Findings reveal CD59 as a critical regulator of Ras-MAPK signaling required for AML growth and nominate its rILYd4-mediated degradation as a therapeutic strategy.
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...
Mu-Tian Cao, L. Cong, Yi-Fei He et al.· Blood Science· 0 citations
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.
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...
Wanxiu Mao, Jia-Yi Cui, Hanqi Su et al.· International Immunopharmaco...· 0 citations
It is found that CD9 overexpression is associated with leukemic T cells that have migrated outside the thymus into peripheral tissues and CD9 expression is heterogeneous, tends to increase at relapse and is enriched in the TAL1 molecular subtype.
J. Quessada, Mathis Nozais, Charlotte Savey et al.· Cancer Gene Therapy· 0 citations
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...
Yi-Ting Meng, Wen-Da Zhu, M. Pospiech et al.· Pharmacological Research· 0 citations