|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
In CML, the BCR-ABL1 fusion gene and its companion messenger RNA offers a unique target differentiating cancer from the normal cell, affording the potential for very sensitive and specific assays.
|
31533919 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
We compared SNAQ test with 2 laboratory developed test at the MD Anderson molecular diagnostic laboratory and Cancer Genetics Institute for analyzing BCR-ABL1 from peripheral blood samples.
|
28682832 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
At current work, the combination of sensors were used to detect the presence of BCR-ABL1 as a mutant gene and CEA as a biomarkers of cancer, such a capability makes the package liable for early and certain detection of acute lymphoblastic leukemia.
|
31295447 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Variant-specific discrepancy when quantitating BCR-ABL1 e13a2 and e14a2 transcripts using the Europe Against Cancer qPCR assay.
|
30985947 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Acute lymphoblastic leukemia (ALL) with BCR-ABL1 translocation is an aggressive malignancy that is usually treated with intensive chemotherapy with the possibility of allogeneic stem cell transplantation.
|
30916583 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Chronic myeloid leukemia (CML) is a hematopoietic stem cell malignancy characterized by the expression of the BCR-ABL1 fusion gene with different chimeric transcripts.
|
29388070 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
PP2A inhibition sensitizes cancer stem cells to ABL tyrosine kinase inhibitors in BCR-ABL<sup>+</sup> human leukemia.
|
29437150 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Also highlighted are the functional consequences of aberrant splice variants (<i>BCR-Abl35INS</i>, <i>BIM-γ</i>, <i>IK6</i>, <i>p61 BRAF V600E</i>, <i>CD19-∆2</i>, <i>AR-V7</i> and <i>PIK3CD-S</i>) in promoting resistance to cancer targeted therapy or immunotherapy.
|
30463359 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
BCR-ABL1 was one of the first tyrosine kinases to be implicated in a human malignancy and the first to be successfully targeted.
|
29455643 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Among 1718 allo-HSCT, 74% were performed for malignancy (ALL 47.2%, AML 26.2%, MDS 10.8%, CML 8.1%, NHL/HD 6.1%, others 2.5%), and 26% for non-malignant disorders (SAA 41%, congenital immunodeficiencies 35.4%, hereditary bone marrow failure 16%, metabolic disorders 7%).
|
29880247 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The repression of MCL-1 renders leukemic cells highly sensitive to synergistic cell death induced by ABT-263 in a mouse model of BCR-ABL<sup>+</sup> B-ALL both <i>in vitro</i> and <i>in vivo</i> Furthermore, DHA synergizes with ABT-263 in human Ph<sup>+</sup> ALL cell lines, and primary patient-derived xenografts of Ph<sup>+</sup> ALL in culture.<b>Conclusions:</b> Our findings suggest that combining DHA with ABT-263 can improve therapeutic response in BCR-ABL<sup>+</sup> B-ALL.<i>Clin Cancer Res; 23(24); 7558-68.©2017 AACR</i>.
|
28974549 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
We propose that FL is a malignancy of cells that acquire both translocation t(14;18) and self-BCR, inducing them to proliferate and mature, resistant to negative selection.
|
27693433 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Notably, BGB324 does not inhibit BCR-ABL1 and consequently inhibits CML independent of BCR-ABL1 mutational status.<b>Conclusions:</b> Our data show that Axl inhibition has therapeutic potential in BCR-ABL TKI-sensitive as well as -resistant CML and support the need for clinical trials.<i>Clin Cancer Res; 23(9); 2289-300.©2016 AACR</i>.
|
27856601 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
However, in internal validation experiments, <i>GUS</i> outperformed <i>ABL</i> in samples collected at diagnosis as the latter produced 80% misclassification rates.<b>Conclusions:</b> Our data suggest that high <i>BCR-ABL</i> transcripts at diagnosis measured using <i>GUS</i> as a reference gene identify patients with CML unlikely to benefit from standard-dose imatinib.<i>Clin Cancer Res; 23(23); 7189-98.©2017 AACR</i>.
|
28928163 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
With the limitations of a small sample size, the results of the current study demonstrate that less frequent monitoring of BCR-ABL1 does not appear to affect outcomes, and that discontinuation of TKIs used as first-line treatment or beyond after resistance or intolerance to first-line treatment appears feasible.Cancer 2017;123:2482-88.© 2017 American Cancer Society.
|
28241101 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
We show that PAK1 and PAK2 are the critical isoforms in a BCR/ABL1<sup>+</sup> haematopoietic malignancy.
|
28707321 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
BCR-ABL1-induced downregulation of WASP in chronic myeloid leukemia involves epigenetic modification and contributes to malignancy.
|
29022901 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Successful clinical trials with Gleevec in CML and gastrointestinal stromal tumors have set up an example for targeted therapy of cancer.
|
26373844 |
2016 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The extraordinary success of imatinib in the treatment of BCR-ABL1 associated cancers underscores the need to identify novel functional gene fusions in cancer.
|
25183062 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The Philadelphia chromosome was the first genetic abnormality discovered in cancer (in 1960), and it was found to be consistently associated with CML.
|
25368816 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Increasing sophisticated information suggests that cancer cells express constitutively active oncogenic kinases such as breakpoint cluster region- c-abl oncogene 1, non-receptor tyrosine kinase (BCR-ABL1) that promote carcinogenesis independent of extrinsic growth factors.
|
23575065 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In this issue of Cancer Discovery, Geng and colleagues report on their use of a combination of promoter cytosine methylation profiling with gene expression and ChIP sequencing to elucidate molecular signatures of adult B-acute lymphoblastic leukemia patient samples with BCR-ABL1, E2A-PBX1, and MLL rearrangements.
|
23148371 |
2012 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Here we present proof-of-principle experiments showing how a conditional transgenic mouse model of BCR-ABLp190-driven B-ALL offers the opportunity to test the hypothesis that the age of the leukemic cells-of-origin of B-ALL influences B-ALL malignancy.
|
21164221 |
2010 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Maternal and infant cancer clones shared the same unique BCR-ABL1 genomic fusion sequence, indicating a shared, single-cell origin.
|
19822752 |
2009 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
However, BCR-ABLp210-induced CML is reversible through the unique elimination of the cancer stem cells (CSCs).
|
19037256 |
2009 |