|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
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
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Analysis of primary ALL samples revealed a significant increase in GPR132 expression in IKZF1-deleted BCR-ABL negative patients, suggesting that levels of wild-type Ikaros may influence the regulation of G2A in B-ALL.
|
27588474 |
2016 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
However, the threshold 70 WT1 copies/104 ABL copies post induction in childhood ALL did not show clinical significance for predicting prognosis (p=0.056).
|
26221900 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study reports the highest ethnic frequency of BCR-ABL FO in pediatric ALL, and is consistent with previous reports from our region.
|
26266519 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Retinoids potentiated the activity of dasatinib in mouse and human BCR-ABL1 ALL, providing an additional therapeutic option in IKZF1-mutated ALL.
|
26321221 |
2015 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We treated thiopurine-sensitive BCR-ABL+Arf-null Tpmt+/+ ALL in Tpmt+/+, +/-, or -/- recipient mice to test the impact of the host polymorphism on antileukemic efficacy.
|
24710003 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Ikaros deletions in BCR-ABL-negative childhood acute lymphoblastic leukemia are associated with a distinct gene expression signature but do not result in intrinsic chemoresistance.
|
24976218 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These efforts have characterized the genetic basis of recently described and poorly understood subtypes of ALL, including early T-cell precursor ALL, Philadelphia chromosome-like (Ph-like) ALL, and ALL with intrachromosomal amplification of chromosome 21, and have identified several rational therapeutic targets in high-risk ALL, notably ABL1-class and JAK-STAT inhibitors in Ph-like ALL.
|
25696852 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
ALL cells carrying a SNX2-ABL1 fusion exhibited a BCR-ABL1+ ALL-like gene expression profile.
|
24215620 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
BCR-ABL fusion gene typically causes a type of acute lymphoblastic leukemia (ALL), known as Ph+ ALL.
|
24112092 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We demonstrated the dPCR is high-sensitive (able to detect a single copy of BCR-ABL1) and reliable (results are comparable to those obtained by BCR-ABL1 quantification with conventional technology), allowing an accurate monitoring of BCR-ABL1-positive ALL patients in complete remission.
|
24630366 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We analyzed cells from peripheral blood and CD34-/CD34+ cells from bone marrow of pediatric acute lymphoblastic leukemia (ALL) patients harboring BCR-ABL or TEL-AML1.
|
25244981 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
This study identified the BCR-ABL gene as an important factor in CML and ALL cases.
|
25520136 |
2014 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We simultaneously detected IKZF1 gene deletions by multiplex ligation-dependent probe amplification and gene expression of IKZF1 isoforms in 206 children with BCR/ABL-negative ALL treated with ALL IC-BFM 2002 protocol, in which risk stratification was not based on minimal residual disease (MRD), and validated the results on a cohort of 189 patients treated with MRD-directed ALL-BFM 2000 protocol.
|
22997141 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
One recently identified subtype of pediatric B-precursor acute lymphoblastic leukemia (ALL) has been termed BCR-ABL1-like or Ph-like because of similarity of the gene expression profile to BCR-ABL1 positive ALL suggesting the presence of lesions activating tyrosine kinases, frequent alteration of IKZF1, and poor outcome.
|
23212523 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Two models of leukemia were used, one genetic (conditional alpha4 ablation of BCR-ABL1 [p210(+)] leukemia) and one pharmacological (anti-functional alpha4 antibody treatment of primary ALL).
|
23319569 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The response of Philadelphia chromosome (Ph(+)) acute lymphoblastic leukemia (ALL) to treatment by BCR-ABL tyrosine kinase inhibitors (TKIs) has been disappointing, often resulting in short remissions typified by rapid outgrowth of drug-resistant clones.
|
23881917 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In contrast, mainly MLL-AF4+ B-ALL but also ETV6-RUNX1+, BCR-ABL+ or B-ALL displaying normal cytogenetics exhibited significantly higher FLT3 expression levels than normal bone marrow, supporting that aberrantly increased transcription of FLT3, rather than activating FLT3 mutations, contributes to the pathogenesis of these B-ALL.
|
22705992 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Pre-B cells transformed with the viral oncogene v-Abl are suspended in an immortalized, cycling state that mimics leukemias with a BCR-ABL1 translocation, such as Chronic Myelogenous Leukemia (CML) and Acute Lymphoblastic Leukemia (ALL).
|
22693568 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Rapid and accurate detection of BCR-ABL fusion proteins is vital for the diagnosis and classification of leukemias, especially chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL).
|
21933042 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Adult patients with acute lymphoblastic leukemia (ALL) were evaluated to determine whether presence/absence of BCR-ABL induced differences in activation of Src, PI3K/Akt and NF-κB or in the expression of anti-apoptotic proteins such as BCL-2 and c-IAP1.
|
22591684 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our data indicate an immediate need for incorporation of tyrosine kinase inhibitors in the treatment of BCR-ABL+ pediatric ALL in this population and the development of facilities for stem cell transplantation.
|
23317202 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Antileukaemia effect of rapamycin alone or in combination with daunorubicin on Ph+ acute lymphoblastic leukaemia cell line.
|
21898527 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We here report the frequency of TEL-AML1, E2A-PBX1, MLL-AF4, and BCR-ABL chimeric transcripts in 264 Iraqi children newly diagnosed with acute lymphoblastic leukemia (ALL), using FTA cards impregnated with bone marrow aspirate or whole blood.
|
22238115 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL) are associated with fusion of the BCR and ABL1 genes by chromosome translocation.
|
22749885 |
2012 |