CD59 organizes the plasma membrane to sustain oncogenic Ras-MAPK signaling and is a targetable vulnerability in acute myeloid leukemia

LPCAT3 is essential for leukemia progression and represents a therapeutic vulnerability in AML

RNA-seq following LPCAT3 loss showed that genes differentially expressed were significantly enriched in granulocyte chemotaxis–related pathways, suggesting a role of LPCAT3 in modulation of leukemic differentiation programs and microenvironmental interactions, established that LPCAT3 as a previously unrecognized mediat...

A PTBP1–CDC42 splicing axis regulates leukemia growth and venetoclax sensitivity in acute myeloid leukemia

PTBP1 is established as a critical regulator of AML cell fitness and a clinically actionable therapeutic combination that exploits AML dependency on PTBP1-CDC42 signaling to enhance the efficacy of venetoclax-based regimens is identified.

ARID1B mutations promote immune evasion in acute myeloid leukemia through upregulating VISTA expression.

Acute myeloid leukemia (AML) is defined by epigenetic heterogeneity, and recurrent mutations in chromatin remodelers are associated with a poor prognosis. Whether these mutations drive treatment resistance through remodeling of the tumor immune microenvironment remains unclear. ARID1B, a recurrently mutated SWI/SNF sub...

Dynamic expression of CD9 protein in T-cell acute lymphoblastic leukemia.

CD36 Influences Leukemia Progression in MLL-AF9-Driven AML by Modulating the Leukemia Immune Microenvironment.

CD36, a fatty-acid translocase, is increasingly implicated in acute myeloid leukemia biology and treatment resistance, yet its contribution to leukemogenesis is still unclear. Using the MLL-AF9 model, we transduced hematopoietic stem/progenitor cells (HSPCs) from Cd36-knockout (KO) or wild-type (WT) mice and assessed l...

ANKRD28 interacts with DOCK180 to activate Rac1-STAT3-Myc signaling and sustain stemness of CD34+ leukemia stem cells in acute myeloid leukemia.