|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Ultra-deep sequencing leads to earlier and more sensitive detection of the tyrosine kinase inhibitor resistance mutation T315I in chronic myeloid leukemia.
|
27102501 |
2016 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Taken together, our data demonstrate that the small molecule AurA inhibitor AKI603 may be used to overcome drug resistance induced by BCR-ABL-T315I mutation in CML.
|
27824120 |
2016 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
The third-generation tyrosine kinase inhibitor (TKI) ponatinib shows activity against all common BCR-ABL1 single mutants, including the highly resistant BCR-ABL1-T315I mutant, improving outcome for patients with refractory chronic myeloid leukemia (CML).
|
26773037 |
2016 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
In summary, this study provides new insight into the biological underpinnings of BCR-ABL-driven CML and potential rationale for investigating novel treatment strategies for patients with T315I CML.
|
27444277 |
2016 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Collectively, by degrading the native and T315I-mutant BCR-ABL, the chimeric ubiquitin ligase SH2-U-box may serve as a potential therapy for both imatinib-sensitive and resistant CML.
|
27329306 |
2016 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Leukemia cells escape BCR-ABL-targeted therapy by developing mutations, such as T315I, in the p210(BCR-ABL) fusion protein in Philadelphia chromosome-positive chronic myeloid leukemia (CML).
|
26846820 |
2016 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Allogeneic Stem Cell Transplantation for Patients with T315I BCR-ABL Mutated Chronic Myeloid Leukemia.
|
26995693 |
2016 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Despite the great success in using tyrosine kinase inhibitors (TKIs) to treat chronic myeloid leukemia (CML), the frequent development of multi-drug resistance, particularly the T315I mutation of BCR-ABL, remains a challenging issue.
|
25900240 |
2015 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Here, we report the hematological, cytogenetic, and molecular response of a patient with refractory CML in chronic phase with e19a2 transcripts, carrying T315I mutation that was successfully treated with ponatinib.
|
24766374 |
2015 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Inhibition of either RAN or XPO1 impaired colony formation of CD34(+) cells from newly diagnosed and TKI-resistant CML patients in the presence of imatinib, without effects on CD34(+) cells from normal cord blood or from a patient harboring the BCR-ABL1(T315I) mutant.
|
25573989 |
2015 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
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 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Moreover, CC(mut3) inhibits colony formation by primary CML CD34(+) cells ex vivo, including a sample expressing the T315I mutant.
|
25721898 |
2015 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
Here we studied mechanisms of acquired resistance of chronic myeloid leukemia (CML) to tyrosine kinase inhibitors (TKIs) by examining genome-wide gene expression changes in KCL-22 CML cells versus their resistant KCL-22M cells that acquire T315I BCR-ABL mutation following TKI exposure.
|
24967705 |
2014 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
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 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
We conclude that T315I, P-loop, and compound mutations may worsen prognosis in CML.
|
25281405 |
2014 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
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.
|
25127392 |
2014 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
In the present study, an allele-specific oligonucleotide reverse transcriptase polymerase chain reaction assay was used to detect T315I mutation in a cohort of 60 imatinib-resistant CML patients.
|
23540562 |
2013 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
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 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
CLINVAR |
Early detection and quantification of mutations in the tyrosine kinase domain of chimerical BCR-ABL1 gene combining high-resolution melting analysis and mutant-allele specific quantitative polymerase chain reaction.
|
22870928 |
2013 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
CLINVAR |
Ponatinib is a pan-BCR-ABL kinase inhibitor: MD simulations and SIE study.
|
24236021 |
2013 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
CLINVAR |
Detection of BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on imatinib.
|
23676790 |
2013 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
CLINVAR |
In the present study, an allele-specific oligonucleotide reverse transcriptase polymerase chain reaction assay was used to detect T315I mutation in a cohort of 60 imatinib-resistant CML patients.
|
23540562 |
2013 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
The quantitative level of T315I mutated BCR-ABL predicts for major molecular response to second-line nilotinib or dasatinib treatment in patients with chronic myeloid leukemia.
|
23065514 |
2013 |
|
Myeloid Leukemia, Chronic
|
|
0.800 |
GeneticVariation
|
BEFREE |
The BCR-ABL T315I mutation confers resistance to currently licensed tyrosine kinase inhibitors in chronic myelogenous leukemia.
|
23716543 |
2013 |