|
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 |
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 |
Biomarker
|
group |
BEFREE |
More is known about what causes CML than any human cancer.
|
8251912 |
1993 |
|
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 |
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 |
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 |
The Ph1 chromosome and CML have provided one of the most exciting stories of oncogene activation in human malignancy, and much more information, at both the level of basic and of clinical science, will result from the investigations currently underway in a number of laboratories.
|
2676087 |
1989 |
|
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 |
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 |
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 |
CML, characterized by the BCR/ABL gene rearrangement has been more extensively studied than any other malignancy.
|
9519773 |
1998 |
|
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 |
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 |
GeneticVariation
|
group |
BEFREE |
To determine the additional value of molecular monitoring during treatment for CML, we performed a prospective, sequential analysis using quantitative Southern blot monitoring of BCR gene rearrangements of blood and marrow samples from Cancer and Leukemia Group B (CALGB) study 8761.
|
8996121 |
1997 |
|
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 |
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 |
Biomarker
|
group |
BEFREE |
However, BCR-ABLp210-induced CML is reversible through the unique elimination of the cancer stem cells (CSCs).
|
19037256 |
2009 |
|
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 |
GeneticVariation
|
group |
BEFREE |
The first clear cut association of an oncogene with a specific cancer is the c-abl translocation in chronic myelogenous leukemia and acute lymphocytic leukemia; it has been observed in 90% of CML cases examined.
|
1684291 |
1991 |
|
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 |
Chromosomes and causation of human cancer and leukemia: XL. The Ph1 and other translocations in CML.
|
6932993 |
1980 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
CML has served as a model for study of pathogenesis, evolution and treatment of malignancy for nearly 150 years and will continue to do so.
|
8251921 |
1993 |
|
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 |