitive Chronic Myeloid Leukaemia Is Associated with mtDNA Mutations and Reduced Oxphos Capacity
Modulating mRNA Translation Fidelity As a Novel Mechanism for AML Chemoresistance
Multi-Pronged Effects of Cohesin Mutations in the Myeloid Leukemia of Down Syndrome
PTBP1, an RNA Binding Protein and Splicing Regulator, Binds RUNX1 and Co-Localizes at Target Gene Promoters in Leukemia
Proximity Proteomics Identifies a Role of MAP2K4 (MKK4) in JAK2 V617F Signaling
SLC25A1 Reprograms Mitochondrial and Fatty Acid Metabolism to Promote the Progression of Acute Myeloid Leukemia
STAT3-VDAC1 Axis Modulates Mitochondrial Function and Plays a Critical Role in the Survival of Leukemic Stem Cells
TET2 and TP53 Mutations Cooperate in Leukemia Development and Modulate the Response to Inflammation
The Exportin, CSE1L, Regulates Ribosome Biogenesis and Is a Selective Dependency in Childhood and Young Adult Acute Myeloid Leukemia
The LMO2-LDB1-TAL1 Complex Regulates Transcription Networks in AML Relapse