Combination small molecule MEK and PI3K inhibition enhances uveal melanoma cell death in a mutant GNAQ- and GNA11-dependent manner. - Wikidata - wikimedia - TriplyDB

Combination small molecule MEK and PI3K inhibition enhances uveal melanoma cell death in a mutant GNAQ- and GNA11-dependent manner.

Combination small molecule MEK and PI3K inhibition enhances uveal melanoma cell death in a mutant GNAQ- and GNA11-dependent manner.

http://www.wikidata.org/entity/Q39325158

about

Upcoming translational challenges for uveal melanoma Trametinib: a MEK inhibitor for management of metastatic melanoma Pathways and therapeutic targets in melanoma Combined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo.Whole-genome sequencing reveals complex mechanisms of intrinsic resistance to BRAF inhibition.Effect of selumetinib vs chemotherapy on progression-free survival in uveal melanoma: a randomized clinical trial.BRD4-targeted therapy induces Myc-independent cytotoxicity in Gnaq/11-mutatant uveal melanoma cells.The genetics of uveal melanoma: current insights ARF6 Is an Actionable Node that Orchestrates Oncogenic GNAQ Signaling in Uveal Melanoma Uveal melanoma: epidemiology, etiology, and treatment of primary disease.Melanoma epidemiology, biology and prognosis.A molecular revolution in uveal melanoma: implications for patient care and targeted therapy Systematic genomic and translational efficiency studies of uveal melanoma.Understanding the biology of melanoma and therapeutic implications The phosphoinositide 3-kinase α selective inhibitor BYL719 enhances the effect of the protein kinase C inhibitor AEB071 in GNAQ/GNA11-mutant uveal melanoma cells.Mutant NRASQ61 shares signaling similarities across various cancer types--potential implications for future therapies.Current and emerging treatment options for uveal melanoma.Positron emission tomography and functional characterization of a complete PBR/TSPO knockout.Update on Molecular Pathology of Cutaneous Melanocytic Lesions: What is New in Diagnosis and Molecular Testing for Treatment?Biology of advanced uveal melanoma and next steps for clinical therapeutics.Simultaneous inhibition of the HGF/MET and Erk1/2 pathways affect uveal melanoma cell growth and migration.Subcellular distribution patterns and elevated expression of GNA11 and GNA14 proteins in the lungs of humans with pulmonary arterial hypertension.Combined PKC and MEK inhibition for treating metastatic uveal melanoma Paracrine Effect of NRG1 and HGF Drives Resistance to MEK Inhibitors in Metastatic Uveal Melanoma Therapeutic interventions to disrupt the protein synthetic machinery in melanoma Patient survival in uveal melanoma is not affected by oncogenic mutations in GNAQ and GNA11 GNAQ and BRAF mutations show differential activation of the mTOR pathway in human transformed cells.The mTOR inhibitor Everolimus synergizes with the PI3K inhibitor GDC0941 to enhance anti-tumor efficacy in uveal melanoma.WT1 shRNA delivery using transferrin-conjugated PEG liposomes in an in vivo model of melanoma.Targeting mechanisms of resistance to anti-EGF receptor therapy in KRAS wild-type colorectal cancer: the path to more personalized medicine.Melanoma mutagenesis and aberrant cell signaling.Latest developments in the biology and management of uveal melanoma.Non-BRAF targeted therapies for melanoma: protein kinase inhibitors in Phase II clinical trials.Towards combinatorial targeted therapy in melanoma: from pre-clinical evidence to clinical application (review).Profile of selumetinib and its potential in the treatment of melanoma.Primary melanocytic tumors of the central nervous system: a review with focus on molecular aspects.Toward precision medicine in glioblastoma: the promise and the challenges.Evolving systemic targeted therapy strategies in uveal melanoma and implications for ophthalmic management: a review.RasGRP3 Mediates MAPK Pathway Activation in GNAQ Mutant Uveal Melanoma.Co-targeting HGF/cMET Signaling with MEK Inhibitors in Metastatic Uveal Melanoma.

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Combination small molecule MEK and PI3K inhibition enhances uveal melanoma cell death in a mutant GNAQ- and GNA11-dependent manner.

http://www.wikidata.org/entity/Q39325158

description

2012 nî lūn-bûn

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

Combination small molecule MEK ...... Q- and GNA11-dependent manner.

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Combination small molecule MEK ...... Q- and GNA11-dependent manner.

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type

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Combination small molecule MEK ...... Q- and GNA11-dependent manner.

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Combination small molecule MEK ...... Q- and GNA11-dependent manner.

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prefLabel

Combination small molecule MEK ...... Q- and GNA11-dependent manner.

@en

Combination small molecule MEK ...... Q- and GNA11-dependent manner.

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1078-0432.CCR-11-3227

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Clinical Cancer Research

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Combination small molecule MEK ...... Q- and GNA11-dependent manner.

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Bita Esmaeli

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Brendan C Hayes

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Gregory Lizee

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Jahan S Khalili

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Ji Wang

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Michael A Davies

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Scott E Woodman

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Xiaoxing Yu

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P2860

Use of data-biased random walks on graphs for the retrieval of context-specific networks from genomic data

Mutations in GNA11 in uveal melanoma

Frequent somatic mutations of GNAQ in uveal melanoma and blue naevi

Discovery of GSK2126458, a Highly Potent Inhibitor of PI3K and the Mammalian Target of Rapamycin

Phase I pharmacokinetic and pharmacodynamic study of the oral, small-molecule mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancers

Effective use of PI3K and MEK inhibitors to treat mutant Kras G12D and PIK3CA H1047R murine lung cancers.

Galphaq expression activates EGFR and induces Akt mediated cardiomyocyte survival: dissociation from Galphaq mediated hypertrophy

Therapeutic implications of the emerging molecular biology of uveal melanoma.

Regulators of G-protein signaling and their Gα substrates: promises and challenges in their use as drug discovery targets.

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

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10.1158/1078-0432.CCR-11-3227

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16

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