NF-κB-activating complex engaged in response to EGFR oncogene inhibition drives tumor cell survival and residual disease in lung cancer - Wikidata - awgldk - TriplyDB

NF-κB-activating complex engaged in response to EGFR oncogene inhibition drives tumor cell survival and residual disease in lung cancer

NF-κB-activating complex engaged in response to EGFR oncogene inhibition drives tumor cell survival and residual disease in lung cancer

http://www.wikidata.org/entity/Q28259999

about

Synthetic lethality in lung cancer and translation to clinical therapies Co-activation of STAT3 and YES-Associated Protein 1 (YAP1) Pathway in EGFR-Mutant NSCLC.Advances in molecular-based personalized non-small-cell lung cancer therapy: targeting epidermal growth factor receptor and mechanisms of resistance.Adaptive and Acquired Resistance to EGFR Inhibitors Converge on the MAPK Pathway.Resisting Resistance: Targeted Therapies in Lung Cancer.Preclinical efficacy of a RAF inhibitor that evades paradoxical MAPK pathway activation in protein kinase BRAF-mutant lung cancer.Genetic polymorphisms in TNIP1 increase the risk of gastric carcinoma.Inactivation of Capicua drives cancer metastasis A module of inflammatory cytokines defines resistance of colorectal cancer to EGFR inhibitors.Gallic acid inhibition of Src-Stat3 signaling overcomes acquired resistance to EGF receptor tyrosine kinase inhibitors in advanced non-small cell lung cancer.Liver X receptors agonist GW3965 re-sensitizes gefitinib-resistant human non-small cell lung cancer cell to gefitinib treatment by inhibiting NF-κB in vitro.Primary Double-Strike Therapy for Cancers to Overcome EGFR Kinase Inhibitor Resistance: Proposal from the Bench.The Emerging Role of Non-traditional Ubiquitination in Oncogenic Pathways.Exploiting Synthetic Lethality and Network Biology to Overcome EGFR Inhibitor Resistance in Lung Cancer.Epithelial NF-κB signaling promotes EGFR-driven lung carcinogenesis via macrophage recruitment.Marsdenia tenacissima extract overcomes Axl- and Met-mediated erlotinib and gefitinib cross-resistance in non-small cell lung cancer cells.Activation of signal transducer and activator of transcription 3 (STAT3) signaling in EGFR mutant non-small-cell lung cancer (NSCLC)A framework for understanding and targeting residual disease in oncogene-driven solid cancers.Neoadjuvant Oncogene-Targeted Therapy in Early Stage Non-Small-Cell Lung Cancer as a Strategy to Improve Clinical Outcome and Identify Early Mechanisms of Resistance Characterizing the last holdouts.Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers.Current Landscape of Targeted Therapy in Lung Cancer.A TNF-JNK-Axl-ERK signaling axis mediates primary resistance to EGFR inhibition in glioblastoma.Suberoylanilide Hydroxamic Acid, an Inhibitor of Histone Deacetylase, Induces Apoptosis in Rheumatoid Arthritis Fibroblast-Like Synoviocytes.Understanding and targeting resistance mechanisms in NSCLC.Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression.Phase I study of the combination of quinacrine and erlotinib in patients with locally advanced or metastatic non small cell lung cancer.Imaging PD-L1 Expression with ImmunoPET.Mechanisms of rapid cancer cell reprogramming initiated by targeted receptor tyrosine kinase inhibitors and inherent therapeutic vulnerabilities.Mechanisms of receptor tyrosine kinase activation in cancer.Negative regulators of cell death pathways in cancer: perspective on biomarkers and targeted therapies.Tumour heterogeneity and resistance to cancer therapies.Anti-Inflammatory Effects of Protein Kinase Inhibitor Pyrrol Derivate.TNF-driven adaptive response mediates resistance to EGFR inhibition in lung cancer.Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma.RNF25 promotes gefitinib resistance in EGFR-mutant NSCLC cells by inducing NF-κB-mediated ERK reactivation.Emerging application of genomics-guided therapeutics in personalized lung cancer treatment.Genomic Profiling on an Unselected Solid Tumor Population Reveals a Highly Mutated Wnt/β-Catenin Pathway Associated with Oncogenic EGFR Mutations.Genetic Alterations of TRAF Proteins in Human Cancers A Novel Role for the Interleukin-1 Receptor Axis in Resistance to Anti-EGFR Therapy

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NF-κB-activating complex engaged in response to EGFR oncogene inhibition drives tumor cell survival and residual disease in lung cancer

http://www.wikidata.org/entity/Q28259999

description

2015 nî lūn-bûn

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2015 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2015 թվականի ապրիլին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年论文

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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NF-κB-activating complex engag ...... esidual disease in lung cancer

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Collin M Blakely

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P2860

Differential expression analysis for sequence count data

An integrated encyclopedia of DNA elements in the human genome

Sphingosine-1-phosphate is a missing cofactor for the E3 ubiquitin ligase TRAF2

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

PKC phosphorylation of TRAF2 mediates IKKalpha/beta recruitment and K63-linked polyubiquitination

Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas

Target binding properties and cellular activity of afatinib (BIBW 2992), an irreversible ErbB family blocker

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

Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors

A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.

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