Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We evaluated the function of Meningioma 1 (MN1), a cofactor of HOXA9 and MEIS1, in human and murine MLL-rearranged leukemia by CRISPR-Cas9 mediated deletion of MN1.
|
31413090 |
2019 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Homeobox A9 (HOXA9) is an oncogene in leukemia and has been implicated in CRC pathology, although its role in disease etiology remains obscure at best.
|
31099823 |
2019 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Expression of mutant JAK3 and HOXA9 led to a rapid development of leukemia originating from multipotent or lymphoid-committed progenitors, with a significant decrease in disease latency compared with JAK3 or HOXA9 alone.
|
29496663 |
2018 |
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
MLL-AF9 is one such rearrangement that recruits the lysine methyltransferase, human disruptor of telomere silencing 1-like (DOT1L) and lysine specific demethylase 1 (LSD1), resulting in elevated expression of the Homeobox protein A9 (HOXA9), and leukemia.
|
29972300 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In a murine bone marrow transplantation model, mice transplanted with cells overexpressing Ednra and Hoxa9 succumbed to leukemia significantly earlier than mice transplanted with cells overexpressing Hoxa9 only.
|
30384975 |
2018 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
<b>Methods:</b> Using the gene expression profiling of TCGA and E-MTAB-3444 datasets, we screened for high co-expression of PBX3 and HOXA9 in NPMc+ leukemia patients.
|
30214626 |
2018 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
To define the role of Flt3 in AML with high Hoxa9/Meis1, we treated mice with Hoxa9/Meis1-induced AML with the Flt3 inhibitor AC220, used an Flt3-ligand (FL-/-) knockout model, and investigated whether overexpression of Flt3 could induce leukemia together with overexpression of Hoxa9.
|
27617578 |
2017 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Finally, Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia.
|
28399410 |
2017 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Genetic characterization of NA9-induced phenotypes suggested interference with PVR (Flt1-4 RTK homolog) signaling, which is similar to functional interactions observed in mammals between Flt3 and HOXA9 in leukemia.
|
27838340 |
2017 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interaction of HOXA9/MEIS1/PBX3 is responsible for hematopoietic system transformation in MLL-rearranged (MLL-r) leukemia.
|
28411381 |
2017 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicate that MLL is crucial for NUP98-HOXA9 leukemia initiation.
|
28210005 |
2017 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Understanding the mechanisms regulating the expression and activity of HOXA9, along with its critical downstream targets, shows promise for the development of more selective and effective leukemia therapies.
|
27258906 |
2016 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Role of HOXA9 in leukemia: dysregulation, cofactors and essential targets.
|
26028034 |
2016 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although MEIS1 alone has only a moderate effect on cell proliferation in vitro, it is essential for the development of HOXA9-induced leukemia in vivo.
|
27018596 |
2016 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Finally, kinetics and severity of disease in transplantation assays indicated that Pbx3/Meis1 dimers are rate-limiting factors for Hoxa9-induced leukemia.
|
25911551 |
2015 |
Childhood Leukemia
|
0.100 |
Biomarker
|
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 |
Childhood Leukemia
|
0.100 |
Biomarker
|
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 |
Childhood Leukemia
|
0.100 |
Biomarker
|
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 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Prdm16, a transcription factor associated with human acute myeloid leukemia, was markedly repressed by HOXB4 but upregulated by HOXA9 and HOXA10, suggesting that Prdm16 downregulation was involved in preventing leukemia in HOXB4 transplanted mice.
|
25082879 |
2014 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data establish microRNA as functional effectors of endogenous HOXA9 and HOX-based leukemia oncoproteins, provide a concise in vivo platform to test RNA therapeutics, and suggest therapeutic value for microRNA antagonists in AML.
|
24334453 |
2014 |
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In addition to DNA binding activity, it was critical that specific CpG residues in the Hoxa9 locus were protected from methylation for leukemia development.
|
23990460 |
2013 |
Childhood 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 |
Childhood Leukemia
|
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 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We report that expression of the reactive oxygen species (ROS) scavenger glutathione peroxidase 3 (GPx3) positively correlates with the frequency of leukemia stem cells (LSCs) in Hoxa9+Meis1-induced leukemias.
|
22508837 |
2012 |
Childhood 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 |