|
rs121913448
|
|
|
0.020 |
GeneticVariation |
BEFREE |
We identified for the first time the mutation Glu255Lys in STI571-naive leukemic samples of Ph+ ALL patients.
|
12663457 |
2003 |
|
rs387906517
|
|
|
0.020 |
GeneticVariation |
BEFREE |
We identified for the first time the mutation Glu255Lys in STI571-naive leukemic samples of Ph+ ALL patients.
|
12663457 |
2003 |
|
rs121913459
|
|
|
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 |
|
rs748843032
|
|
|
0.070 |
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 |
|
rs121913452
|
|
|
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 |
|
rs121913459
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The observation of responses in 3 patients with T315I phenotype-refractory CML or Ph-positive ALL, at doses of MK-0457 associated with no significant extramedullary toxicity, is very encouraging.
|
16990603 |
2007 |
|
rs121913448
|
|
|
0.020 |
GeneticVariation |
BEFREE |
Rottlerin also enhanced the cytotoxic effect of imatinib in leukemic cells from patients with CML blast crisis and Ph-positive ALL or a cell line expressing the imatinib-resistant E255K BCR/ABL mutant.
|
17130834 |
2007 |
|
rs387906517
|
|
|
0.020 |
GeneticVariation |
BEFREE |
Rottlerin also enhanced the cytotoxic effect of imatinib in leukemic cells from patients with CML blast crisis and Ph-positive ALL or a cell line expressing the imatinib-resistant E255K BCR/ABL mutant.
|
17130834 |
2007 |
|
rs121913459
|
|
|
0.100 |
GeneticVariation |
BEFREE |
We suggest that use of VX-680 together with a second effective drug as first-line treatment for Ph-positive ALL is likely to be safer and more useful than second-line treatment with VX-680 as monotherapy for drug-resistant T315I Ph-positive ALL.
|
20388735 |
2010 |
|
rs121913459
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Establishment of a new Philadelphia chromosome-positive acute lymphoblastic leukemia cell line (SK-9) with T315I mutation.
|
20471447 |
2010 |
|
rs121913459
|
|
|
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 |
|
rs121913459
|
|
|
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 |
|
rs121913459
|
|
|
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 |
|
rs121913459
|
|
|
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 |
|
rs748843032
|
|
|
0.070 |
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 |
|
rs121913459
|
|
|
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 |
|
rs121913459
|
|
|
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 |
|
rs121913459
|
|
|
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 |
|
rs748843032
|
|
|
0.070 |
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 |
|
rs748843032
|
|
|
0.070 |
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 |
|
rs138470268
|
|
|
0.010 |
GeneticVariation |
BEFREE |
CAR T cells exhibited marked cytotoxicity against Ph(+)ALL regardless of T315I mutation.
|
25108652 |
2014 |
|
rs387906695
|
|
|
0.010 |
GeneticVariation |
BEFREE |
CAR T cells exhibited marked cytotoxicity against Ph(+)ALL regardless of T315I mutation.
|
25108652 |
2014 |
|
rs121913459
|
|
|
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 |
|
rs748843032
|
|
|
0.070 |
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 |
|
rs375678155
|
|
|
0.010 |
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 |