Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Of the total 631 cases, 52.9% (n=334) were acute lymphoblastic leukemia (ALL), 43.9% (n=277) acute myeloid leukemia (AML), 2.2% (n=14) mixed phenotypic acute leukemia (MPAL), 0.5% (n=3) acute undifferentiated leukemia (AUL) and 0.5% (n=3) chronic myeloid leukemia in blast crisis (CML-BC).
|
30858955 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
At the 60<sup>th</sup> month, estimated CBMR and CEMR incidences were, respectively, 14.3 (5.1)% and 25.9 (6.6)% in ALL, 25.8 (5.9)% and 15.5 (4.8)% in AML, and 61.5 (16.5)% and 17.9 (13.4)% in CML.
|
30116013 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We searched for original articles and reviews describing the pharmacology and clinical use of dasatinib in ALL with BCR-ABL1.
|
30916583 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
BCR-ABL1 signal patterns were analyzed using FISH in 243 CML-chronic phase (CML-CP), 17 CML-blast phase (CML-BP) and 52 BCR-ABL1 positive acute lymphoblastic leukemia (ALL) patients.
|
31594548 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
To address this, we studied 142 adults with ALL treated with hyperCVAD over a 10-year period who had MRD assessed by either multi-parameter flow cytometry or (for patients with Philadelphia chromosome positive ALL) reverse transcriptase polymerase chain reaction for the BCR-ABL1 translocation.
|
29318644 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
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
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
CD25 (IL-2RA) and CD26 (DPPIV) were expressed on LSCs in Ph<sup>+</sup> ALL exhibiting BCR/ABL1<sub>p210</sub>, whereas in Ph<sup>+</sup> ALL with BCR/ABL1<sub>p190</sub>, LSCs variably expressed CD25 but did not express CD26.
|
29772458 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Philadelphia chromosome-positive (Ph+) B-cell precursor acute lymphoblastic leukemia (ALL) expressing BCR-ABL1 oncoprotein is a major subclass of ALL with poor prognosis.
|
28579617 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Phosphatase of regenerating liver-3 <i>(PRL-3/PTP4A3)</i> is upregulated in multiple cancers, including BCR-ABL1- and ETV6-RUNX-positive acute lymphoblastic leukemia (ALL).
|
29423065 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
To our knowledge, this is the first successful use of nilotinib in BCR-ABL1-like phenotype ALL.
|
30121665 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
This case illustrates the major interest of interphase FISH for BCR-ABL1 rearrangement on blood neutrophils as a decisive method to discriminate a lymphoid blast crisis of CML from a de novo BCR-ABL1 positive ALL.
|
28444777 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
E14a3 breakpoint cluster region (BCR)/ABL proto-oncogene 1, non-receptor tyrosine kinase (ABL) fusion transcript is rare in Philadelphia chromosome positive disease, particularly in acute lymphoblastic leukemia (ALL).
|
29434963 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Of particular importance is the translocation t(9;22)(q34;q11.2) that leads to the formation of the BCR-ABL1 fusion gene, encoding a constitutively active chimeric tyrosine kinase (TK): BCR-ABL1 that is present in ~3% of pediatric ALL patients with B-immunophenotype and is associated with a poor outcome.
|
28748759 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Although "paired box 5" (PAX5)-related fusion genes are well documented in childhood B-cell precursor acute lymphoblastic leukemia (ALL), these types of fusion with the exception of PAX5-JAK2 are rarely seen in patients with gene expression profiles similar to those of BCR-ABL1 (Philadelphia)-positive ALL (Ph-like ALL).
|
27870151 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We investigated the frequency, predictors, and evolution of acute lymphoblastic leukemia (ALL) in patients with CNS relapse and introduced a novel method for studying BCR-ABL1 protein variants in cDNA from bone marrow (BM) and cerebrospinal fluid (CSF) blast cells.
|
28451802 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Fusion genes were detected by F-qRT-PCR in 97.3% of patients with CML, followed by 69.4% with AML, 33.3% with acute lymphoblastic leukemia (ALL), 9.1% with myelodysplastic syndromes (MDS), and 0% with chronic lymphocytic leukemia (CLL).
|
28743306 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Genetic alterations of IKZF1 encoding the lymphoid transcription factor IKAROS are a hallmark of high-risk B-progenitor acute lymphoblastic leukemia (ALL), such as BCR-ABL1-positive (Ph+) and Ph-like ALL, and are associated with poor outcome even in the era of contemporary chemotherapy incorporating tyrosine kinase inhibitors.
|
27865806 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Therefore, we recommend further investigations on CML-like <i>BCR-ABL1</i>-positive ALL.
|
28331056 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
To characterize the subset of ALL with normal karyotype or failed CBA, we performed fluorescence in situ hybridization (FISH) or PCR for BCR-ABL1 and MLL rearrangements as well as array comparative genomic hybridization (aCGH) in 186 adult patients.
|
26449660 |
2016 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
In 16 samples of normal karyotype ALL (n=9), ALL with no cytogentic result (n=4) and CML with no Philadelphia chromosome (n=3), fusion transcripts were detected.
|
26925663 |
2016 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
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 |
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 |
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 |
As tyrosine kinase inhibitors (TKIs) fail to induce long-term response in blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL), novel therapies targeting leukemia-dysregulated pathways are necessary.
|
23970380 |
2013 |
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 |