|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Pediatric ALL had higher prevalence of ETV6-RUNX1, TCF3-PBX1, and STIL-TAL1, while BCR-ABL1 and SET-NUP214 were more common in adult ALL.
|
30125757 |
2018 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
SETDB2 expression is maintained as a direct target gene of the chimeric transcription factor E2A-PBX1 in a subset of ALL and suppresses expression of the cell-cycle inhibitor CDKN2C through histone H3K9 tri-methylation, thus establishing an oncogenic pathway subordinate to E2A-PBX1 that silences a major tumor suppressor in ALL.
|
29694893 |
2018 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
To determine whether methylation differences between mostly fatal TCF3-HLF and curable TCF3-PBX1 pediatric acute lymphoblastic leukemia subtypes can be associated with differential gene expression and remission.
|
29334255 |
2018 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Pediatric acute lymphoblastic leukemia with t(1;19)/TCF3-PBX1 in Taiwan.
|
28436581 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In this study, we developed a multiplex RT-PCR assay for detection of the 4 most frequent translocations in ALL (BCR-ABL, TEL-AML1, MLL-AF4, and E2A- PBX1).
|
26925663 |
2016 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Virus infection efficiently induced T-cell, B-cell, and biphenotypic ALL in E2A-PBX1 cKI mice.
|
27088431 |
2016 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using an integrated approach, we uncovered distinct mutation, gene expression and drug response profiles in TCF3-HLF-positive and treatment-responsive TCF3-PBX1-positive ALL.
|
26214592 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, our data suggest a collaborative action between autophagy and ubiquitination in the degradation of E2A/Pbx1, thereby revealing a novel strategy for targeted preventive or treatment therapy on the pediatric ALL.
|
25615280 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data support conditional E2A-PBX1 mice as a model of human ALL and suggest targeting pre-BCR signaling and JAK kinases as potential therapeutic strategies.
|
26301816 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This study was conducted to determine the frequency of common fusion transcripts BCR-ABL, TEL-AML1, MLL-AF4 and E2A-PBX1 for B-ALL and SIL-TAL1 for T-ALL as seen at a tertiary care center in India.
|
26264145 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Outcome of TCF3-PBX1 positive pediatric acute lymphoblastic leukemia patients in Japan: a collaborative study of Japan Association of Childhood Leukemia Study (JACLS) and Children's Cancer and Leukemia Study Group (CCLSG).
|
24578304 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
E2A-PBX1 is expressed as a result of the t(1;19) chromosomal translocation in nearly 5% of cases of childhood acute lymphoblastic leukemia.
|
24503810 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
TCF3 rearrangement mostly t(1;19) (q23;p13)/ TCF3-PBX1 gene is associated with favorable outcome in acute lymphoblastic leukemia (ALL) upon treatment with intensification protocols; however, it is associated with higher incidence of central nervous system (CNS) relapse which may affect outcome of patients.
|
25116187 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both kinases were overexpressed in ALL and AML patients (P<0.0002), especially in E2A-PBX1-translocated ALL cases (P<0.002), compared with normal bone-marrow mononuclear cells.
|
22940834 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The observed in vitro and in vivo anti-leukemic potency of the αCD19-AON immunoconjugate provides the first preclinical proof-of-principle that t(1;19)(+) high risk B-lineage ALL can be treated with leukemia-specific biotherapeutic agents that knock-down E2A-PBX1 expression.
|
22990208 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
None of the T-ALL and E2A-PBX1+ B-ALL overexpressed FLT3.
|
22705992 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Prognostic impact of t(1;19)/ TCF3-PBX1 in childhood acute lymphoblastic leukemia in the context of Berlin-Frankfurt-Münster-based protocols.
|
21534874 |
2011 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Folylpolyglutamate synthetase (FPGS) activity was higher in B vs T lineage ALL (p<0.005), MTX influx and FPGS activity were higher in hyperdiploid vs non-hyperdiploid ALL (p<0.03), MTX influx and FPGS activity were lower in the t(12;21) (ETV6-RUNX1) subtype (p<0.05), and the ratio of FPGS to γ-glutamyl hydrolase (GGH) activity was lower in the t(1;19) (TCF3-PBX1) subtype (p<0.03) than other genetic subtypes.
|
21152005 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data suggest that GAS6/Mer axis regulates homing and survival of the E2A/PBX1-positive B-cell precursor ALL in the bone marrow niche.
|
19922767 |
2010 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Most remarkably, miR-708 was 250- up to 6500-fold higher expressed in 57 TEL-AML1, BCR-ABL, E2A-PBX1, hyperdiploid and B-other cases than in 20 MLL-rearranged and 15 T-ALL cases (0.0001<P<0.01), whereas the expression of miR-196b was 500-fold higher in MLL-rearranged and 800-fold higher in 5 of 15 T-ALL cases as compared with the expression level in the remaining precursor B-ALL cases (P<0.001).
|
18923441 |
2009 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The prevalence of E2A-PBX1 in Mexican pediatric cases supports the existence of ethnic differences in the frequency of molecular markers of ALL.
|
18455790 |
2008 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In ALL, ZAP-70 expression is associated with the E2A/PBX1 rearrangement and pre-B stage and may have a prognostic role and be a candidate molecule for targeted therapies.
|
16160012 |
2006 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Adult patients with acute lymphoblastic leukemia (ALL) and t(1;19)/E2A-PBX1 or t(4;11)/MLL-AF4 have a poor outcome.
|
17039234 |
2006 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The (1;19)(q23;p13) translocation, leading to the production of the E2A/PBX1 fusion transcript, is one of the most common translocations in pediatric B-lineage acute lymphoblastic leukemia (ALL).
|
16396770 |
2006 |