|
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 |
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 |
|
Neoplasms
|
|
0.060 |
GeneticVariation
|
BEFREE |
Moreover, in mouse tumor xenografts, S116836 significantly inhibits the growth and volume of tumors expressing the WT or T315I mutant BCR-ABL without causing significant cardiotoxicity.
|
31837444 |
2020 |
|
Neoplasms
|
|
0.060 |
GeneticVariation
|
BEFREE |
The in vivo efficacy validation of p-niclosamide, a water soluble derivative of niclosamide, showed that p-niclosamide significantly inhibited the tumor burden of nude mice subcutaneously bearing T315I-BCR-ABL-expressing CML cells, and prolonged the survival of allografted leukemic mice harboring BaF3-T315I-BCR-ABL.
|
29358661 |
2018 |
|
Neoplasms
|
|
0.060 |
GeneticVariation
|
BEFREE |
In vitro studies showed that SHC004-221A1 inhibited the proliferation of tumor cell lines carrying native and T315I mutant BCR-ABL.
|
28595903 |
2017 |
|
Neoplasms
|
|
0.060 |
GeneticVariation
|
BEFREE |
Finally, combined in vivo treatment significantly suppressed BaF3/T315I tumor growth and prolonged survival in an allogeneic mouse model.
|
25465126 |
2015 |
|
Neoplasms
|
|
0.060 |
GeneticVariation
|
BEFREE |
NVP-BEZ235 in combination with nilotinib also inhibited tumor growth in a xenograft model and inhibited the growth of primary T315I mutant cells and ponatinib-resistant cells.
|
24100660 |
2014 |
|
Neoplasms
|
|
0.060 |
GeneticVariation
|
BEFREE |
AP24534 inhibited all tested BCR-ABL mutants in cellular and biochemical assays, suppressed BCR-ABL(T315I)-driven tumor growth in mice, and completely abrogated resistance in cell-based mutagenesis screens.
|
19878872 |
2009 |
|
Blast Phase
|
|
0.070 |
GeneticVariation
|
BEFREE |
Pre- and post-transplant ponatinib for a patient with acute megakaryoblastic blast phase chronic myeloid leukemia with T315I mutation who underwent allogeneic hematopoietic stem cell transplantation.
|
30879266 |
2019 |
|
Blast Phase
|
|
0.070 |
GeneticVariation
|
BEFREE |
Here, we demonstrate that JNJ-26854165, an inhibitor of MDM2, inhibits proliferation and triggers cell death in a p53-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant.
|
27999193 |
2017 |
|
Blast Phase
|
|
0.070 |
GeneticVariation
|
BEFREE |
ARDAP derivative <b>10</b> inhibited the proliferation of BCR/ABL-expressing KU812 and LAMA84 cells from chronic myeloid leukemia (CML) patients in blast crisis and of hematopoietic cells ectopically expressing the imatinib mesylate (IM)-sensitive KBM5-WT or its IM-resistant KBM5-T315I mutation.
|
28523104 |
2017 |
|
Blast Phase
|
|
0.070 |
GeneticVariation
|
BEFREE |
Adults with Ph+ chronic phase (CP)-, accelerated phase (AP)- or blast phase (BP)-CML, or ALL and documented BCR-ABL T315I mutation were treated with a 5-day continuous infusion of MK-0457 administered every 14 days at 40 mg/m(2)/h, 32 mg/m(2)/h or 24 mg/m(2)/h.
|
25127392 |
2014 |
|
Blast Phase
|
|
0.070 |
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 |
|
Blast Phase
|
|
0.070 |
GeneticVariation
|
BEFREE |
BMS-214662 was cytotoxic against CML blast crisis stem/progenitor cells, particularly in combination with a tyrosine kinase inhibitor and equally effective in cell lines harboring wild-type vs mutant BCR-ABL, including the T315I mutation.
|
18156496 |
2008 |
|
Blast Phase
|
|
0.070 |
GeneticVariation
|
BEFREE |
P-loop and T315I mutations were particularly frequent in advanced-phase chronic myeloid leukemia and Ph+ ALL patients, and often accompanied progression from chronic phase to accelerated phase/blast crisis.
|
17189410 |
2006 |
|
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 |
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 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Collectively, the present results suggest that in the treatment of leukemia, taxodione has potential as a compound with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.
|
29859988 |
2018 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
T315I mutation of BCR-ABL1 into human Philadelphia chromosome-positive leukemia cell lines by homologous recombination using the CRISPR/Cas9 system.
|
29967475 |
2018 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Antitumor Effects of Blocking Protein Neddylation in T315I-BCR-ABL Leukemia Cells and Leukemia Stem Cells.
|
29321163 |
2018 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
T315I mutation of BCR-ABL1 into human Philadelphia chromosome-positive leukemia cell lines by homologous recombination using the CRISPR/Cas9 system.
|
29967475 |
2018 |
|
Childhood Leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Collectively, the present results suggest that in the treatment of leukemia, taxodione has potential as a compound with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.
|
29859988 |
2018 |
|
leukemia
|
|
0.100 |
GeneticVariation
|
BEFREE |
Antitumor Effects of Blocking Protein Neddylation in T315I-BCR-ABL Leukemia Cells and Leukemia Stem Cells.
|
29321163 |
2018 |
|
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 |
|
Childhood 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 |