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 |
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 |
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 |
More is known about what causes CML than any human cancer.
|
8251912 |
1993 |
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 |
Retroviral vector design for gene therapy of cancer: specific inhibition and tagging of BCR-ABLp190 cells.
|
8900540 |
1996 |
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 |
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 |
Novel FISH probes designed to detect IGK-MYC and IGL-MYC rearrangements in B-cell lineage malignancy identify a new breakpoint cluster region designated BVR2.
|
16888615 |
2006 |
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 |
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 |
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 |
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 |
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 |
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 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 |
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 |