|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Tyrosine kinase inhibitors (TKIs) targeting breakpoint cluster region-ABL are the first-line therapy for most CML patients and have drastically improved the prognosis of CML.
|
26284455 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Dasatinib is a small-molecule inhibitor of the tyrosine kinases SRC and ABL that has been approved for the treatment of chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia.
|
25842192 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
To discover novel inhibitors against drug-resistant CML bearing T315I mutation, we applied a physics-based hierarchical virtual screening approach to dock a large chemical library against ATP binding pockets of both wild-type (WT) and T315I mutant ABL kinases in a combinatorial fashion.
|
26501568 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In total, 95 CML and 20 Ph + ALL patients with positive PCR transcripts were identified, of which 10 (10.5%) and 4 (20.0%), respectively, were found to have pre-HSCT ABL kinase mutations known to confer TKI resistance.
|
25300870 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The non-receptor tyrosine kinase ABL drives myeloid progenitor expansion in human chronic myeloid leukemia.
|
25803821 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We investigated the influence of p210BCR-ABL breakpoint variants and imatinib treatment on expression and proteolytic activity of Separase as measured with a specific fluorogenic assay on CML cell lines (b2a2: KCL-22, BV-173; b3a2: K562, LAMA-84).
|
26087013 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The introduction of highly selective ABL-tyrosine kinase inhibitors (TKIs) has revolutionized therapy for chronic myeloid leukemia (CML).
|
26304963 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Co-expression of p96(ABL/BCR) abolished the capacity of p185(BCR/ABL) to induce a CML-like disease and led to the induction of ALL.
|
25919613 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Bosutinib has shown activity against all phases of resistant chronic myeloid leukemia that do not harbor the T315I or V299L ABL kinase domain mutations.
|
24490604 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
ABL-specific tyrosine kinase inhibitors (TKIs) induce minimal apoptosis in CML progenitor cells, yet exert potent antiproliferative effects, through as yet poorly understood mechanisms.
|
24806995 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Treatment of chronic myeloid leukemia (CML) has been drastically changed by the emergence of the ABL tyrosine kinase inhibitor (TKI), imatinib mesylate.
|
24258348 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Imatinib, an ABL tyrosine kinase inhibitor (TKI), has shown clinical efficacy against chronic myeloid leukemia (CML).
|
24100660 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we report a novel BCR (breakpoint cluster region)-ABL (c-abl oncogene 1, non-receptor tyrosine kinase)/GATA1/microRNA-138 (miR-138) circuitry in chronic myeloid leukemia (CML). miR-138 expression is downregulated in K562 cells and primary CML samples, which is restored after imatinib treatment.
|
23208504 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
MK-0457, a pan-aurora kinase inhibitor that also inhibits the ABL T315I mutant, was evaluated to treat patients with chronic myelogenous leukemia (CML) or Philadelphia chromosome (Ph+) acute lymphoblastic leukemia (ALL) with the T315I mutation.
|
25127392 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The ABL kinase inhibitor imatinib is highly effective in treating most, but not all, patients with chronic myeloid leukemia (CML).
|
24775308 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Roles of the complex in regulation of response or resistance to ABL and JAK2 inhibitors were investigated in BCR-ABL (+) cells and primary CML stem/progenitor cells and in immunodeficient NSG mice.All statistical tests were two-sided.
|
23446755 |
2013 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Because a substantial number of patients with chronic myeloid leukemia acquire resistance to ABL tyrosine kinase inhibitors (TKIs), their management remains a challenge.
|
23684619 |
2013 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Patients in the chronic phase (CP) of chronic myelogenous leukemia (CML) have been treated successfully following the advent of ABL kinase inhibitors, but once they progress to the blast crisis (BC) phase the prognosis becomes dismal.
|
24098673 |
2013 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Integrating in vitro sensitivity and dose-response slope is predictive of clinical response to ABL kinase inhibitors in chronic myeloid leukemia.
|
24062017 |
2013 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The presence of ABL mutations in 45 CML patients resistant to imatinib was evaluated by direct sequencing and was correlated with the results of the cytogenetic study (performed in 39 cases).
|
23433665 |
2013 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The aim of this study was to evaluate proliferation inhibition and apoptosis induction by down-regulating PPP2R5C gene expression in the imatinib-sensitive and imatinib-resistant CML cell lines K562, K562R (imatinib resistant without an Abl gene mutation), 32D-Bcr-Abl WT (imatinib-sensitive murine CML cell line with a wild type Abl gene) and 32D-Bcr-Abl T315I (imatinib resistant with a T315I Abl gene mutation) and primary cells from CML patients by RNA interference.
|
24004697 |
2013 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The t(9;22)(q34;q11) translocation between bcr and abl genes plays a pivotal role in the pathogenesis and diagnosis of chronic myelogenous leukemia (CML).
|
23417967 |
2013 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Imatinib, a small molecule inhibitor of ABL, PDGFR and C-KIT, has revolutionized treatment of chronic myeloid leukaemia (CML).
|
21221851 |
2012 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
ABL tyrosine kinase inhibitor (TKI) therapy induces clinical remission in chronic myeloid leukemia (CML) patients but early relapses and later emergence of TKI-resistant disease remain problematic.
|
22623184 |
2012 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
We investigated the influence of IM and p210BCR-ABL on Separase as a potential driver of centrosomal amplification in CML.
|
22870341 |
2012 |