Beneficial effects of combining nilotinib and imatinib in preclinical models of BCR-ABL+ leukemias. - Wikidata - awgldk - TriplyDB

Beneficial effects of combining nilotinib and imatinib in preclinical models of BCR-ABL+ leukemias.

Beneficial effects of combining nilotinib and imatinib in preclinical models of BCR-ABL+ leukemias.

http://www.wikidata.org/entity/Q35642790

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Sustained proliferation in cancer: Mechanisms and novel therapeutic targets Optimizing combination therapies with existing and future CML drugs Imatinib and nilotinib inhibit hematopoietic progenitor cell growth, but do not prevent adhesion, migration and engraftment of human cord blood CD34+ cells Dynamics and management of cytopenias associated with dasatinib therapy in patients with chronic myeloid leukemia in chronic phase after imatinib failure.Combination of low-dose imatinib plus nilotinib for the treatment of chronic-phase chronic myeloid leukaemia after imatinib failure.A phase I study of single-agent nilotinib or in combination with imatinib in patients with imatinib-resistant gastrointestinal stromal tumors.Nilotinib for the treatment of chronic myeloid leukemia: An evidence-based review Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors.Imatinib assay by high-performance liquid chromatography in tandem mass spectrometry with solid-phase extraction in human plasma.Development and targeted use of nilotinib in chronic myeloid leukemia.Monitoring response and resistance to treatment in chronic myeloid leukemia.ABC transporters in multi-drug resistance and ADME-Tox of small molecule tyrosine kinase inhibitors.An LC-MS/MS method for rapid and sensitive high-throughput simultaneous determination of various protein kinase inhibitors in human plasma.Potentiation of antileukemic therapies by the dual PI3K/PDK-1 inhibitor, BAG956: effects on BCR-ABL- and mutant FLT3-expressing cells.SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib.Targeted therapy in chronic myeloid leukemia.Clinical perspectives of concepts on neoplastic stem cells and stem cell-resistance in chronic myeloid leukemia.Nilotinib: a phenylamino-pyrimidine derivative with activity against BCR-ABL, KIT and PDGFR kinases.Interaction of nilotinib, dasatinib and bosutinib with ABCB1 and ABCG2: implications for altered anti-cancer effects and pharmacological properties Induction of apoptosis by directing oncogenic Bcr-Abl into the nucleus.Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.Nilotinib for the treatment of Philadelphia-chromosome-positive chronic myeloid leukemia.Refining targeted therapies in chronic myeloid leukemia: development and application of nilotinib, a step beyond imatinib.Tyrosine kinase inhibitors as modulators of ATP binding cassette multidrug transporters: substrates, chemosensitizers or inducers of acquired multidrug resistance?Nilotinib: a novel, selective tyrosine kinase inhibitor.Use of tyrosine kinase inhibitors for chronic myeloid leukemia: management of patients and practical applications for pharmacy practitioners.Tyrosine kinase inhibitor-induced hypothyroidism: incidence, etiology, and management.Combination therapy with nilotinib for drug-sensitive and drug-resistant BCR-ABL-positive leukemia and other malignancies.Suppression of programmed cell death 4 (PDCD4) protein expression by BCR-ABL-regulated engagement of the mTOR/p70 S6 kinase pathway.Nilotinib: evaluation and analysis of its role in chronic myeloid leukemia.Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia cells.Nilotinib for the treatment of chronic myeloid leukemia.Synergistic activity of the Src/Abl inhibitor bosutinib in combination with imatinib.Imatinib-resistant chronic myeloid leukemia (CML): Current concepts on pathogenesis and new emerging pharmacologic approaches.Nilotinib-mediated inhibition of ABCB1 increases intracellular concentration of dasatinib in CML cells: implications for combination TKI therapy.Tyrosine kinase inhibitors enhanced the efficacy of conventional chemotherapeutic agent in multidrug resistant cancer cells.Combining nilotinib and imatinib improves the outcome of imatinib-resistant blast phase CML.

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Beneficial effects of combining nilotinib and imatinib in preclinical models of BCR-ABL+ leukemias.

http://www.wikidata.org/entity/Q35642790

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Andrew L Kung

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Arghya Ray

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Daisy Moreno

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Doriano Fabbro

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Elizabeth Hall-Meyers

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Ellen Weisberg

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James D Griffin

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Jamie L DellaGatta

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Jingrui Jiang

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Juergen Mestan

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P2860

Structural mechanism for STI-571 inhibition of abelson tyrosine kinase

Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL

Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells

Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors

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

Overriding imatinib resistance with a novel ABL kinase inhibitor

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

A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias.

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

Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop

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