H3K79 Methylation Profiles Define Murine and Human MLL-AF4 Leukemias [PDF]
We created a mouse model wherein conditional expression of an Mll-AF4 fusion oncogene induces B precursor acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Gene expression profile analysis of the ALL cells demonstrated significant overlap with human MLL-rearranged ALL.
Madeleine Lemieux +2 more
exaly +5 more sources
The full transforming capacity of MLL-Af4 is interlinked with lymphoid lineage commitment. [PDF]
Abstract Chromosome rearrangements involving the mixed-lineage leukemia gene (MLL) create MLL-fusion proteins, which could drive both acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). The lineage decision of MLL-fusion leukemia is influenced by the fusion partner and microenvironment.
Lin S +4 more
europepmc +4 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 fuses MLL in-frame with the AF4 gene producing MLL-AF4 and AF4-MLL fusion proteins.
Godfrey L +10 more
europepmc +6 more sources
A conditional model of MLL-AF4 B-cell tumourigenesis using invertor technology [PDF]
MLL-AF4 fusion is the most common consequence of chromosomal translocations in infant leukaemia and is associated with a poor prognosis. MLL-AF4 is thought to be required in haematopoietic stem cells to elicit leukaemia and may be involved in tumour phenotype specification as it is only found in B-cell tumours in humans.
Markus Metzler +2 more
exaly +4 more sources
Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene [PDF]
MLL-AF4 fusion is a hallmark genetic abnormality in infant B-acute lymphoblastic leukemia (B-ALL) known to arise in utero. The cellular origin of leukemic fusion genes during human development is difficult to ascertain. The bone marrow (BM) microenvironment plays an important role in the pathogenesis of several hematological malignances. BM mesenchymal
Menendez, Pablo +9 more
openaire +6 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 +2 more sources
MLL-AF4, a double-edged sword for iPSC respecification into HSPCs. [PDF]
The successful derivation of human embryonic stem cells (hESCs) in 1998 (1) and later of induced pluripotent stem cells (iPSCs) in 2006/2007 (2, 3) led to huge excitement and held great promise to revolutionize several fields, from basic research to regenerative and personalized medicine, as these human pluripotent cells (hPSCs) have the potential when
Zeisig BB, So CWE.
europepmc +4 more sources
Venetoclax in combination with chidamide and azacitidine for the treatment of relapsed/refractory B-cell acute lymphoblastic leukemia with the MLL-AF4 gene: a case report and literature review [PDF]
B-cell acute lymphoblastic leukemia (B-ALL) with the MLL-AF4 fusion gene has a poor prognosis, and the mortality rate exceeds 90%, particularly in cases of extramedullary relapse (EMR).
Xuelian Jin, Zhigang Liu, Yu Wu, Jie Ji
doaj +2 more sources
Activity of immunoproteasome inhibitor ONX-0914 in acute lymphoblastic leukemia expressing MLL–AF4 fusion protein [PDF]
Proteasome inhibitors bortezomib and carfilzomib are approved for the treatment of multiple myeloma and mantle cell lymphoma and have demonstrated clinical efficacy for the treatment of acute lymphoblastic leukemia (ALL). The t(4;11)(q21;q23) chromosomal
Tyler W. Jenkins +8 more
doaj +2 more sources
t(4;11) leukemias display addiction to MLL-AF4 but not to AF4-MLL [PDF]
The most frequent MLL-gene rearrangement found in leukemia is a reciprocal translocation with AF4 on chromosome 4 resulting in the formation of the MLL-AF4 and the AF4-MLL fusion genes. The oncogenic role of MLL-AF4 is documented but the significance of the reciprocal product - AF4-MLL in leukemia is less clear.
Ashish Kumar, John H Kersey, Quanzhi Li
exaly +3 more sources

