Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition. - Wikidata - awgldk - TriplyDB

Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition.

Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition.

http://www.wikidata.org/entity/Q35146471

about

Resistant mechanisms to BRAF inhibitors in melanoma Targeting cancer with kinase inhibitors P-Rex1 cooperates with PDGFRβ to drive cellular migration in 3D microenvironments Concomitant BRAF and PI3K/mTOR blockade is required for effective treatment of BRAF(V600E) colorectal cancer.Impact of MET expression on outcome in BRAF(V600E/K) advanced melanoma.A novel AKT1 mutant amplifies an adaptive melanoma response to BRAF inhibition Effects of AKT inhibitor therapy in response and resistance to BRAF inhibition in melanoma.Non-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistance Primary cross-resistance to BRAFV600E-, MEK1/2- and PI3K/mTOR-specific inhibitors in BRAF-mutant melanoma cells counteracted by dual pathway blockade Negative feedback regulation of the ERK1/2 MAPK pathway Functional profiling of live melanoma samples using a novel automated platform From bench to bedside: lessons learned in translating preclinical studies in cancer drug development Strategies for modern biomarker and drug development in oncology.PDGFRα up-regulation mediated by sonic hedgehog pathway activation leads to BRAF inhibitor resistance in melanoma cells with BRAF mutation.Genome-scale transcriptional activation by an engineered CRISPR-Cas9 complex.Melanoma: clinical features and genomic insights.The HSP90 inhibitor XL888 overcomes BRAF inhibitor resistance mediated through diverse mechanisms BRAF-mutant melanoma: treatment approaches, resistance mechanisms, and diagnostic strategies.Inhibition of HSP90 by AT13387 delays the emergence of resistance to BRAF inhibitors and overcomes resistance to dual BRAF and MEK inhibition in melanoma models Angiotropism, pericytic mimicry and extravascular migratory metastasis in melanoma: an alternative to intravascular cancer dissemination.Overcoming resistance to BRAF inhibition in BRAF-mutated metastatic melanoma Epigenetic changes of EGFR have an important role in BRAF inhibitor-resistant cutaneous melanomas Therapeutic destruction of insulin receptor substrates for cancer treatment.The broad-spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF-mutant melanoma cells in combination with other signaling pathway inhibitors.Inhibitors of pan-PI3K Signaling Synergize with BRAF or MEK Inhibitors to Prevent BRAF-Mutant Melanoma Cell Growth.Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.Targeting mutant BRAF in melanoma: current status and future development of combination therapy strategies Complexity in the signaling network: insights from the use of targeted inhibitors in cancer therapy.Combinatorial therapies to overcome B-RAF inhibitor resistance in melanomas.Drosophila Cancer Models Identify Functional Differences between Ret Fusions.Downregulation of the Ubiquitin Ligase RNF125 Underlies Resistance of Melanoma Cells to BRAF Inhibitors via JAK1 Deregulation.Therapeutic interventions to disrupt the protein synthetic machinery in melanoma Resistance to BRAF inhibitors induces glutamine dependency in melanoma cells Melanoma whole-exome sequencing identifies (V600E)B-RAF amplification-mediated acquired B-RAF inhibitor resistance Overexpression of ATP-binding cassette transporter ABCG2 as a potential mechanism of acquired resistance to vemurafenib in BRAF(V600E) mutant cancer cells.Preexisting MEK1 exon 3 mutations in V600E/KBRAF melanomas do not confer resistance to BRAF inhibitors Pilot study on "pericytic mimicry" and potential embryonic/stem cell properties of angiotropic melanoma cells interacting with the abluminal vascular surface.Melanoma adapts to RAF/MEK inhibitors through FOXD3-mediated upregulation of ERBB3 MEK inhibition affects STAT3 signaling and invasion in human melanoma cell lines Polymer nanofiber-embedded microchips for detection, isolation, and molecular analysis of single circulating melanoma cells.

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Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition.

http://www.wikidata.org/entity/Q35146471

description

2011 nî lūn-bûn

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2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի օգոստոսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Combinatorial treatments that ...... ells to V600EB-RAF inhibition.

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Combinatorial treatments that ...... ells to V600EB-RAF inhibition.

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type

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Combinatorial treatments that ...... ells to V600EB-RAF inhibition.

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Combinatorial treatments that ...... ells to V600EB-RAF inhibition.

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Combinatorial treatments that ...... ells to V600EB-RAF inhibition.

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Combinatorial treatments that ...... ells to V600EB-RAF inhibition.

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Cancer Research

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Combinatorial treatments that ...... ells to V600EB-RAF inhibition.

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Antoni Ribas

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Hubing Shi

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Roger S Lo

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Xiangju Kong

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P2860

Activation of N-ras in a human melanoma cell line

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

Inhibition of Mutated, Activated BRAF in Metastatic Melanoma

Mutations of the BRAF gene in human cancer

Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K

COT drives resistance to RAF inhibition through MAP kinase pathway reactivation

Inhibition of mTORC1 leads to MAPK pathway activation through a PI3K-dependent feedback loop in human cancer

Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity

Multiple signaling pathways must be targeted to overcome drug resistance in cell lines derived from melanoma metastases.

4E-BP1 is a key effector of the oncogenic activation of the AKT and ERK signaling pathways that integrates their function in tumors.

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