|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Compared with the other BCP-ALL cell lines in use, the HXEX-ALL1 cells have a special karyotype represented by trisomy 8 and 9p and 17p deletions with a multidrug resistance phenotype, especially highly resistant to asparaginase.
|
31168295 |
2019 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Downregulation of H4R3sme2 by PRMT5 silencing induced BCP-ALL cell differentiation from the pre-B to immature B stage, whereas overexpressed PRMT5 with enhanced H4R3sme2 promoted human mature B cells to dedifferentiate back to the pre-B II/immature B stages <i>in vitro</i>.
|
30635341 |
2019 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The IC50 of clofarabine in 79 BCP-ALL cell lines was approximately 20 times lower than that of Ara-C.
|
29473342 |
2018 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results indicate that incorporation of VS-5584/ATO combination into BCP-ALL therapeutic protocols can improve treatment and the survival of patients.
|
29574283 |
2018 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
During diagnostic immunophenotyping of 573 childhood B-cell precursor ALL (BCP-ALL), we identified eight cases with this immunophenotype among "B-other ALL" (BCP-ALL cases negative for routinely tested chromosomal/genetic aberrations).
|
28395118 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
ERG-related patients have remarkably favorable outcome despite a high incidence of inauspicious IKZF1 aberrations.We describe clinical and genomic features of the ERG-related cases in an unselected cohort of B-other BCP ALL pediatric patients enrolled in the AIEOP ALL 2000 therapeutic protocol.
|
28415578 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
86.6% of the promoter-associated differentially methylated sites were hypermethylated in BCP ALL.
|
29125853 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
After genotyping an additional 2525 cases and 3575 controls, we identify new susceptibility loci for BCP-ALL mapping to 10q26.13 (rs35837782, LHPP, P=1.38 × 10<sup>-11</sup>) and 12q23.1 (rs4762284, ELK3, P=8.41 × 10<sup>-9</sup>).
|
27694927 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Specifically in BCP-ALL, we identified ATRX as a novel putative driver gene and uncovered an association between somatic mutations in the Notch signaling pathway at ALL diagnosis and increased risk of relapse.
|
27590521 |
2016 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Altogether, our data suggest that genetic predisposition aligned with chance haa an additive effect in BCP-ALL outcome.
|
25150625 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We also discuss the relationship between the hyperdiploid karyotype and genetic alterations in the RAS/MAPK pathway in BCP-ALL.
|
24072241 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Taken together, our results indicate that BTG1 deletions may act as "drivers" of leukemogenesis in specific BCP-ALL subgroups, in which they can arise independently in multiple subclones at sites that are prone to aberrant RAG1/RAG2-mediated recombination events.
|
22359517 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
HOXA3-4, HOXA7, and HOXB3-4 genes were differentially expressed between BCP-ALL and T-ALL subgroups, and among genotypically defined MLL/AF4, TEL/AML1, BCR/ABL, hyperdiploid and normal karyotype subgroups.
|
20672366 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study disclosed RUNX1 alterations in the ETV6/RUNX1-negative group of BCP-ALL that encourages the investigation of RUNX1 at a large scale with longer follow-up, which will focus on the prognostic importance and the underlying biology of disease.
|
18728978 |
2008 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We identified interleukin (IL)-10 expression as a significant adverse prognostic indicator in childhood BCP-ALL.
|
16751110 |
2006 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
T-cell ALL samples were significantly more sensitive than BCP ALL and N BM samples.
|
16051737 |
2005 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
DNA samples from 149 healthy controls, from 26 fresh frozen childhood cases of acute lymphoblastic leukemia (ALL) (B-, BCP- and T-ALL) and from 12 paraffin-embedded osteosarcomas were investigated.
|
15642675 |
2005 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
CDKN2/p16 deletion was seen in 23 of the 83 (28%) BCP-ALL and 15 of the 22 (68%) T-ALL cases.
|
9089742 |
1997 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This study shows that TEL-AML1 transcripts are frequently detected in pediatric BCP-ALLs and that these transcripts are molecular targets that will simplify the strategy of MRD monitoring in childhood BCP-ALL.
|
8704188 |
1996 |