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

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

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

http://www.wikidata.org/entity/Q24681743

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ABL tyrosine kinases: evolution of function, regulation, and specificity Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemia Antitumour activity of MDV3100 in castration-resistant prostate cancer: a phase 1-2 study AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance New Developments in Chronic Myeloid Leukemia: Implications for Therapy Cancer Stem Cell Hierarchy in Glioblastoma Multiforme Morphogenetic fields in embryogenesis, regeneration, and cancer: non-local control of complex patterning Resistance to tyrosine kinase inhibition therapy for chronic myelogenous leukemia: a clinical perspective and emerging treatment options Conformational Control Inhibition of the BCR-ABL1 Tyrosine Kinase, Including the Gatekeeper T315I Mutant, by the Switch-Control Inhibitor DCC-2036 Structural and Spectroscopic Analysis of the Kinase Inhibitor Bosutinib and an Isomer of Bosutinib Binding to the Abl Tyrosine Kinase Domain Characteristics and outcome of chronic myeloid leukemia patients with F317L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors.Resistant mutations in CML and Ph(+)ALL - role of ponatinib.Structural insight into selectivity and resistance profiles of ROS1 tyrosine kinase inhibitors.Overcoming mutation-based resistance to antiandrogens with rational drug design Current developments in molecular monitoring in chronic myeloid leukemia Modeling of Chronic Myeloid Leukemia: An Overview of In Vivo Murine and Human Xenograft Models Secondary mutations as mediators of resistance to targeted therapy in leukemia Stochastic Tunneling of Two Mutations in a Population of Cancer Cells NMR reveals the allosteric opening and closing of Abelson tyrosine kinase by ATP-site and myristoyl pocket inhibitors.ABL fusion oncogene transformation and inhibitor sensitivity are mediated by the cellular regulator RIN1.Dasatinib or imatinib in newly diagnosed chronic-phase chronic myeloid leukemia: 2-year follow-up from a randomized phase 3 trial (DASISION).A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias The role of genetic diversity in cancer.Aurora kinase inhibitors--rising stars in cancer therapeutics?Toward the design of mutation-resistant enzyme inhibitors: further evaluation of the substrate envelope hypothesis.The mutator phenotype in cancer: molecular mechanisms and targeting strategies Targeting the cancer kinome through polypharmacology.Inhibition of mitotic kinase Aurora suppresses Akt-1 activation and induces apoptotic cell death in all-trans retinoid acid-resistant acute promyelocytic leukemia cells Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia.Addiction to multiple oncogenes can be exploited to prevent the emergence of therapeutic resistance.Overlooking evolution: a systematic analysis of cancer relapse and therapeutic resistance research.Results of allogeneic hematopoietic stem cell transplantation for chronic myelogenous leukemia patients who failed tyrosine kinase inhibitors after developing BCR-ABL1 kinase domain mutations.Practical management of patients with chronic myeloid leukemia who develop tyrosine kinase inhibitor-resistant BCR-ABL1 mutations.Cancer stem cell plasticity and tumor hierarchy.Progress in understanding melanoma propagation.Targeted inhibition of kinases in cancer therapy Endogenous Voltage Potentials and the Microenvironment: Bioelectric Signals that Reveal, Induce and Normalize Cancer.Monitoring response and resistance to treatment in chronic myeloid leukemia.Outcome of patients with chronic myeloid leukemia with multiple ABL1 kinase domain mutations receiving tyrosine kinase inhibitor therapy The novel Aurora A kinase inhibitor MLN8237 is active in resistant chronic myeloid leukaemia and significantly increases the efficacy of nilotinib

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

http://www.wikidata.org/entity/Q24681743

description

2007 nî lūn-bûn

@nan

2007 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

2007年の論文

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2007年論文

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2007年論文

@zh-hant

2007年論文

@zh-hk

2007年論文

@zh-mo

2007年論文

@zh-tw

2007年论文

@wuu

name

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@ast

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@en

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@nl

type

label

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@ast

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@en

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@nl

prefLabel

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@ast

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@en

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@nl

P1433

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P1433

Journal of Clinical Investigation

P1476

Sequential ABL kinase inhibito ...... with altered oncogenic potency

@en

P2093

Brian J Skaggs

http://www.w3.org/2001/XMLSchema#string

Charles L Sawyers

http://www.w3.org/2001/XMLSchema#string

John M Nicoll

http://www.w3.org/2001/XMLSchema#string

Neil P Shah

http://www.w3.org/2001/XMLSchema#string

Ronald L Paquette

http://www.w3.org/2001/XMLSchema#string

Susan Branford

http://www.w3.org/2001/XMLSchema#string

Timothy P Hughes

http://www.w3.org/2001/XMLSchema#string

P2860

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

Structural mechanism for STI-571 inhibition of abelson tyrosine kinase

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants

Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias

Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia

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

Overriding imatinib resistance with a novel ABL kinase inhibitor

Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases

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

P304

2562-9

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scholarly article

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2277092

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P356

10.1172/JCI30890

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P407

P433

9

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P478

117

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P577

2007-09-01T00:00:00Z

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P698

17710227

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P932

1940237

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