|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, MA selectively inhibits proliferation and causes apoptosis in MLL-rearranged leukemia cells and downregulates the expression of MLL fusion target genes, including HOXA9 and MEIS1.
|
30951287 |
2019 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
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 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Serving as an effective inhibitor, 28d demonstrates the mechanism of cell killing in both cell cycle arrest and apoptotic effect as well as downregulation of the pivotal mixed lineage leukemia (MLL) fusion target genes such as HOXA9 and MEIS1, which reflects the critical roles of type I PRMTs in MLL leukemia.
|
29019697 |
2017 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicate that MLL is crucial for NUP98-HOXA9 leukemia initiation.
|
28210005 |
2017 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Recently, SALL4 has been further linked to the functions of MLL and its target gene homeobox A9 (HOXA9).
|
28974232 |
2017 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
HOXA9 and MEIS1 are considered to be the most critical targets of MLL fusions and their coexpression rapidly induces AML.
|
26747896 |
2016 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
CCI-007 altered the characteristic MLL-r gene expression signature in sensitive cells with downregulation of the expression of HOXA9, MEIS1, CMYC and BCL2, important drivers in MLL-r leukemia, within a few hours of treatment.
|
27317766 |
2016 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mixed-lineage leukemia (MLL) maintains the expression of cellular memory genes during development, while leukemic MLL fusion proteins aberrantly maintain expression of hematopoietic stem cell program genes such as HOXA9 to cause leukemia.
|
24465000 |
2014 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mixed lineage leukemia (MLL) fusion proteins directly activate the expression of key downstream genes such as MEIS1, HOXA9 to drive an aggressive form of human leukemia.
|
24445817 |
2014 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Although high expression of Hoxa9 in MLL fusion leukemia is supposed to be responsible for the recruitment of EZH2, our data also suggest that there may be some other mechanisms independent of Hoxa9 activation to suppress p16 expression, because expression levels of Hoxa9 and p16 were not inversely related between MLL/ENL and Hoxa9/Meis1 transduced cells.
|
24612037 |
2014 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, our both in vitro and in vivo functional studies demonstrate that Tet1 plays an indispensable oncogenic role in the development of MLL-rearranged leukemia, through coordination with MLL-fusion proteins in regulating their critical cotargets, including homeobox A9 (Hoxa9)/myeloid ecotropic viral integration 1 (Meis1)/pre-B-cell leukemia homeobox 3 (Pbx3) genes.
|
23818607 |
2013 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
And, although Nup98-HOXA9, MEIS1-HOXA9, and E2A-Hlf could transform ME-deficient cells, both MLL-AF9 and MLL-ENL were ineffective, indicating that the ME requirement is specific to MLL fusion leukemia.
|
24021671 |
2013 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, we observed that SALL4 interacted with mixed-lineage leukemia (MLL) and co-occupied the HOXA9 promoter region with MLL in AML leukemic cells, which suggests that a SALL4/MLL pathway may control HOXA9 expression.
|
24051379 |
2013 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Through interactions with the polymerase-associated factor complex (PAFc), mixed lineage leukemia (MLL) fusion proteins activate genes critical for blocking differentiation, such as HOXA9.
|
23900238 |
2013 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
With regard to the mechanism of therapy using AAV8-IL24 in MLL/AF4-positive ALL, we demonstrated the antiangiogenicity and effects on the ER stress pathway and unreported pathways through inhibition of S100A6 and HOXA9, which is specific to MLL/AF4-positive ALL.
|
22025528 |
2012 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Collectively, our data indicate that both truncated and full-length forms of HOXA9 are highly expressed in human MLL-rearranged leukemia, and the truncated isoform of HOXA9 might also play an oncogenic role by cooperating with canonical HOXA9 in cell transformation and leukemogenesis.
|
22633751 |
2012 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Chromatin immunoprecipitation followed by quantitative polymerase chain reaction was used to determine how binding of associating proteins compare across Hoxa9 and Meis1 in cell lines with and without MLL fusion proteins and how binding is altered during gene down-regulation and differentiation.
|
20854876 |
2011 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
IGF-1R expression correlated with endogenous HoxA9 expression in a small panel of mixed lineage leukemia (MLL)/AF4 cell lines. siRNA knockdown of endogenous HoxA9 expression in the MLL/AF4-positive cell line RS4;11 resulted in loss of IGF-1R expression.
|
18337761 |
2008 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Co-expression of HoxA9 and Meis1 genes in the KP-L-RY cell line indicated possible functional similarity between MLL-AF4 and MLL-AF5q31.
|
12399976 |
2002 |