|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
t(17;19)(q21-q22;p13), responsible for TCF3-HLF fusion, is a rare translocation in childhood B-cell precursor acute lymphoblastic leukemia(BCP-ALL). t(1;19)(q23;p13), producing TCF3-PBX1 fusion, is a common translocation in childhood BCP-ALL.
|
31305009 |
2019 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These findings indicate that isoform profiles and SNP genotypes of the GR gene may be useful indicators of GC sensitivity in BCP-ALL.
|
28850694 |
2018 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The distinguishable DNA whole genome methylation profile of 2 cases of pediatric precursor B acute lymphoblastic leukaemia (BCP ALL) with prodromal, preleukemic phase: A case report.
|
30334962 |
2018 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These so-called BCR-ABL1-like fusions are mutually exclusive with the sentinel translocations in BCP-ALL (BCR-ABL1, ETV6-RUNX1, TCF3-PBX1, and KMT2A (MLL) rearrangements) and have the promising prospect to be sensitive to tyrosine kinase inhibitors similar to BCR-ABL1.
|
28709134 |
2017 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
86.6% of the promoter-associated differentially methylated sites were hypermethylated in BCP ALL.
|
29125853 |
2017 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our findings suggest that BCP-ALL are arrested at different cellular stages, which relates to the expression pattern of the pre-BCR components that could serve as prognostic markers for high-risk pediatric BCP-ALL patients.
|
27611867 |
2016 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, the spectrum of MLL translocation partners in adult T-ALL much more resembles that of AML than that of BCP ALL and thus the mechanisms by which MLL contributes to leukemogenesis in adult T-ALL appear to differ from those in BCP ALL.
|
22927255 |
2012 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The abnormalities with the most significant impact for treatment and management of BCP-ALL are t(9;22)(q34;q11)/BCR-ABL1, t(4;11)(q21;q23)/MLL-AFF1 and near-haploidy/low hypodiploidy for high risk stratification and, to a lesser extent, t(12;21)(p13;q22)/ETV6-RUNX1 and high hyperdiploidy for good risk management.
|
20701601 |
2010 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Five 'hot topics' are presented in which cytogenetics and related techniques have been instrumental in understanding the role of genetics in leukaemogenesis: (i) genetic changes are integral to the biology of T-cell ALL; (ii) intrachromosomal amplification of chromosome 21 is a new recurrent abnormality in precursor-B ALL (BCP-ALL); (iii) the immunoglobulin heavy chain gene (IGH@) is significant in BCP-ALL; (iv) alterations in genes involved in B-cell development and cell cycle control contribute to the pathogenesis of BCP-ALL; (v) age-related cytogenetic profiles define ALL in children and adolescents as distinct biological entities.
|
19006567 |
2009 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
B-cell precursor acute lymphoblastic leukemia (BCP-ALL/B-precursor ALL) is characterized by a high rate of tissue infiltration.
|
18245480 |
2008 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL.
|
18328947 |
2008 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Unlike other chromosomal translocations, which are usually specific for a given lineage, the chromosomal translocation t(12;13)(p12;q14) has been observed in both B-cell and T-cell precursor acute lymphoblastic leukemia (BCP-, TCP-ALL), in differentiated and undifferentiated acute myeloblastic leukemia (AML), and in chronic myeloid leukemia (CML) at progression to blast crisis.
|
10379868 |
1999 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
At the mRNA level FLT3R was expressed by most (80-100%) cases of AML (acute myeloid leukemia) throughout the different morphological subtypes (MO-M7), of ALL(acute lymphoblastic leukemia) of the immunological subtypes T-ALL and BCP-ALL (B cell precursor ALL including pre-pre B-ALL, cALL and pre B-ALL), of AMLL (acute mixed-lineage leukemia), and of CML (chronic myeloid leukemia) in lymphoid or mixed blast crisis.
|
8618433 |
1996 |
|
Acute lymphocytic 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 |