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rs748843032
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|
0.100 |
GeneticVariation |
BEFREE |
Discovery of (E)-N-(4-((4-methylpiperazin-1-yl)methyl)-3-(trifluoromethyl)phenyl)-3-((3-(2-(pyridin-2-yl)vinyl)-1H-indazol-6-yl)thio)propanamide (CHMFL-ABL-121) as a highly potent ABL kinase inhibitor capable of overcoming a variety of ABL mutants including T315I for chronic myeloid leukemia.
|
30317026 |
2018 |
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rs748843032
|
|
|
0.100 |
GeneticVariation |
BEFREE |
We have now demonstrated that protein expression of human estrogen receptor alpha 36 (ERα36), an alternative splicing variant of human estrogen receptor alpha 66 (ERα66), is highly increased in TKI-insensitive CD34+ chronic myeloid leukemia (CML) cells and BCR-ABL-T315I mutant cells, and is abnormally localized in plasma membrane and cytoplasm.
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28599273 |
2017 |
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rs748843032
|
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|
0.100 |
GeneticVariation |
BEFREE |
The emergence of drug resistance of the BCR-ABL kinase inhibitor imatinib, especially toward the T315I gatekeeper mutation, poses a great challenge to targeted therapy in treating chronic myeloid leukemia (CML) patients.
|
26501568 |
2015 |
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rs748843032
|
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0.100 |
GeneticVariation |
BEFREE |
Ponatinib is approved for the treatment of adults with T315I-positive chronic-, accelerated- or blast-phase chronic myeloid leukaemia (CML), or Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia (ALL) [in the EU and the USA], as well as those with chronic-, accelerated- or blast-phase CML, or Ph+ ALL who are resistant or intolerant to prior tyrosine kinase inhibitor therapy (EU) or for whom no other tyrosine kinase inhibitor therapy is indicated (USA).
|
24807266 |
2014 |
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rs748843032
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0.100 |
GeneticVariation |
BEFREE |
A phase 2 study of MK-0457 in patients with BCR-ABL T315I mutant chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia.
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25127392 |
2014 |
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rs748843032
|
|
|
0.100 |
GeneticVariation |
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 |
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rs748843032
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|
0.100 |
GeneticVariation |
BEFREE |
Rapid quantitative detection of the T315I mutation in patients with chronic myelogenous leukemia.
|
22306673 |
2012 |
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rs748843032
|
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0.100 |
GeneticVariation |
BEFREE |
Ex vivo exposure of CML cells from patients harboring BCR-ABL or BCR-ABL(T315I) to DCC-2036 revealed marked inhibition of colony formation and reduced phosphorylation of the direct BCR-ABL target CrkL.
|
21505103 |
2011 |
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rs748843032
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0.100 |
GeneticVariation |
BEFREE |
Expanded distribution of the T315I mutation among hematopoietic stem cells and progenitors in a chronic myeloid leukemia patient during imatinib treatment.
|
20963643 |
2010 |
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rs748843032
|
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|
0.100 |
GeneticVariation |
BEFREE |
The aim of this study was to evaluate the behavior of T315I mutated cells and to study the presence of potential additional mutations in progenitors and stem cells from a patient with CML.
|
20929330 |
2010 |
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rs748843032
|
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0.100 |
GeneticVariation |
BEFREE |
The second-generation BCR-ABL inhibitors nilotinib (Tasigna; Novartis) and dasatinib (Sprycel; Bristol-Myers Squibb) have shown significant activity after imatinib failure in clinical trials, but still face similar obstacles to imatinib, including negligible activity against the frequent BCR-ABL T315I mutation and modest effects in advanced phases of CML.
|
17853901 |
2007 |
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rs748843032
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0.100 |
GeneticVariation |
BEFREE |
We conclude that (a) amino acid substitutions at seven residues (M244V, G250E, Y253F/H, E255K/V, T315I, M351T, and F359V) account for 85% of all resistance-associated mutations; (b) the search for mutations is important both in case of imatinib failure and in case of loss of response at the hematologic or cytogenetic level; (c) advanced-phase chronic myeloid leukemia and Ph+ ALL patients have a higher likelihood of developing imatinib-resistant mutations; and (d) the presence of either P-loop or T315I mutations in imatinib-treated patients should warn the clinician to reconsider the therapeutic strategy.
|
17189410 |
2006 |
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rs754736070
|
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|
0.010 |
GeneticVariation |
BEFREE |
We conclude that (a) amino acid substitutions at seven residues (M244V, G250E, Y253F/H, E255K/V, T315I, M351T, and F359V) account for 85% of all resistance-associated mutations; (b) the search for mutations is important both in case of imatinib failure and in case of loss of response at the hematologic or cytogenetic level; (c) advanced-phase chronic myeloid leukemia and Ph+ ALL patients have a higher likelihood of developing imatinib-resistant mutations; and (d) the presence of either P-loop or T315I mutations in imatinib-treated patients should warn the clinician to reconsider the therapeutic strategy.
|
17189410 |
2006 |