|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Remarkable progress has been achieved in understanding the molecular pathogenesis of AML1-ETO leukemia.
|
28299657 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, deregulation of both AML1 and Notch target genes is required for the development of AE9a-driven leukemia.
|
28360416 |
2017 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Space-Time Clustering of Childhood Leukemia: Evidence of an Association with ETV6-RUNX1 (TEL-AML1) Fusion.
|
28129329 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Activation of STUB1 could be a promising therapeutic strategy for RUNX1-RUNX1T1 leukemia.
|
28536267 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, as will be discussed in other chapters, both RUNX1 and CBFB are involved in recurrent chromosomal rearrangements in leukemia.
|
28299663 |
2017 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
MiR-221-regulated KIT level by wild type or leukemia mutant RUNX1: a determinant of single myeloblast fate decisions that - collectively - drives or hinders granulopoiesis.
|
29156756 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
ETV6/RUNX1-like acute lymphoblastic leukemia: A novel B-cell precursor leukemia subtype associated with the CD27/CD44 immunophenotype.
|
28395118 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Previous studies showed that the interaction between CBFβ-smooth muscle myosin heavy chain (SMMHC; encoded by <i>CBFB-MYH11</i>) and RUNX1 plays a critical role in the pathogenesis of this leukemia.
|
29018080 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The 8;21 chromosomal rearrangement disrupts the key hematopoietic RUNX1 transcription factor, and contributes to leukemia through recruitment of co-repressor complexes to RUNX1 target genes, altered subnuclear localization, and deregulation of the myeloid gene regulatory program.
|
28611288 |
2017 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our findings represent the first characterization of this CASC15 in RUNX1-translocated leukemia, and point towards a mechanistic basis for its action.
|
28724437 |
2017 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Areas covered: Available techniques include multi-color flow cytometry (MFC) of leukemia associated immunophenotypes (LAIP), quantitative reverse transcriptase polymerase chain reaction (QRT-PCR) for detecting fusion and mutated genes (RUNX1-RUNX1T1, CBFB-MYH11, and NPM1), overexpression of genes such as WT1, and next generation sequencing (NGS) for MRD.
|
28475434 |
2017 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Additionally, the ETV6-RUNX1 fusion was found to encode putative neoepitopes in a high proportion (69.6%) of the pediatric leukemia harboring this fusion.
|
28854978 |
2017 |
|
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Honokiol induces proteasomal degradation of AML1-ETO oncoprotein via increasing ubiquitin conjugase UbcH8 expression in leukemia.
|
28043811 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Presence of ETV6/RUNX1 alone is usually not sufficient for leukemia onset, and additional genetic alterations have to occur in ETV6/RUNX1-positive cells to cause transformation.
|
26919255 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Secondary chromosomal aberrations are necessary for development of overt leukemia in t(12;21)/ETV6-RUNX1-positive acute lymphoblastic leukemia (ALL).
|
27215399 |
2016 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
To better define the genetic landscape in AML and distinguish driver from passenger mutations, we compared the mutational profiles of AML1-ETO-driven mouse models of leukemia with the mutational profiles of human AML patients.
|
26666262 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Clinical data suggest that CBL mutations are a frequent event in t(8;21) AML, but the role of CBL in AML1-ETO-induced leukemia has not been investigated.
|
26449661 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Collectively, these data describe a pivotal role for MEIS2 in AML1-ETO-induced leukemia.
|
27346355 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both RUNX1 and CBFβ are frequently mutated in human leukemia.
|
27428424 |
2016 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The RUNX1 transcription factor is an essential regulator of hematopoiesis and is a frequent target of point mutations and chromosomal alterations in leukemia.
|
26060100 |
2016 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
RUNX1/AML1 is among the most commonly mutated genes in human leukemia.
|
26745853 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In our previous study, we showed that APP is highly expressed and regulates leukemia cell migration in AML1‑ETO-positive (AE) leukemia.
|
27460334 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
All together, our study defined a unique lncRNA expression signature associated with ETV6/RUNX1-positive BCP-ALL and identified lnc-RTN4R-1 and lnc-NKX2-3-1 as lncRNAs that might be functionally implicated in the biology of this prevalent subtype of human leukemia.
|
27650541 |
2016 |
|
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We conclude that the distal P1-Runx1 promoter is a direct transcriptional target of Wnt/β-catenin signaling that may be important in normal hematopoiesis or its transition into malignant stem cells during the onset or progression of leukemia.
|
26580584 |
2016 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Altogether, RUNX1 dosage could explain the differential phenotype according to RUNX1 mutations, with a haploinsufficiency leading to thrombocytopenia alone in a majority of cases whereas a more complete gene deletion predisposes to leukemia.
|
25490895 |
2015 |