KMT2A, lysine methyltransferase 2A, 4297

N. diseases: 535; N. variants: 65
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 GeneticVariation disease BEFREE MLL rearrangements play a crucial role in leukemogenesis and comprise a poor prognosis. 31417187 2019
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Highlighting the central role of BCL6 in <i>MLL-</i>rearranged B-ALL, conditional deletion and pharmacological inhibition of BCL6 compromised leukemogenesis in transplant recipient mice and restored sensitivity to vincristine chemotherapy in <i>MLL-</i>rearranged B-ALL patient samples. 31395741 2019
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Furthermore, PCR analysis showed that the chromosome 11 breakpoint was at the APOA5/APOA4 locus at 11q23.3, which is associated with malignancy, and that the chromosome 22 breakpoint was at the SEPT5 intron 1 locus, which also plays a role in leukemogenesis through formation of a fusion gene with MLL. 30680670 2019
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Numerous <i>in vitro</i> and <i>in vivo</i> studies have demonstrated that the <i>KMT2A</i>/MLLT3 super elongation complex subunit (<i>MLLT3</i>) fusion gene on the derivative chromosome 11 serves a crucial role in leukemogenesis. 31807181 2019
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Our findings demonstrate that the abnormal elevated expression of circAF4 regulates the cell growth via the circAF4/miR-128-3p/MLL-AF4 axis, which could contribute to leukemogenesis, suggesting that circAF4 may be a novel therapeutic target of MLL-AF4 leukemia. 31623653 2019
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Overall, this study suggests that the fetal liver Mll-AF4+ LSK cells are sensitive to direct exposure to inflammatory stimuli, especially poly(I:C); however, maternal immune activation induced by a single exposure to poly(I:C) is not sufficient to initiate MLL-AF4 leukemogenesis. 31381950 2019
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Whereas WNT/β-catenin signaling has previously been shown to support MLL-AF9-driven leukemogenesis, the mechanism underlying this relationship remains unclear. 30528456 2019
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE MLL-fusion proteins, AF9 and ENL, play an essential role in the recruitment of DOT1L and the H3K79 hypermethylation of MLL target genes, which is pivotal for leukemogenesis. 30258537 2018
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE In addition, a mouse model of MLL-AF9-driven leukemogenesis was used to study the role of Baf200 in malignant hematopoiesis. 29482581 2018
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE The DOT1L histone H3 lysine 79 (H3K79) methyltransferase plays an oncogenic role in MLL-rearranged leukemogenesis. 29343685 2018
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE These results uncover a dependency for SETD2 during MLL-leukemogenesis, revealing a novel actionable vulnerability in this disease. 29777171 2018
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 AlteredExpression disease BEFREE Aberrant fusion proteins involving the MLL histone methyltransferase (HMT) lead to recruitment of DOT1L, to a multi-protein complex resulting in aberrant methylation of histone H3 lysine 79 at MLL target genes, and ultimately enhanced expression of critical genes for hematopoietic differentiation, including HOXA9 and MEIS1, and as such defines the established mechanism for leukemogenesis in MLL-rearrangement (MLL-r) leukemias. 28229434 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Conditional deletion of <i>Mof</i> in a mouse model of <i>MLL-AF9</i>-driven leukemogenesis reduced tumor burden and prolonged host survival. 28202522 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE This review provides an overview of different MLL-FP mouse model systems and discusses how well they have recapitulated aspects of the human disease as well as highlights the biological insights each model has provided into MLL-FP leukemogenesis. 28179274 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Epigenetic dysregulation is considered a key driver of MLL-r leukemogenesis, which theoretically supports the use of epigenetic modifiers as a treatment option. 28675638 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Using an MLL-AF9 murine leukemia model and serial transplantation studies, we show that ZFP521 is not required for leukemogenesis, although its absence leads to a significant delay in leukemia onset. 28615219 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 AlteredExpression disease BEFREE We further demonstrate that the designed photo-controllable azo-peptidomimetics affect the transcription of the MLL1-target gene Deptor, which regulates hematopoiesis and leukemogenesis, and inhibit the growth of leukemia cells. 28970883 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 AlteredExpression disease BEFREE In MLL1 fusion-driven leukemia, aberrant activation of HOXA genes is epigenetically mediated by the TrxG complex and HOXA gene expression and leukemogenesis are critically dependent on the protein-protein interaction between the TrxG proteins MLL1 and menin. 27888797 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE In this study, we utilized two well-established murine models of human AML induced by MLL-AF9 or AML1-ETO9a to determine the role of Necdin in leukemogenesis. 29152105 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE In this issue of Cancer Cell, Chen et al. describe complementary approaches demonstrating that MLL1 is dispensable for MLL-fusion-mediated leukemogenesis. 28609652 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 AlteredExpression disease BEFREE Proteomic data resolve association of dimerized MLL with gene expression modulators, and inhibiting dimerization disrupts formation of these complexes while completely abrogating leukemogenesis in mice. 29062045 2017
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Our data reveal a molecular dependency on MLL1 function in NUP98-fusion-driven leukemogenesis. 27889185 2016
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE We found that although mice receiving MLL-AF9-transduced FL or BM cells develop AML, loss of Id1 significantly prolonged the median survival of mice receiving FL cells but accelerated leukemogenesis in recipients of BM cells. 26944543 2016
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Through inhibiting expression of TET1 and its downstream targets, forced expression of miR-26a significantly suppresses the growth/viability of human MLL-rearranged AML cells, and substantially inhibits MLL-fusion-mediated mouse hematopoietic cell transformation and leukemogenesis. 26791235 2016
CUI: C0598766
Disease: Leukemogenesis
Leukemogenesis
0.100 Biomarker disease BEFREE Forced Dnmt3b expression induced widespread DNA hypermethylation inMyc-Bcl2-induced leukemias, preferentially at gene bodies.MLL-AF9-induced leukemogenesis showed much less pronounced DNA hypermethylation upon Dnmt3b expression. 26729896 2016