Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK. - Wikidata - wikimedia - TriplyDB

Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK.

Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK.

http://www.wikidata.org/entity/Q34938204

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P1343

ALK Signaling and Target Therapy in Anaplastic Large Cell Lymphoma Crystal structure of EML1 reveals the basis for Hsp90 dependence of oncogenic EML4-ALK by disruption of an atypical β-propeller domain ALK mutations confer differential oncogenic activation and sensitivity to ALK inhibition therapy in neuroblastoma Crizotinib: A comprehensive review Clinical use of crizotinib for the treatment of non-small cell lung cancer Crizotinib resistance: implications for therapeutic strategies The role of the ALK receptor in cancer biology Recent Advances in Targetable Therapeutics in Metastatic Non-Squamous NSCLC Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs ALK inhibitors in non-small cell lung cancer: the latest evidence and developments Molecular Pathology and Personalized Medicine: The Dawn of a New Era in Companion Diagnostics-Practical Considerations about Companion Diagnostics for Non-Small-Cell-Lung-Cancer Oncogene Overdose: Too Much of a Bad Thing for Oncogene-Addicted Cancer Cells ALK and ROS1 as targeted therapy paradigms and clinical implications to overcome crizotinib resistance Crizotinib as a personalized alternative for targeted anaplastic lymphoma kinase rearrangement in previously treated patients with non-small-cell lung cancer Ganetespib: research and clinical development Genomically driven precision medicine to improve outcomes in anaplastic thyroid cancer Predictive biomarkers in precision medicine and drug development against lung cancer Molecular testing in lung cancer in the era of precision medicine Combating acquired resistance to tyrosine kinase inhibitors in lung cancer Ligand-triggered resistance to molecular targeted drugs in lung cancer: roles of hepatocyte growth factor and epidermal growth factor receptor ligands ALK and ROS1 as a joint target for the treatment of lung cancer: a review Targeting EML4-ALK driven non-small cell lung cancer (NSCLC)Review of the current targeted therapies for non-small-cell lung cancer Targeted therapies in development for non-small cell lung cancer Acquired Resistance to Crizotinib from a Mutation in CD74 – ROS1 The ALK Inhibitor Ceritinib Overcomes Crizotinib Resistance in Non-Small Cell Lung Cancer Molecular pathology of lung cancer: key to personalized medicine.A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors.ALK mutations conferring differential resistance to structurally diverse ALK inhibitors.Crizotinib-resistant mutants of EML4-ALK identified through an accelerated mutagenesis screen.Differential inhibitor sensitivity of anaplastic lymphoma kinase variants found in neuroblastoma.Mechanisms of resistance to crizotinib in patients with ALK gene rearranged non-small cell lung cancer.Mechanisms of acquired crizotinib resistance in ALK-rearranged lung Cancers.Safety and activity of crizotinib for paediatric patients with refractory solid tumours or anaplastic large-cell lymphoma: a Children's Oncology Group phase 1 consortium study.Two novel ALK mutations mediate acquired resistance to the next-generation ALK inhibitor alectinib Brigatinib, an anaplastic lymphoma kinase inhibitor, abrogates activity and growth in ALK-positive neuroblastoma cells, Drosophila and mice.Focus on Alectinib and Competitor Compounds for Second-Line Therapy in ALK-Rearranged NSCLC ALK and crizotinib: after the honeymoon…what else? Resistance mechanisms and new therapies to overcome it Targeted Therapies in Non-Small Cell Lung Cancer-Beyond EGFR and ALK Inhibitors of the anaplastic lymphoma kinase

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P2860

Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK.

http://www.wikidata.org/entity/Q34938204

description

2011 nî lūn-bûn

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2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年學術文章

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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Therapeutic strategies to over ...... the fusion oncogene EML4-ALK.

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PNAS.1019559108

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Therapeutic strategies to over ...... g the fusion oncogene EML4-ALK

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A John Iafrate

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Alice T Shaw

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Cyril Benes

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Eugene Lifshits

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Jeffrey A Engelman

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Tahsin M Khan

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Victor M Rivera

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William C Shakespeare

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P2860

MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

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

Novel mutant-selective EGFR kinase inhibitors against EGFR T790M

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

Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.

Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors.

Activity of IPI-504, a novel heat-shock protein 90 inhibitor, in patients with molecularly defined non-small-cell lung cancer.

Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer.

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7535-7540

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scholarly article

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10.1073/PNAS.1019559108

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18

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108

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Ryohei Katayama

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2011-04-18T00:00:00Z

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51060261

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21502504

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3088626

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