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Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

http://www.wikidata.org/entity/Q33850665

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Beyond BRAF: where next for melanoma therapy?Advances in targeted proteomics and applications to biomedical research Combinatorial drug screening and molecular profiling reveal diverse mechanisms of intrinsic and adaptive resistance to BRAF inhibition in V600E BRAF mutant melanomas.Change or die: targeting adaptive signaling to kinase inhibition in cancer cells.Amuvatinib has cytotoxic effects against NRAS-mutant melanoma but not BRAF-mutant melanoma.Phosphoproteomic analysis of basal and therapy-induced adaptive signaling networks in BRAF and NRAS mutant melanoma.Evaluating kinase ATP uptake and tyrosine phosphorylation using multiplexed quantification of chemically labeled and post-translationally modified peptides.The broad-spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF-mutant melanoma cells in combination with other signaling pathway inhibitors.Quantitative Profiling of Protein Tyrosine Kinases in Human Cancer Cell Lines by Multiplexed Parallel Reaction Monitoring Assays Large-Scale Interlaboratory Study to Develop, Analytically Validate and Apply Highly Multiplexed, Quantitative Peptide Assays to Measure Cancer-Relevant Proteins in Plasma.Parsing interindividual drug variability: an emerging role for systems pharmacology.Proteomic Findings in Melanoma.A Timely Shift from Shotgun to Targeted Proteomics and How It Can Be Groundbreaking for Cancer Research.PDGFR-alpha inhibits melanoma growth via CXCL10/IP-10: a multi-omics approach.Adolescent and young adult patients with cancer: a milieu of unique features.ER stress-induced autophagy in melanoma.Proteomic profiling predicts drug response to novel targeted anticancer therapeutics.Emerging power of proteomics for delineation of intrinsic tumor subtypes and resistance mechanisms to anti-cancer therapies.Vertical inhibition of the MAPK pathway enhances therapeutic responses in NRAS-mutant melanoma.Inhibition of PI3K/Akt/mTOR signaling in PI3KR2-overexpressing colon cancer stem cells reduces tumor growth due to apoptosis.1-Benzyl-indole-3-carbinol is a highly potent new small molecule inhibitor of Wnt/β-catenin signaling in melanoma cells that coordinately inhibits cell proliferation and disrupts expression of microphthalmia-associated transcription factor isoform-M Intercellular Resistance to BRAF Inhibition Can Be Mediated by Extracellular Vesicle-Associated PDGFRβ.Comparison of Quantitative Mass Spectrometry Platforms for Monitoring Kinase ATP Probe Uptake in Lung Cancer.Proteomic interrogation of HSP90 and insights for medical research.The FLT3 and PDGFR inhibitor crenolanib is a substrate of the multidrug resistance protein ABCB1 but does not inhibit transport function at pharmacologically relevant concentrations.Acetylsalicylic Acid Governs the Effect of Sorafenib in RAS- Mutant Cancers.Targeting CDK2 overcomes melanoma resistance against BRAF and Hsp90 inhibitors.Combined BRAF and HSP90 Inhibition in Patients with Unresectable -Mutant Melanoma

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Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

http://www.wikidata.org/entity/Q33850665

description

2014 nî lūn-bûn

@nan

2014 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի ապրիլին հրատարակված գիտական հոդված

@hy

2014年の論文

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2014年論文

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2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

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name

Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

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Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

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type

label

Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

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Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

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prefLabel

Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

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Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

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MCP.M113.037424

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Molecular & Cellular Proteomics

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Evaluating melanoma drug response and therapeutic escape with quantitative proteomics

@en

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Amod Sarnaik

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

Elizabeth Wood

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

Geoffrey T Gibney

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

H Eirik Haarberg

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

Inna V Fedorenko

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

John M Koomen

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

Kim H T Paraiso

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

Vernon K Sondak

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

Vito W Rebecca

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

Yi Chen

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

P2860

Quantitative analysis of HSP90-client interactions reveals principles of substrate recognition

Relief of profound feedback inhibition of mitogenic signaling by RAF inhibitors attenuates their activity in BRAFV600E melanomas

Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation

Improved survival with vemurafenib in melanoma with BRAF V600E mutation

Absolute quantification of proteins and phosphoproteins from cell lysates by tandem MS

Pharmacodynamic effects and mechanisms of resistance to vemurafenib in patients with metastatic melanoma.

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

Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.

A genome-scale RNA interference screen implicates NF1 loss in resistance to RAF inhibition.

MEK162 for patients with advanced melanoma harbouring NRAS or Val600 BRAF mutations: a non-randomised, open-label phase 2 study.

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1844-1854

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10.1074/MCP.M113.037424

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7

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13

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Keiran S M Smalley

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2014-04-23T00:00:00Z

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24760959

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4083119

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