Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Clinical, cytogenetic and molecular features of acute myeloid leukemia with a MLL-SEPT5 fusion gene are reviewed.
|
23725386 |
2014 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
In the <i>MLL-AF9</i> AML mouse model, treatment with Pam3CSK4 provided proof of concept for in vivo therapeutic efficacy.
|
29296851 |
2017 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Ras activation seems to complement the MLLT3-MLL oncogene in transformation with features of de novo and t-AML with MLLT3-MLL being similar.
|
20395514 |
2010 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
This interaction is critical for the maintenance of <i>MLL</i> translocation driven AML by targeting MLL fusion proteins to the target genes <i>Meis1</i> and <i>Hoxa9</i>.
|
29774127 |
2018 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The presence of the MLL gene rearrangements or the age at onset had no impact on the outcome of infant AML.
|
11739161 |
2001 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
FTO is highly expressed in AMLs with t(11q23)/MLL rearrangements, t(15;17)/PML-RARA, FLT3-ITD, and/or NPM1 mutations.
|
28017614 |
2017 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Involvement of the MLL gene located at chromosome region 11q23 is a frequent occurrence in both acute myelocytic leukemia and acute lymphoblastic leukemia.
|
14580777 |
2003 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Although MLL-AF9 caused by the chromosomal translocation t(9;11) has a critical role in acute myeloid leukemia, the molecular pathogenesis is poorly understood.
|
22902925 |
2012 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Here, we studied the distribution and characteristics of Tregs in the LHME, investigated the effects of Treg ablation on leukemia progression, explored the mechanisms leading to Treg accumulation, and studied whether blocking Treg migration to the LHME delayed leukemia progression in MLL-AF9-induced mouse acute myeloid leukemia (AML) models using wildtype (WT) and Foxp3<sup>DTR/GFP</sup> mice.
|
31669202 |
2020 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
MLL gene amplification in acute myeloid leukemia and myelodysplastic syndromes is associated with characteristic clinicopathological findings and TP53 gene mutation.
|
25387813 |
2015 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Mixed lineage leukemia [MLL; now known as lysine methyltransferase 2A (KMT2A)] rearrangement-positive acute myeloid leukemia (AML) and juvenile myelomonocytic leukemia (JMML) are distinct diseases, although age of susceptibility (infancy or early childhood) and abnormal monocytosis are common clinical features.
|
30143999 |
2018 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Thus, restoration of miR-26a expression/function holds therapeutic potential to treat MLL-rearranged AML.
|
26791235 |
2016 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
The MLL gene was found to be rearranged in 14 out of 14 cases, and in three out of six cases the breakpoint was at the telomeric part of the gene, as observed in most cases of AML following therapy with topoisomerase II inhibitors.
|
11552977 |
2001 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
We modeled the frequent co-occurrence of <i>miR-125b</i> overexpression and <i>MLL</i> translocations by examining functional cooperation between <i>miR-125b</i> and <i>MLL-AF9</i> By generating a knock-in mouse model in which <i>miR-125b</i> overexpression is controlled by doxycycline induction, we demonstrated that <i>miR-125b</i> significantly enhances <i>MLL-AF9</i>-driven AML in vivo, and the resultant leukemia is partially dependent on continued overexpression of <i>miR-125b</i> Surprisingly, <i>miR-125b</i> promotes AML cell expansion and suppresses apoptosis involving a non-cell-intrinsic mechanism.
|
28053194 |
2017 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
This case report helps to better understand the rare but potentially severe impact of KMT2A- FLNA fusions in infants with AML to improve prognostic stratification of therapy and clinical management.
|
28253492 |
2016 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
t(11;22)(q23;q11.2) In acute myeloid leukemia of infant twins fuses MLL with hCDCrel, a cell division cycle gene in the genomic region of deletion in DiGeorge and velocardiofacial syndromes.
|
9600980 |
1998 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Stabilization of NF-κB-Inducing Kinase Suppresses MLL-AF9-Induced Acute Myeloid Leukemia.
|
29320732 |
2018 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
We found that DNMT3A and NPM1 mutations and MLL translocations predicted an improved outcome with high-dose induction chemotherapy in patients with AML.
|
22417203 |
2012 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Our study indicates that the MLL gene rearrangements are similar both in AML that develops de novo and in t-AML.
|
8260707 |
1993 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Here, we characterize the in vivo migratory behavior of AML cells and their response to chemotherapy and CXCR4 antagonism, using high-resolution 2-photon and confocal intravital microscopy of mouse calvarium BM and the well-established MLL-AF9-driven AML mouse model.
|
30422351 |
2019 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
We have recently reported the detection by Southern blot of ALL-1 gene rearrangements in adult patients with acute myeloid leukemia lacking cytogenetic evidence of 11q23 translocations.
|
8016145 |
1994 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Moreover, secondary acute myeloid leukemias (AML) that occur as the result of chemotherapy agents, which are known to inhibit DNA topoisomerase II, often manifest the same MLL abnormalities.
|
8932918 |
1996 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Rearrangement of the MLL gene in acute lymphoblastic and acute myeloid leukemias with 11q23 chromosomal translocations.
|
8361504 |
1993 |
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
We recently showed that the combined loss of Runx1/Cbfb inhibited the development of MLL-AF9-induced AML.
|
27819671 |
2017 |
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Rearrangements of the MLL (11q23) gene in AML are usually related to the morphological phenotype FAB M5.
|
16044313 |
2005 |