|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Sensitivity assays demonstrated that AMP-E can detect <i>MLL-AFF1</i> in MV4-11 cell dilutions of 10<sup>-7</sup> and transcripts down to 0.005 copies/ng.<b>Implications:</b> This study demonstrates a NGS methodology with improved sensitivity compared with current diagnostic methods for <i>MLL</i>-rearranged leukemia.
|
29133595 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In gene reporter assays, the leukemia-specific fusion protein KMT2A-MLLT3 transactivated the intragenic BRE promoter.
|
28871137 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
They could markedly down-regulate the expressions of the c-Myc, Bcl-2 and CDK6 oncogenes in MV4-11 in the qRT-PCR and western blot studies, which further demonstrated that compound 1 and its derivatives could serve as a promising therapeutic strategy for MLL leukemia by targeting BRD4_BD1 protein.
|
29730189 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
SETD2-mediated crosstalk between H3K36me3 and H3K79me2 in MLL-rearranged leukemia.
|
29249820 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We show that the MLL genetic partner could have implications in allo-HSCT response, and we propose three genes whose expression could be useful for the prognosis of this leukemia in patients undergoing allo-HSCT: 3' region of MLL, EVI1, and FLT3.
|
29384595 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, HOTAIR knockdown reduced infiltration of leukemic blasts, decreased frequency of LSC, and prolonged overall survival in MLL-AF9-induced murine leukemia, suggesting that HOTAIR is required for the maintenance of AML.
|
30172749 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PAF complex regulation of Prmt5 facilitates the progression and maintenance of MLL fusion leukemia.
|
28945229 |
2018 |
|
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mixed-lineage leukemia (MLL) protein is the best-characterized member of SET family of histone 3 lysine 4 methyltransferase, known for its transcriptional-activation role during development. mll gene rearrangements cause multiple kinds of aggressive leukemia in both children and adults.
|
30489191 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Heterogeneous effects of M-CSF isoforms on the progression of MLL-AF9 leukemia.
|
29363207 |
2018 |
|
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We have shown that antagomiR inhibition of miRNA miR-21 and miR-196b activity is sufficient to ablate MLL-AF9 leukemia stem cells (LSC) in vivo.
|
29997117 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, DOT1L is believed to be involved in the development of MLL-rearranged leukemia driven by the MLL (mixed-lineage leukemia) fusion proteins, which thus to be a crucial target for leukemia therapy.
|
29534934 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, genome editing enables modeling of human acute <i>MLL-</i>rearranged leukemia in vivo, reflecting the genetic simplicity of this disease, and provides an experimental platform for biological and disease-modeling applications.
|
29650777 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the present study, we assessed by FISH whether exposure to low concentrations (0.1 μm, 72 hours) of permethrin and malathion induce aberrations in KMT2A and IGH genes, which are involved in the etiology of leukemia and lymphoma.
|
29741206 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Blocking these interactions may represent a novel therapeutic approach for MLL-rearranged leukemia.
|
30258537 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Functional investigation of 128 conserved MLL-fusion-interactors identifies a specific role for the lysine methyltransferase SETD2 in MLL-leukemia.
|
29777171 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The druggability of MLL1 PPIs for leukemia were also discussed.
|
29254892 |
2018 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Among the three age groups, older patients more often had higher risk ALL due to T-ALL (32%/25%/9%, P<0.001), KMT2A rearrangements (6%/5%/3%, P<0.001) and higher day 29 residual leukemia for B-lineage (P<0.001), but not T-ALL (P=0.53).
|
28819280 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The histone H3 lysine 4 (H3K4) presenter WDR5 forms protein complexes with H3K4 methyltransferases MLL1-MLL4 and binding partner proteins including RBBP5, ASH2L, and DPY30, and plays a key role in histone H3K4 trimethylation, chromatin remodeling, transcriptional activation of target genes, normal biology, and diseases such as MLL-rearranged leukemia.
|
30488017 |
2018 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our results provide new insight into the biology of KMT2A-R leukemia with subclonal signaling mutations and highlight the importance of activated signaling as a contributing driver.
|
29720585 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In a mouse model of human MLL-AF9 leukemia, fPrdm16 extended latency, while sPrdm16 shortened latency and induced a strong inflammatory signature, including several cytokines and chemokines that are associated with myelodysplasia and with a worse prognosis in human AML.
|
29878897 |
2018 |
|
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We show that the critical function of ZFP64 in leukemia is to maintain MLL expression via binding to the MLL promoter, which is the most enriched location of ZFP64 occupancy in the human genome.
|
30503706 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study demonstrates the therapeutic potential for targeting DOT1L in <i>MLL-r</i> leukemia and lays the groundwork for future combination approaches in this patient population.
|
29724899 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The role of Cdc42 in hematopoietic cell transformation and leukemia progression has been studied in an acute myeloid leukemia model using the MLL-AF9 oncogene-induced transformation and a Cdc42 conditional gene-targeted mouse model.
|
30062418 |
2018 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We present a leukemia case that exhibits a chromosomal translocation t(11;16)(q23;q23), which results in the expression of a novel KMT2A fusion gene.
|
30107050 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using mouse models carrying primary human acute lymphoblast leukemia derived from MLL-AF9-overexpressing human hematopoietic stem cells, we demonstrate that allogeneic lymphocyte infusion (ALI)-mediated graft-vs.-leukemia effects selectively spare leukemia cells in the bone marrow.
|
29603337 |
2018 |