|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
MLL rearrangement most often results from translocation or partial tandem duplication, although recent published reports suggest a different mechanism by which MLL might participate in leukemogenesis: MLL amplification.
|
12034519 |
2002 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
MLL (ALL-1) chimeric fusions and MLL partial tandem duplications (PTD) may have mechanistically distinct contributions to leukemogenesis.
|
15774615 |
2005 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
MLL-AF4 may be sufficient on its own for leukemogenesis or the gene-fusion product may alternatively predispose transformed cells to global genetic instability, enhancing the acquisition of additional key mutations.
|
23893660 |
2013 |
|
Leukemogenesis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MLL(DNMT1 CXXC)-AF9 shows robust in vitro colony forming activity and in vivo leukemogenesis, similar to MLL-AF9.
|
23990460 |
2013 |
|
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 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
MLL rearrangements play a crucial role in leukemogenesis and comprise a poor prognosis.
|
31417187 |
2019 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
A number of experiments show that the resulting MLL fusion genes directly contribute to leukemogenesis.
|
15269783 |
2004 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
A relevant role of septins in leukemogenesis has been uncovered by their involvement as fusion partners in MLL-related leukemia.
|
19445675 |
2009 |
|
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 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additional genetic changes, such as ETV6 loss, extra RUNX1, ETV6/RUNX1 duplication, and MLL aberrations in the ETV6/RUNX1-positive group, supported the hypothesis of the ETV6/RUNX1 leukemogenic model that these secondary changes are necessary for leukemogenesis rather than progression of disease.
|
18728978 |
2008 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
AF4 antibodies should be useful for further elucidation of the function of AF4 in normal cellular physiology, as well as the function of MLL-AF4 in leukemogenesis.
|
9808577 |
1998 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Besides its importance in endocrine organs, menin has been shown to interact with the mixed lineage leukemia (MLL) protein, a histone H3 lysine 4 methyltransferase, and plays a critical role in hematopoiesis and leukemogenesis.
|
21740816 |
2011 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
CBP is the first partner gene of MLL containing well defined structural and functional motifs that provide unique insights into the potential mechanisms by which these translocations contribute to leukemogenesis.
|
9238046 |
1997 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Collectively, our data suggest that PBX3 is a critical cofactor of HOXA9 in leukemogenesis, and targeting their interaction is a feasible strategy to treat presently therapy resistant CA-AML (eg, MLL-rearranged leukemia) in which HOXA/PBX3 genes are overexpressed.
|
23264595 |
2013 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Common genetic aberrations responsible for lymphomagenesis are deletions of 6q, loss of p53, and amplification of the 3q27 and the MLL gene regions.(Blood.2000;95:1180-1187)
|
10666188 |
2000 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Complementary FISH helped us identify involvement of TP53, MLL, and RUNX1/AML1 genes in 82% of cases, confirming their probable role in leukemogenesis.
|
15721632 |
2005 |
|
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 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Deletions of MLL that abolish interactions with PAFc also eliminate MLL-AF9 mediated immortalization indicating an essential function for this interaction in leukemogenesis.
|
20541477 |
2010 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
DNA damage response and inflammatory signaling limit the MLL-ENL-induced leukemogenesis in vivo.
|
22516260 |
2012 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
DNA structural properties of AF9 are similar to MLL and could act as recombination hot spots resulting in MLL/AF9 translocations and leukemogenesis.
|
10861294 |
2000 |
|
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 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
For instance, the MLL-AF9 fusion oncogene is thought to contribute to myeloid leukemogenesis by driving a hematopoietic stem cell-like "self-renewal" gene expression signature in committed myeloid progenitors.
|
22613471 |
2012 |
|
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 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Forced expression of miR-150 dramatically inhibited leukemic cell growth and delayed MLL-fusion-mediated leukemogenesis, likely through targeting FLT3 and MYB and thereby interfering with the HOXA9/MEIS1/FLT3/MYB signaling network, which in turn caused downregulation of MYC/LIN28.
|
23079661 |
2012 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further analysis of this novel type of MLL fusion protein would provide new insights into leukemogenesis.
|
15897884 |
2005 |