| The ENL moiety of the childhood leukemia-associated MLL-ENL oncoprotein recruits human Polycomb 3. | leukemia, |
| myeloid gene dysregulation is dispensable in leukemic transformation mediated by MLL fusion proteins; dysregulation of HOX gene family members is implicated as a dominant mechanism of leukemic transformation induced by chimeric MLL oncogenes | leukemia, |
| Identification of CBL, a proto-oncogene at 11q23.3, as a novel MLL fusion partner in a patient with de novo acute myeloid leukemia. | leukemia, |
| Partial duplication of the MLL oncogene in patients with aggressive acute myeloid leukemia. | leukemia, |
| The TCR gene rearrangements in childhood B-lineage acute lymphoblastic leukemia was associated with expression of MLL chimeric oncogene. | leukemia, |
| The incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression. | leukemia, |
| Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities. | leukemia, |
| Mixed-lineage leukemia (MLL) is a proto-oncogene frequently involved in chromosomal translocations associated with acute leukemia. | leukemia, |
| c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis. | leukemia, |
| Acute myeloid leukemia with t(9;11)(p21-22;q23): common properties of dysregulated ras pathway signaling and genomic progression characterize de novo and therapy-related cases. | leukemia, |
| Regardless of the precise mechanism, a consistent effect of MLL fusion oncogenes in human leukemia is to induce high level expression of HOXA and MEIS1 genes. | leukemia, |
| Grist for the MLL: how do MLL oncogenic fusion proteins generate leukemia stem cells?. | leukemia, |
| data provide a structural basis for understanding the role of menin as a tumor suppressor protein and as an oncogenic co-factor of mixed lineage leukemia fusion proteins | leukemia, |
| Identification of genes that define transcription factor networks and important genetic pathways acting during progression of leukemia induced by MLL fusion oncogenes. | leukemia, |
| Data show that MLL fusion oncogenes maintain leukemia-associated Rac GTPases activity by regulating Frat gene expression, specifically Frat2. | leukemia, |
| Report oncogenic potential of MLL-NEBL and NEBL-MLL fusion genes in acute myeloid leukemia. | leukemia, |
| model whereby cotranscriptional recruitment of Rnf20 at MLL-fusion target genes leads to amplification of Dot1l-mediated H3K79 methylation, thereby rendering leukemia cells dependent on Rnf20 to maintain their oncogenic transcriptional program | leukemia, |
| Abrogation of Rac1 signaling causes DNA double-strand breaks in acute monocytic leukemia cells harbouring the MLL-AF9 oncogene. | leukemia, |
| MicroRNA-142-3p inhibits cell proliferation in human acute lymphoblastic leukemia by targeting the MLL-AF4 oncogene. | leukemia, |
| The leukemia-associated Mll-Ell oncoprotein induces fibroblast growth factor 2 (Fgf2)-dependent cytokine hypersensitivity in myeloid progenitor cells. | leukemia, |