|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib-Induced Graft-versus-Host Disease/Graft-versus-Leukemia Effect in a Patient with Philadelphia-Positive Acute Lymphoblastic Leukemia without the T315I Mutation Relapsing after Allogeneic Transplant.
|
28810255 |
2017 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
In the United States, ponatinib has received accelerated approval for adults with T315I-positive chronic myeloid leukemia (CML) or T315I (gatekeeper mutation)-positive, Philadelphia chromosome-positive, acute lymphoblastic leukemia (Ph + ALL), and patients with CML or Ph + ALL for whom no other TKI therapy is indicated.
|
28184964 |
2017 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib-Induced Graft-versus-Host Disease/Graft-versus-Leukemia Effect in a Patient with Philadelphia-Positive Acute Lymphoblastic Leukemia without the T315I Mutation Relapsing after Allogeneic Transplant.
|
28810255 |
2017 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Surprisingly, inhibition of AurA by AKI603 induced leukemia cell senescence in both BCR-ABL wild type and T315I mutation cells.
|
27824120 |
2016 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Surprisingly, inhibition of AurA by AKI603 induced leukemia cell senescence in both BCR-ABL wild type and T315I mutation cells.
|
27824120 |
2016 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
In BCR/ABL- or BCR/ABL-T315I-driven murine leukemia as well as in xenograft models of primary Ph+ leukemia harboring the T315I, PF-114 significantly prolonged survival to a similar extent as ponatinib.
|
25394714 |
2015 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
In BCR/ABL- or BCR/ABL-T315I-driven murine leukemia as well as in xenograft models of primary Ph+ leukemia harboring the T315I, PF-114 significantly prolonged survival to a similar extent as ponatinib.
|
25394714 |
2015 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
One patient with lymphoid BC/Ph+ ALL who harbored a T315I ABL mutation and was treated with ponatinib was found to have developed a newly acquired V216M TP53 mutation (12% of transcripts) when becoming resistant to ponatinib.
|
25894969 |
2015 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here we combine comprehensive drug sensitivity and resistance profiling of patient cells ex vivo with structural analysis to establish the VEGFR tyrosine kinase inhibitor axitinib as a selective and effective inhibitor for T315I-mutant BCR-ABL1-driven leukaemia.
|
25686603 |
2015 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib is the only currently approved tyrosine kinase inhibitor (TKI) that suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph(+)) leukemia, including the recalcitrant BCR-ABL1(T315I) mutant.
|
25132497 |
2014 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
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.
|
25127392 |
2014 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib is the only currently approved tyrosine kinase inhibitor (TKI) that suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph(+)) leukemia, including the recalcitrant BCR-ABL1(T315I) mutant.
|
25132497 |
2014 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib is a valuable treatment option for adults with T315I-positive chronic-, accelerated- or blast-phase CML, or Ph+ ALL, 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, but before starting treatment, clinicians need to consider whether the potential benefits of therapy will outweigh the risks.
|
24807266 |
2014 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
Eight of 18 patients with BCR-ABL T315I-mutated chronic myelogenous leukemia (44%) had hematologic responses and one of three patients (33%) with Philadelphia chromosome-positive acute lymphoblastic leukemia obtained complete remission.
|
22772060 |
2013 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
MK-0457 has important activity in patients with leukemias expressing the highly resistant T315I BCR-ABL mutation.
|
22772060 |
2013 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
One mutation, T315I, for example, renders the leukemia resistant to all first- and second-line TKIs.
|
23666688 |
2013 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
One mutation, T315I, for example, renders the leukemia resistant to all first- and second-line TKIs.
|
23666688 |
2013 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
MK-0457, an Aurora kinase and BCR-ABL inhibitor, is active in patients with BCR-ABL T315I leukemia.
|
22772060 |
2013 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Given the fact that all AKIs fail to inhibit BCR/ABL harboring the 'gatekeeper' mutation T315I, we investigated the effects of AKIs in combination with the allosteric inhibitor GNF2 in Ph + leukemia.
|
22985168 |
2012 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
T315I mutation in Ph-positive acute lymphoblastic leukemia is associated with a highly aggressive disease phenotype: three case reports.
|
22593461 |
2012 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
The efficacy of this approach on the leukemogenic potential of BCR/ABL was studied in Ba/F3 cells, primary murine bone marrow cells, and untransformed Rat-1 fibroblasts expressing BCR/ABL or BCR/ABL-T315I as well as in patient-derived long-term cultures (PDLTC) from Ph + ALL-patients.
|
22985168 |
2012 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
These data indicate that the emergence of the T315I mutation among Ph + ALL patients treated with dasatinib is, in part, dependent on plasma dasatinib pharmacokinetics.
|
22587422 |
2012 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Given the fact that all AKIs fail to inhibit BCR/ABL harboring the 'gatekeeper' mutation T315I, we investigated the effects of AKIs in combination with the allosteric inhibitor GNF2 in Ph + leukemia.
|
22985168 |
2012 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
The results of 12 serial samples from 2 patients (case A: Philadelphia-positive acute lymphoblastic leukemia and case B: CML) with the T315I mutant clone were compared with those of direct sequencing or 2 kinds of allele-specific oligonucleotide (ASO)-PCR.
|
21867983 |
2011 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Allogeneic stem cell transplantation for patients harboring T315I BCR-ABL mutated leukemias.
|
21926354 |
2011 |