|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest that anti-CD19 CAR-T cells therapy with a remarkable MRD eradicating ability might be an effective option for patients with relapsed and refractory E2A-PBX1 positive B-ALL.
|
30714847 |
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 |
Although survival rate is usually high after the initial chemotherapy, many TCF3-PBX1 BCP-ALL patients relapse and subsequently develop treatment resistance, resulting in poor prognosis.
|
30631148 |
2019 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
All children in Hong Kong diagnosed with ALL with TCF3-PBX1 rearrangement over the past two decades were included.
|
30051646 |
2018 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
A novel PAX5 rearrangement in TCF3-PBX1 acute lymphoblastic leukemia: a case report.
|
30563523 |
2018 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
TCF3-PBX1 BCP-ALL patients typically benefit from chemotherapy; however, many relapse and subsequently develop resistant disease with few effective treatment options.
|
27461063 |
2017 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We reviewed the roles of miRNA here with emphasis on their function in human leukemia and the mechanisms of the TEL/AML1, BCR/ABL, MLL/AF4 and TCF3/PBX1 oncoproteins on miRNAs expression in acute lymphoblastic leukemia.
|
27431573 |
2016 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Virus infection efficiently induced T-cell, B-cell, and biphenotypic ALL in E2A-PBX1 cKI mice.
|
27088431 |
2016 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
To address this, we interrogated activated signaling pathways in a comparative analysis of mouse and human leukemias expressing the fusion protein E2A-PBX1, which is present in 5%-7% of pediatric and 50% of pre-B-cell receptor (preBCR<sup>+</sup>) acute lymphocytic leukemia (ALL).
|
27758892 |
2016 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Investigation for TCF3(E2A)-PBX1 rearrangements may be useful in BCL6-positive B-lymphoblastic leukemia.
|
25780007 |
2015 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Clinical features and prognostic significance of TCF3-PBX1 fusion gene in Chinese children with acute lymphoblastic leukemia by using a modified ALL-BFM-95 protocol.
|
25551271 |
2015 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This study reviewed the clinical characteristics of 112 pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) patients with TCF3-PBX1 fusion treated according to the Japan Association of Childhood Leukemia Study (JACLS) ALL02 protocol (n = 82) and Children's Cancer and Leukemia Study Group (CCLSG) ALL 2004 protocol (n = 30).
|
24578304 |
2014 |
|
Acute lymphocytic leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
For example, whereas the E2A portion of the E2A-Pbx1 leukemia fusion protein mediates robust transcriptional activation in t(1;19) acute lymphoblastic leukemia, the transcriptional activity of wild-type E2A is silenced by high levels of corepressors, such as the AML1-ETO fusion protein in t(8;21) acute myeloid leukemia and ETO-2 in hematopoietic cells.
|
24064250 |
2014 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
GCN5 acetylates and regulates the stability of the oncoprotein E2A-PBX1 in acute lymphoblastic leukemia.
|
23044487 |
2013 |
|
Acute lymphocytic 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 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
E2A-PBX1 fusion gene caused by t(1;19)(q23;p13), has been well characterized in acute lymphoid leukemia (ALL).
|
23688269 |
2013 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In E2A-PBX1-positive B-ALLs, aberrant DNA methylation patterning was strongly associated with direct fusion protein binding as shown by the E2A-PBX1 chromatin immunoprecipitation (ChIP) sequencing (ChIP-seq), suggesting that E2A-PBX1 fusion protein directly remodels the epigenome to impose an aggressive B-ALL phenotype.
|
23107779 |
2012 |
|
Acute lymphocytic leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
E2A, 1 of 3 E-protein-encoding genes, is implicated in the induction of acute lymphoblastic leukemia through its involvement in the chromosomal translocation 1;19 and consequent expression of the E2A-PBX1 oncoprotein.
|
22972988 |
2012 |