|
Malignant Neoplasms
|
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 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Finally, we observe that the ABL1 cancer mutants display an increased cytosolic localization, which is associated with the oncogenic properties of the ABL1 kinase.
|
26758680 |
2016 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These studies involve the identification of the first cancer-associated chromosomal abnormality and the subsequent development of tyrosine kinase inhibitors (TKIs) that inhibit BCR-ABL kinase activity in CML.
|
23483480 |
2013 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In summary, our data show a novel multikinase modulator that might be therapeutically effective in BCR-ABL1-STAT5-related malignancies.
|
30687103 |
2018 |
|
Malignant Neoplasms
|
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 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
CML, characterized by the BCR/ABL gene rearrangement has been more extensively studied than any other malignancy.
|
9519773 |
1998 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Activity of tyrosine kinase inhibitors against human NUP214-ABL1-positive T cell malignancies.
|
18401417 |
2008 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Using BCR-ABL-induced chronic myeloid leukemia (CML) as a cancer model, we recently identified arachidonate 5-lipoxygenase (5-LO) gene (Alox5) as a critical regulator for leukemia stem cells (LSCs) in CML.
|
19823023 |
2009 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Consistently, inhibition of ABL suppresses cancer invasion in mice.
|
25432929 |
2015 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The introduction of kinase inhibitors in cancer medicine has transformed chronic myeloid leukemia from a fatal disease into a leukemia subtype with a favorable prognosis by interfering with the constitutively active kinase BCR-ABL.
|
26321002 |
2015 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Because it has been difficult to perform lineage studies of the Ph chromosome, we investigated the use of fluorescence in situ hybridization (FISH) with probes for BCR (on chromosome 22) and ABL (on chromosome 9) to study lineage involvement in Ph+ lymphoblastic malignancies.
|
8656674 |
1996 |
|
Malignant Neoplasms
|
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 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Abnormalities of tyrosine kinase proteins are well recognised in myeloid malignancies, mutation in the cytoplasmic tyrosine kinase JAK2 (V617F) is key in the pathogenesis of myeloproliferative neoplasms, and translocations involving ABL key in the development of chronic myeloid leukaemia.
|
21722956 |
2011 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Because the propensity for on- versus off-target resistance varies across cancer types, a deeper understanding of the mutational burden in drug targets could rationalize treatment outcomes and prioritize pan-target inhibitors for indications where on-target mutations are most likely.<b>Experimental Design:</b> To measure and model the mutational landscape of a drug target at high resolution, we integrated single-molecule Duplex Sequencing of the ABL1 gene in Philadelphia-positive (Ph<sup>+</sup>) leukemias with computational simulations.<b>Results:</b> A combination of drug target mutational burden and tumor-initiating cell fraction is sufficient to predict that most patients with chronic myeloid leukemia are unlikely to harbor ABL1 resistance mutations at the time of diagnosis, rationalizing the exceptional success of targeted therapy in this setting.
|
30042204 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, the clinical significance and prognostic impact of several inflammatory markers were evaluated in patients with BCR/ABL-negative myeloproliferative malignancies.
|
28946149 |
2017 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Collectively, our findings support clinical investigation of ATP-competitive TKIs in malignancies harboring ABL1 point mutations, and sequencing of BCR-ABL1 and ABL1 1b in patients with acquired resistance to allosteric ABL1 inhibitors.
|
27890928 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The most dramatic example of targeted therapy in cancer to date is the use of targeted BCR-ABL protein tyrosine kinase inhibitors (TKI), which has revolutionized the treatment of chronic myeloid leukemia (CML).
|
24246694 |
2013 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Targeting ABL1-mediated oxidative stress adaptation in fumarate hydratase-deficient cancer.
|
25490448 |
2014 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
T cell malignancies harboring the ABL1 fusion genes are sensitive to many cytotoxic agents, but up to date complete remissions have not been achieved.
|
27821800 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CML was the first cancer to be associated with a defined genetic abnormality, BCR-ABL, that is necessary and sufficient for initiating chronic phase disease as well as the first cancer to be treated with molecular targeted therapy.
|
18539972 |
2008 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The existence of a minor "pool" of blasts of greater clonogenic capacity along with significantly higher expression level of BCR-ABL, individually or in conjunction with other cancer and adhesion-related genes, might also signify clonal evolution toward subsequent increased malignancy and lower therapeutic sensitivity.
|
18452548 |
2008 |
|
Malignant Neoplasms
|
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 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
STI-571 is a small molecule that selectively inhibits the enzymatic activity of the ABL, platelet-derived growth factor receptor, and KIT tyrosine kinases and the BCR-ABL fusion protein and is a landmark development in cancer therapy.
|
12094371 |
2002 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Resistance to imatinib (Gleevec®) in cancer cells is frequently because of acquired point mutations in the kinase domain of BCR-ABL.
|
24586514 |
2014 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Abl1 is a protein tyrosine kinase whose aberrant activation due to mutations is the culprit of several cancers, most notably chronic myeloid leukaemia.
|
30684523 |
2019 |