Source: ALL
Variant | Gene | Risk Allele | Score vda | Association Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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0.100 | GeneticVariation | BEFREE | Establishment of a new Philadelphia chromosome-positive acute lymphoblastic leukemia cell line (SK-9) with T315I mutation. | 20471447 | 2010 |
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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 |
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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 |