BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships - Wikidata - awgldk - TriplyDB

BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships

BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships

http://www.wikidata.org/entity/Q36542821

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Evolutionary dynamics of cancer in response to targeted combination therapy Targeting cancer with kinase inhibitors Resistant mutations in CML and Ph(+)ALL - role of ponatinib.Current developments in molecular monitoring in chronic myeloid leukemia Drug resistance missense mutations in cancer are subject to evolutionary constraints Interferon-α Revisited: Individualized Treatment Management Eased the Selective Pressure of Tyrosine Kinase Inhibitors on BCR-ABL1 Mutations Resulting in a Molecular Response in High-Risk CML Patients Imatinib binding to human c-Src is coupled to inter-domain allostery and suggests a novel kinase inhibition strategy A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias Haematological complete remission by ponatinib and bortezomib in a patient with relapsed, Ph⁺ pre-B acute lymphoblastic leukaemia.Clonal distribution of BCR-ABL1 mutations and splice isoforms by single-molecule long-read RNA sequencing.Patients with Philadelphia-positive leukemia with BCR-ABL kinase mutations before allogeneic transplantation predominantly relapse with the same mutation.cFinder: definition and quantification of multiple haplotypes in a mixed sample.Discovery of a small molecule targeting SET-PP2A interaction to overcome BCR-ABLT315I mutation of chronic myeloid leukemia.ABCB1 Overexpression Is a Key Initiator of Resistance to Tyrosine Kinase Inhibitors in CML Cell Lines A coiled-coil mimetic intercepts BCR-ABL1 dimerization in native and kinase-mutant chronic myeloid leukemia Novel oral transforming growth factor-β signaling inhibitor EW-7197 eradicates CML-initiating cells.Quantitative Analysis of Mutant Subclones in Chronic Myeloid Leukemia: Comparison of Different Methodological Approaches.European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013.Acute lymphoblastic leukemia in pregnancy: a case report with literature review BCR-ABL1 kinase domain mutations may persist at very low levels for many years and lead to subsequent TKI resistance Targeting methyltransferase PRMT5 eliminates leukemia stem cells in chronic myelogenous leukemia.Exploiting Temporal Collateral Sensitivity in Tumor Clonal Evolution.Molecular dynamics reveal BCR-ABL1 polymutants as a unique mechanism of resistance to PAN-BCR-ABL1 kinase inhibitor therapy.Molecular techniques for the personalised management of patients with chronic myeloid leukaemia.Novel multiple tyrosine kinase inhibitor ponatinib inhibits bFGF-activated signaling in neuroblastoma cells and suppresses neuroblastoma growth in vivo.Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia.Chronic myeloid leukemia: overview of new agents and comparative analysis.Ever-advancing chronic myeloid leukemia treatment.Definition and treatment of resistance to tyrosine kinase inhibitors in chronic myeloid leukemia.Outcomes of chronic-phase chronic myeloid leukemia beyond first-line therapy.Individualizing kinase-targeted cancer therapy: the paradigm of chronic myeloid leukemia.Do we need more drugs for chronic myeloid leukemia?Chronic myeloid leukemia: advances in understanding disease biology and mechanisms of resistance to tyrosine kinase inhibitors.A review of the European LeukemiaNet recommendations for the management of CML.Computational analysis of ABL kinase mutations allows predicting drug sensitivity against selective kinase inhibitors.Chronic Myeloid Leukemia in the Era of Tyrosine Kinase Inhibitors: An Evolving Paradigm of Molecularly Targeted Therapy.Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.Deep molecular response by IFN-α and dasatinib combination in a patient with T315I-mutated chronic myeloid leukemia.Efficacy of the dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with nilotinib against BCR-ABL-positive leukemia cells involves the ABL kinase domain mutation The Role of Early Molecular Response in the Management of Chronic Phase CML.

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BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships

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BCR-ABL1 compound mutations in ...... uency and clonal relationships

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Alistair G Reid

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Anthony D Pomicter

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Christopher A Eide

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Clinton C Mason

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David J Anderson

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David Marin

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Ira L Kraft

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Jamshid S Khorashad

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Johanna C Estrada

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Lauren T Adrian

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P2860

AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance

Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency

The cancer genome

Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia

Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification

Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study.

Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance.

Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia.

Identifying cancer driver genes in tumor genome sequencing studies.

Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia.

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Brian J. Druker

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233881305

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