Combined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo. - Test2 - elhamkhani - TriplyDB

Combined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo.

Combined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo.

http://www.wikidata.org/entity/Q27852093

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Phytochemicals for the Management of Melanoma Pathways and therapeutic targets in melanoma Beyond BRAF: where next for melanoma therapy?Activated Ras as a Therapeutic Target: Constraints on Directly Targeting Ras Isoforms and Wild-Type versus Mutated Proteins CIViC database Metformin and trametinib have synergistic effects on cell viability and tumor growth in NRAS mutant cancer.Mutant HRAS as novel target for MEK and mTOR inhibitors Primary cross-resistance to BRAFV600E-, MEK1/2- and PI3K/mTOR-specific inhibitors in BRAF-mutant melanoma cells counteracted by dual pathway blockade Targeting the mTOR Complex by Everolimus in NRAS Mutant Neuroblastoma.The phosphoinositide 3-kinase pathway and therapy resistance in cancer PI3K and cancer: lessons, challenges and opportunities Combination of the PI3K inhibitor ZSTK474 with a PSMA-targeted immunotoxin accelerates apoptosis and regression of prostate cancer MicroRNA-1301 inhibits proliferation of human glioma cells by directly targeting N-Ras.Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways Treatment of NRAS-mutated advanced or metastatic melanoma: rationale, current trials and evidence to date Molecular therapy for acute myeloid leukaemia.Molecular pathways: targeting NRAS in melanoma and acute myelogenous leukemia.Melanoma: clinical features and genomic insights.MiR-124 governs glioma growth and angiogenesis and enhances chemosensitivity by targeting R-Ras and N-Ras MiR-143 acts as a tumor suppressor by targeting N-RAS and enhances temozolomide-induced apoptosis in glioma.Mutant NRASQ61 shares signaling similarities across various cancer types--potential implications for future therapies.Genotyping of cutaneous melanoma.A preclinical orthotopic model for glioblastoma recapitulates key features of human tumors and demonstrates sensitivity to a combination of MEK and PI3K pathway inhibitors.Prenylation inhibition-induced cell death in melanoma: reduced sensitivity in BRAF mutant/PTEN wild-type melanoma cells RSK1 activation promotes invasion in nodular melanoma.Amuvatinib has cytotoxic effects against NRAS-mutant melanoma but not BRAF-mutant melanoma.SDF-1/CXCL12 induces directional cell migration and spontaneous metastasis via a CXCR4/Gαi/mTORC1 axis.Genetic events that limit the efficacy of MEK and RTK inhibitor therapies in a mouse model of KRAS-driven pancreatic cancer Empirical inference of circuitry and plasticity in a kinase signaling network Combined inhibition of MEK and mTOR has a synergic effect on angiosarcoma tumorgrafts Combined Inhibition of MEK and Plk1 Has Synergistic Antitumor Activity in NRAS Mutant Melanoma.Tumor-Targeted Synergistic Blockade of MAPK and PI3K from a Layer-by-Layer Nanoparticle.Melanoma Cell-Intrinsic PD-1 Receptor Functions Promote Tumor Growth.MIG6 Is MEK Regulated and Affects EGF-Induced Migration in Mutant NRAS Melanoma.miR-98 functions as a tumor suppressor in salivary adenoid cystic carcinomas Targeting mutant NRAS signaling pathways in melanoma.Acyl protein thioesterase 1 and 2 (APT-1, APT-2) inhibitors palmostatin B, ML348 and ML349 have different effects on NRAS mutant melanoma cells Rationale-based therapeutic combinations with PI3K inhibitors in cancer treatment Searching for the Chokehold of NRAS Mutant Melanoma.Combined targeting of mTOR and AKT is an effective strategy for basal-like breast cancer in patient-derived xenograft models.

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P2860

Combined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo.

http://www.wikidata.org/entity/Q27852093

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2013 nî lūn-bûn

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2013 թուականի Մարտին հրատարակուած գիտական յօդուած

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2013 թվականի մարտին հրատարակված գիտական հոդված

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Combined targeting of MEK and ...... melanoma in vitro and in vivo.

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Proceedings of the National Academy of Sciences of the United States of America

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Combined targeting of MEK and ...... melanoma in vitro and in vivo.

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Adil I Daud

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Anoosheh Ebaee

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Christian Posch

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Gary A Green

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Homayoun Moslehi

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Kim Chong

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Lily Peng

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Luzviminda Feeney

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Michelle T Dimon

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Philip E LeBoit

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P2860

Binding of ras to phosphoinositide 3-kinase p110alpha is required for ras-driven tumorigenesis in mice

Combined targeting of BRAF and CRAF or BRAF and PI3K effector pathways is required for efficacy in NRAS mutant tumors

Identification of 4-(2-(4-amino-1,2,5-oxadiazol-3-yl)-1-ethyl-7-{[(3S)-3-piperidinylmethyl]oxy}-1H-imidazo[4,5-c]pyridin-4-yl)-2-methyl-3-butyn-2-ol (GSK690693), a novel inhibitor of AKT kinase

Reversing melanoma cross-resistance to BRAF and MEK inhibitors by co-targeting the AKT/mTOR pathway.

Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF

BRAF mutation predicts sensitivity to MEK inhibition

Distinct sets of genetic alterations in melanoma

Hyperactive Ras in developmental disorders and cancer

Theoretical basis, experimental design, and computerized simulation of synergism and antagonism in drug combination studies

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

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