|
Acute lymphoblastic leukemia with lymphomatous features
|
|
0.700 |
GeneticVariation
|
CLINVAR |
MK-0457, an Aurora kinase and BCR-ABL inhibitor, is active in patients with BCR-ABL T315I leukemia.
|
22772060 |
2013 |
|
Acute lymphoblastic leukemia with lymphomatous features
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
Acute lymphoblastic leukemia with lymphomatous features
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation.
|
11861307 |
2002 |
|
Acute lymphocytic leukemia
|
|
0.050 |
GeneticVariation
|
BEFREE |
The BCR-ABL T315I kinase domain mutation is insensitive to dasatinib therapy for Philadelphia-positive acute lymphoid leukemia (Ph + ALL) patients.
|
22587422 |
2012 |
|
Acute lymphocytic leukemia
|
|
0.050 |
GeneticVariation
|
BEFREE |
Three patients with T315I abl-mutated chronic myeloid leukemia (CML) or Philadelphia chromosome (Ph)-positive acute lymphocytic leukemia (ALL) have achieved clinical responses to doses of MK-04547 that are not associated with adverse events.
|
16990603 |
2007 |
|
Acute lymphocytic leukemia
|
|
0.050 |
GeneticVariation
|
BEFREE |
This cell line may provide a useful model for in vitro and in vivo cellular and molecular studies of BCR-ABL-positive ALL with T315I mutation.
|
20471447 |
2010 |
|
Acute lymphocytic leukemia
|
|
0.050 |
GeneticVariation
|
BEFREE |
The objectives of this retrospective observational study were to estimate overall and progression-free survival for chronic myeloid leukemia in chronic-phase (CP), accelerated-phase (AP), or blastic-phase (BP) and Philadelphia chromosome-positive (Ph)(+) acute lymphoblastic leukemia (ALL) patients with T315I mutation.
|
19843886 |
2009 |
|
Acute lymphocytic leukemia
|
|
0.050 |
GeneticVariation
|
BEFREE |
It suppressed primary Ph+ acute lymphatic leukemia-derived long-term cultures that either displayed nonmutational resistance or harbor the T315I.
|
25394714 |
2015 |
|
Adult Acute Lymphocytic Leukemia
|
|
0.020 |
GeneticVariation
|
BEFREE |
This cell line may provide a useful model for in vitro and in vivo cellular and molecular studies of BCR-ABL-positive ALL with T315I mutation.
|
20471447 |
2010 |
|
Adult Acute Lymphocytic Leukemia
|
|
0.020 |
GeneticVariation
|
BEFREE |
The objectives of this retrospective observational study were to estimate overall and progression-free survival for chronic myeloid leukemia in chronic-phase (CP), accelerated-phase (AP), or blastic-phase (BP) and Philadelphia chromosome-positive (Ph)(+) acute lymphoblastic leukemia (ALL) patients with T315I mutation.
|
19843886 |
2009 |
|
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 |
|
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 |
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 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ponatinib is a third-generation TKI that is currently approved as per label when no other TKIs are indicated for the treatment of patients with CML and Ph+ ALL after failing treatment with second-generation TKIs or if presence of T315I mutation is discovered.
|
30251548 |
2019 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
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 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
This specific combination of Nutlin-3 and Tanshinone IIA is also effective in preventing the recurrence of refractory leukemia, such as Ph+ ALL with the ABL kinase T315I mutation and AML with the FLT3-ITD mutation.
|
30389549 |
2019 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
0.100 |
GeneticVariation
|
BEFREE |
The clonal evolution of two distinct T315I-positive BCR-ABL1 subclones in a Philadelphia-positive acute lymphoblastic leukemia failing multiple lines of therapy: a case report.
|
28779753 |
2017 |
|
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 |
|
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 |
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 |
|
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 |
|
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 |
|
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 |
|
B Acute Lymphoblastic Leukemia with t(9;22)(q34.1;q11.2); BCR-ABL1
|
|
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 |