Epigenetic regulator genes direct lineage switching in MLL/AF4 leukemia. [PDF]
Key Points • Myeloid relapse can originate from various differentiation stages of MLL/AF4+ ALL.• Dysregulation of epigenetic regulators underpins fundamental lineage reprogramming.
Tirtakusuma R +56 more
europepmc +7 more sources
The RNA-binding protein IGF2BP3 is critical for MLL-AF4-mediated leukemogenesis. [PDF]
Despite recent advances in therapeutic approaches, patients with MLL-rearranged leukemia still have poor outcomes. Here, we find that the RNA-binding protein IGF2BP3, which is overexpressed in MLL-translocated leukemia, strongly amplifies MLL-Af4 ...
Tran TM +13 more
europepmc +7 more sources
circRNA circAF4 functions as an oncogene to regulate MLL-AF4 fusion protein expression and inhibit MLL leukemia progression [PDF]
Background Circular RNAs (circRNAs) represent a type of endogenous noncoding RNAs that are generated by back-splicing events and favor repetitive sequences.
Wei Huang +12 more
doaj +3 more sources
Mll-AF4 Confers Enhanced Self-Renewal and Lymphoid Potential during a Restricted Window in Development [PDF]
MLL-AF4+ infant B cell acute lymphoblastic leukemia is characterized by an early onset and dismal survival. It initiates before birth, and very little is known about the early stages of the disease’s development.
Neil A. Barrett +7 more
doaj +3 more sources
Enhanced hemato-endothelial specification during human embryonic differentiation through developmental cooperation between AF4-MLL and MLL-AF4 fusions [PDF]
The t(4;11)(q21;q23) translocation is associated with high-risk infant pro-B-cell acute lymphoblastic leukemia and arises prenatally during embryonic/fetal hematopoiesis.
Clara Bueno +17 more
doaj +3 more sources
Targeting IGF2BP3 enhances antileukemic effects of menin-MLL inhibition in MLL-AF4 leukemia. [PDF]
Key Points • Knockdown of IGF2BP3 sensitizes MLL-AF4 leukemia to menin-MLL inhibition.• These data support the role of IGF2BP3 as an oncogenic amplifier in MLL-AF4 leukemogenesis and its therapeutic potential.
Lin TL +10 more
europepmc +2 more sources
MLL-AF4 binds directly to a BCL-2 specific enhancer and modulates H3K27 acetylation. [PDF]
Survival rates for children and adults carrying mutations in the Mixed Lineage Leukemia (MLL) gene continue to have a very poor prognosis. The most common MLL mutation in acute lymphoblastic leukemia is the t(4;11)(q21;q23) chromosome translocation that ...
Godfrey L +10 more
europepmc +5 more sources
MiR-27a downregulates 14-3-3θ, RUNX1, AF4, and MLL-AF4, crucial drivers of blast transformation in t(4;11) leukemia cells. [PDF]
The chromosomal translocation t(4;11)(q21;q23), a hallmark of an aggressive form of acute lymphoblastic leukemia (ALL), encodes mixed‐lineage leukemia (MLL)‐AF4 oncogenic chimera that triggers aberrant transcription of genes involved in lymphocyte ...
Fioretti T +8 more
europepmc +2 more sources
H3K79me2/3 controls enhancer-promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells. [PDF]
MLL gene rearrangements (MLLr) are a common cause of aggressive, incurable acute lymphoblastic leukemias (ALL) in infants and children, most of which originate in utero. The most common MLLr produces an MLL-AF4 fusion protein.
Godfrey L +20 more
europepmc +2 more sources
Nuclear FGFR2 Interacts with the MLL-AF4 Oncogenic Chimera and Positively Regulates <i>HOXA9</i> Gene Expression in t(4;11) Leukemia Cells. [PDF]
The chromosomal translocation t(4;11) marks an infant acute lymphoblastic leukemia associated with dismal prognosis. This rearrangement leads to the synthesis of the MLL-AF4 chimera, which exerts its oncogenic activity by upregulating transcription of ...
Fioretti T +7 more
europepmc +2 more sources

