A functional landscape of resistance to ALK inhibition in lung cancer. - Wikidata - awgldk - TriplyDB

A functional landscape of resistance to ALK inhibition in lung cancer.

A functional landscape of resistance to ALK inhibition in lung cancer.

http://www.wikidata.org/entity/Q35438912

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Crizotinib resistance: implications for therapeutic strategies Tyrosine Kinase Receptor Landscape in Lung Cancer: Therapeutical Implications Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine Oncogenic kinase fusions: an evolving arena with innovative clinical opportunities Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs Novel ALK inhibitor AZD3463 inhibits neuroblastoma growth by overcoming crizotinib resistance and inducing apoptosis.Narrowing the focus: a toolkit to systematically connect oncogenic signaling pathways with cancer phenotypes Discovering and understanding oncogenic gene fusions through data intensive computational approaches Genomic Aberrations in Crizotinib Resistant Lung Adenocarcinoma Samples Identified by Transcriptome Sequencing.Sensitivity Analysis of the NPM-ALK Signalling Network Reveals Important Pathways for Anaplastic Large Cell Lymphoma Combination Therapy.Original insights on thrombospondin-1-related antireceptor strategies in cancer.Detection of ALK fusion transcripts in FFPE lung cancer samples by NanoString technology RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK-positive lung cancer.Isothiocyanatostilbenes as novel c-Met inhibitors.Functional screening implicates miR-371-3p and peroxiredoxin 6 in reversible tolerance to cancer drugs.Evolution from genetics to phenotype: reinterpretation of NSCLC plasticity, heterogeneity, and drug resistance.Novel multiple tyrosine kinase inhibitor ponatinib inhibits bFGF-activated signaling in neuroblastoma cells and suppresses neuroblastoma growth in vivo.Novel Src/Abl tyrosine kinase inhibitor bosutinib suppresses neuroblastoma growth via inhibiting Src/Abl signaling.Akt Activation Mediates Acquired Resistance to Fibroblast Growth Factor Receptor Inhibitor BGJ398.Coupling an EML4-ALK-centric interactome with RNA interference identifies sensitizers to ALK inhibitors.Emergence of resistance to tyrosine kinase inhibitors in non-small-cell lung cancer can be delayed by an upfront combination with the HSP90 inhibitor onalespib.High-throughput Phenotyping of Lung Cancer Somatic Mutations Elucidation of Resistance Mechanisms to Second-Generation ALK Inhibitors Alectinib and Ceritinib in Non-Small Cell Lung Cancer Cells.EMT is associated with, but does not drive resistance to ALK inhibitors among EML4-ALK non-small cell lung cancer.Central nervous system involvement in ALK-rearranged NSCLC: promising strategies to overcome crizotinib resistance.Acquired Resistance to Clinical Cancer Therapy: A Twist in Physiological Signaling.Multifunctional roles of PKCδ: Opportunities for targeted therapy in human disease Extracellular purines, purinergic receptors and tumor growth.Monocarboxylate transporter 1 contributes to growth factor-induced tumor cell migration independent of transporter activity.Integrating functional genomics to accelerate mechanistic personalized medicine.New systemic strategies for overcoming resistance to targeted therapies in non-small cell lung cancer.Targeting ALK: Precision Medicine Takes on Drug Resistance.Anaplastic lymphoma kinase rearrangements in non-small-cell lung cancer: novel applications in diagnostics and treatment.Systematic Functional Characterization of Resistance to PI3K Inhibition in Breast Cancer.Update in Lung Cancer 2015.Anaplastic Lymphoma Kinase Is a Regulator of Alcohol Consumption and Excitatory Synaptic Plasticity in the Nucleus Accumbens Shell.KEAP1 loss modulates sensitivity to kinase targeted therapy in lung cancer.Integrating phosphoproteomics into the clinical management of prostate cancer Co-dependency of PKCδ and K-Ras: inverse association with cytotoxic drug sensitivity in KRAS mutant lung cancer.Data driven polypharmacological drug design for lung cancer: analyses for targeting ALK, MET, and EGFR.

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A functional landscape of resistance to ALK inhibition in lung cancer.

http://www.wikidata.org/entity/Q35438912

description

2015 nî lūn-bûn

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2015 թուականի Մարտին հրատարակուած գիտական յօդուած

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2015 թվականի մարտին 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年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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name

A functional landscape of resistance to ALK inhibition in lung cancer.

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A functional landscape of resistance to ALK inhibition in lung cancer.

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A functional landscape of resistance to ALK inhibition in lung cancer.

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A functional landscape of resistance to ALK inhibition in lung cancer.

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A functional landscape of resistance to ALK inhibition in lung cancer

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A functional landscape of resistance to ALK inhibition in lung cancer.

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A functional landscape of resistance to ALK inhibition in lung cancer.

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J.CCELL.2015.02.005

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A functional landscape of resistance to ALK inhibition in lung cancer.

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Cory M Johannessen

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David E Root

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Eliezer M Van Allen

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Federica Piccioni

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Frederick H Wilson

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Jeffrey A Engelman

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Jong Wook Kim

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Pablo Tamayo

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Steven M Corsello

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Tanaz Sharifnia

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P2860

MED12 controls the response to multiple cancer drugs through regulation of TGF-β receptor signaling

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

The participation of plasma membrane hemichannels to purinergic signaling

The ALK Inhibitor Ceritinib Overcomes Crizotinib Resistance in Non-Small Cell 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.

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.

EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors.

A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors.

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10.1016/J.CCELL.2015.02.005

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Jill P. Mesirov

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Levi A Garraway

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