|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
In the B-ALL children, BCR-ABL was detected in 26/218 (11.9%), E2A-PBX1 in 13/218 (5.9%), TEL-AML1 in 16/218 (7.3%) and MLL-AF4 in 3/218 (1.4%) patients.
|
26264145 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
With intensive chemotherapy and allogeneic HSCT, favorable outcome of children (≥1 year old) with MLL-AF4-positive ALL was observed.
|
26410102 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Poor prognostic factors included age ≤90 days at diagnosis, MLL-R ALL and white cell count ≥50,000/μl.
|
25399948 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
In contrast to infant cases, MLL-R leukemia in older children had more somatic mutations (mean of 6.5 mutations/case versus 1.3 mutations/case, P = 7.15 × 10(-5)) and had frequent mutations (45%) in epigenetic regulators, a category of genes that, with the exception of MLL, was rarely mutated in infant MLL-R ALL.
|
25730765 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
For this, we performed gene expression profiling after siRNA-mediated repression of MLL-AF4, MLL-ENL, and AF4-MLL in MLL-rearranged ALL cell line models.
|
25793396 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Molecular studies reveal a MLL-MLLT3 gene fusion displaced in a case of childhood acute lymphoblastic leukemia with complex karyotype.
|
25843568 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Thus, implementing FDA-approved PI3K inhibitors in current treatments may potentially improve the GC response and prognosis in patients with MLL-rearranged ALL.
|
23958920 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The aims of this multicenter study were to determine the prevalence of the four most common gene rearrangements [ETV6-RUNX1, TCF3-PBX1, BCR-ABL1, and MLL rearrangements] and to explore their relationship with mortality rates during the first year of treatment in ALL children from Mexico City.
|
25692130 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
MLL fusion-driven activation of CDK6 potentiates proliferation in MLL-rearranged infant ALL.
|
24736461 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Children with the IKZF1 SNP had an increased risk of developing MLL-germline ALL in white children.
|
24564228 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Combined approaches including flow cytometry, Western blot, obatoclax treatment with death pathway inhibition, microarray analyses, and/or electron microscopy indicated a unique killing mechanism involving apoptosis, necroptosis, and autophagy in MLL-AF4 ALL cell lines and primary MLL-R and MLL-G infant ALL cells.
|
23393050 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study assesses whether an ethnic influence has an effect on the frequency of any of the four fusion genes: BCR-ABL1, ETV6-RUNX1, TCF3-PBX1, and MLL-AFF1 found in ALL.
|
23859904 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
In addition, the Src kinase inhibitor PP2 markedly sensitized MLL-rearranged ALL cells otherwise resistant to prednisolone, via downregulation of S100A8 and S100A9, which allowed prednisolone-induced Ca(2+) fluxes to reach the mitochondria and trigger apoptosis.
|
22282267 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Using the median FLT3 expression as cut-off value we found that high-level FLT3 expression is associated with an extremely poor 1-year overall survival (OS; 0 vs 71%; P=0.002) and disease-free survival (DFS; 0 vs 43%; P=0.03) in MLL-AF4+ B-ALL but not in MLL-germline B-ALL.
|
22705992 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Although the majority of children with acute lymphoblastic leukemia (ALL) are cured with current therapy, the event-free survival (EFS) of infants with ALL, particularly those with mixed lineage leukemia (MLL) gene rearrangements, is only 30% to 40%.
|
21135279 |
2011 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The chromosomal translocation t(4;11)(q21;q23) is a frequent genetic aberration of the mixed lineage leukemia (MLL) gene, predominantly associated with high-risk acute lymphoblastic leukemia (ALL) in pediatric patients.
|
21233834 |
2011 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Translocations involving the mixed-lineage leukemia (MLL) gene, localized at 11q23, comprise 15 to 20% of all pediatric acute myeloid leukemia (AML) cases.
|
21566656 |
2011 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
However, in children an increased risk of ALL (odds ratio [OR] = 1.88; 95% confidence interval [CI], 1.16-3.07; P = .010) and AML (OR = 2.74; 95% CI, 1.07-7.01; P = .036) was observed with the MTR 2756 GG genotype; the association was most pronounced for cases with the MLL translocation (OR = 4.90; 95% CI, 1.30-18.45; P = .019).
|
20101025 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
In this cohort of Taiwanese children, the relative frequencies of the 4 translocations of B-lineage ALL were 8% with ALL-type t(9;22)/BCR-ABL1, 4% with (1;19)/TCF-PBX1, 2% with t(4;11)/MLL-AF4, and 17.6% with t(12;21)/ETV6-RUNX1.
|
20930648 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our data show that MLL germline infant ALL specifies a gene expression pattern that is different from both MLL-rearranged infant ALL and pediatric precursor B-ALL.
|
20032505 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Moreover, the 11q23/MLL subtype of ALL showed similarities with non-hematopoietic tissues.
|
20211010 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk acute lymphoblastic leukemia (ALL).
|
20194896 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Expression of miR-196b is not exclusively MLL-driven but is especially linked to activation of HOXA genes in pediatric acute lymphoblastic leukemia.
|
20494936 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Acute lymphoblastic leukemia (ALL) in infants is characterized by a high frequency of MLL gene rearrangements.
|
19665068 |
2009 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
MLL-AF4 is known to be the most frequent fusion transcript, but the exact frequencies of MLL aberrations in CD10(-) adult BCP-ALL are unknown.
|
19144982 |
2009 |