|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Aberrant transcriptional regulation of the MLL fusion partner EEN by AML1-ETO and its implication in leukemogenesis.
|
16990610 |
2007 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
AML1-MTG8 generated by t(8;21) contributes to leukemic transformation, but additional events are required for full leukemogenesis.
|
15902284 |
2005 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, AML-1-ETO may contribute to leukemogenesis by specifically inhibiting C/EBP-alpha- and AML-1B-dependent activation of myeloid promoters and blocking differentiation.
|
9418879 |
1998 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In particular, there exists strong evidence that leukemic RUNX1-fusions such as RUNX1-ETO disrupt genomic integrity and induce a "mutator" phenotype during the early stages of leukemogenesis.
|
28299675 |
2017 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
FLT3 mutation and AML/ETO in a case of Myelodysplastic syndrome in transformation corroborates the two hit model of leukemogenesis.
|
17079011 |
2007 |
|
Leukemogenesis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
ETO and AML1 phosphoproteins are expressed in CD34+ hematopoietic progenitors: implications for t(8;21) leukemogenesis and monitoring residual disease.
|
8781439 |
1996 |
|
Leukemogenesis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined.
|
10435586 |
1999 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
It is now widely known that formation of AML1-MTG8 by t(8;21) translocation is a very early event in leukemogenesis, and AML1-MTG8 alone might have limited proliferative potential.
|
16162359 |
2006 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We show in this study that both overexpression and knockout of microRNA (miR)-126 surprisingly result in enhanced leukemogenesis in cooperation with the t(8;21) fusion genes AML1-ETO/RUNX1-RUNX1T1 and AML1-ETO9a (a potent oncogenic isoform of AML1-ETO).
|
26361793 |
2015 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition to blocking differentiation, AML1-ETO is also shown to induce growth arrest in AML cells, which is unfavorable for leukemogenesis harboring the t(8;21) translocation.
|
16741927 |
2006 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, our results shed new light on post-translational regulation of MTG8, perturbation of which, in AML1-MTG8 protein, probably contributes to leukemogenesis.
|
10076566 |
1999 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results would shed new insights for understanding mechanisms of AML1-ETO-associated leukemogenesis.
|
17367753 |
2007 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, t(8;21)-positive AMLs appear to overexpress the AML1-ETO fusion protein, which may be responsible for differentiation block and leukemogenesis in AML.
|
9579874 |
1998 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.
|
15650049 |
2005 |
|
Leukemogenesis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These results suggest that the high-level expression of TIS11b contributes to AML1-MTG8-mediated leukemogenesis.(Blood.2000;96:655-663)
|
10887131 |
2000 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Altered PU.1 function is possibly implicated in leukemogenesis, as PU.1 gene mutations were identified in some patients with acute myeloid leukemia (AML) and as several oncogenic products (AML1-ETO, promyelocytic leukemia-retinoic acid receptor alpha, FMS-like receptor tyrosine kinase 3 internal tandem duplication) are associated with PU.1 downregulation.
|
17361223 |
2007 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
AML1-ETO, the most common fusion oncoprotein by t (8;21) in acute myeloid leukaemia (AML), enhances hematopoietic self-renewal and leukemogenesis.
|
31119862 |
2019 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We identified TET2 and PTPN11 mutations in both mouse and human AML and then demonstrated the ability of Tet2 loss and PTPN11 D61Y to initiate leukemogenesis in concert with expression of AML1-ETO in vivo.
|
26666262 |
2016 |
|
Leukemogenesis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
AML1-ETO promotes SIRT1 expression to enhance leukemogenesis of t(8;21) acute myeloid leukemia.
|
27725192 |
2017 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
RUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1).
|
20589720 |
2010 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The contribution of activated c-Kit signaling to PML/RARalpha- and AML-1/ETO-induced leukemogenesis was investigated in a murine transduction/transplantation leukemia model.
|
19424569 |
2009 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
AML1-ETO mediates hematopoietic self-renewal and leukemogenesis through a COX/β-catenin signaling pathway.
|
23645839 |
2013 |
|
Leukemogenesis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
AML associated oncofusion proteins PML-RARA, AML1-ETO and CBFB-MYH11 target RUNX/ETS-factor binding sites to modulate H3ac levels and drive leukemogenesis.
|
28030795 |
2017 |
|
Leukemogenesis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
GSEA analysis confirmed similar altered gene expression patterns in the truncated RUNX1 and RUNX1/ETO models, with both models showing alterations in genes involved in self-renewal and leukemogenesis, including homeobox genes, primitive erythroid genes and leukemogenic transcription factors.
|
25798834 |
2016 |
|
Leukemogenesis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, these data support the notion that VPA might effectively target AML1/ETO-driven leukemogenesis through disruption of aberrant HDAC1 function and that VPA should be integrated in novel therapeutic approaches for AML1/ETO-positive AML.
|
17389244 |
2007 |