602. Myeloid Oncogenesis: Basic: Poster II

Epigenetic basis of MDS MPN overlap syndrome with compound loss of Kmt2c and Dnmt3a

HDAC inhibitors potentiate the efficacy of antineoplastic agents in acute megakaryoblastic leukemia via dual activation of apoptosis and pyroptosis

Deciphering the mechanistic role of mixed lineage leukemia partial tandem duplications MLLPTD in MDS and AML

Chromodomain helicase DNA binding protein CHD2 interacts with TET2 and regulates lineage defining transcription in hematopoietic stem and progenitor cells

Oncofetal RNA binding proteins IGF2BP suppress innate immunity signaling pathways in leukemia stem cells

PSF3 recruits DNA polymerase theta Polθ to stalled replication forks to promote DNA repair and survival of myeloid malignant cells

Unravelling the epigenetic drivers of chip – MDS CMML – AML progression through novel methylation sensitive regulatory elements

RAS G12 and Q61 codon mutations confer distinct disease characteristics in Acute Myeloid Leukemia and exhibit differential response to RAS ON inhibitor RMC 7977

ZBTB7A loss promotes RUNX1 RUNX1T19a driven leukemia by enhancing the block of erythroid differentiation

Transgenic expression of enhanced AsCas12a in mice enables In Vivo multiplex genetic editing and development of diverse novel models of myeloid neoplasms

Cooperative activation of NF κB by inv 3 t 3 3 and NRAS mutations drives myeloid leukemogenesis

Tissue specific requirement for the inv 16 oncogene CBFB MYH11 implies unique leukemia survival mechanisms in the bone marrow microenvironment

Inhibition of CPT1A reverses AML1 ETO induced differentiation blockage by activating BCL 2 MYC signaling and metabolic reprogramming