Response of BRAF-mutant melanoma to BRAF inhibition is mediated by a network of transcriptional regulators of glycolysis. - Wikidata - wikimedia - TriplyDB

Response of BRAF-mutant melanoma to BRAF inhibition is mediated by a network of transcriptional regulators of glycolysis.

Response of BRAF-mutant melanoma to BRAF inhibition is mediated by a network of transcriptional regulators of glycolysis.

http://www.wikidata.org/entity/Q33946905

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Targeting hypoxic response for cancer therapy Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis MYC, Metabolism, and Cancer Combination Therapies to Inhibit the RAF/MEK/ERK Pathway in Melanoma: We are not Done Yet Pathways and therapeutic targets in melanoma Mitogen-Inducible Gene-6 Mediates Feedback Inhibition from Mutated BRAF towards the Epidermal Growth Factor Receptor and Thereby Limits Malignant Transformation Combinatorial drug screening and molecular profiling reveal diverse mechanisms of intrinsic and adaptive resistance to BRAF inhibition in V600E BRAF mutant melanomas.In-depth genomic data analyses revealed complex transcriptional and epigenetic dysregulations of BRAFV600E in melanoma.Non-invasive metabolic imaging of brain tumours in the era of precision medicine.CVE: an R package for interactive variant prioritisation in precision oncology.Potential clinical implications of BRAF mutations in histiocytic proliferations.Phenotype switching in melanoma: implications for progression and therapy.Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume.Transketolase-like 1 ectopic expression is associated with DNA hypomethylation and induces the Warburg effect in melanoma cells.Feeling energetic? New strategies to prevent metabolic reprogramming in melanoma Comparison of the Lonidamine Potentiated Effect of Nitrogen Mustard Alkylating Agents on the Systemic Treatment of DB-1 Human Melanoma Xenografts in Mice Targeting mitochondrial complex I using BAY 87-2243 reduces melanoma tumor growth.BMI1 induces an invasive signature in melanoma that promotes metastasis and chemoresistance Resistance to BRAF inhibitors induces glutamine dependency in melanoma cells Targeting metabolic flexibility by simultaneously inhibiting respiratory complex I and lactate generation retards melanoma progression.Overcoming melanoma resistance to vemurafenib by targeting CCL2-induced miR-34a, miR-100 and miR-125b Correlation of BRAFV600E Mutation and Glucose Metabolism in Thyroid Cancer Patients: An ¹⁸F-FDG PET Study.Synergistic effects of ion transporter and MAP kinase pathway inhibitors in melanoma.A new mechanism of trastuzumab resistance in gastric cancer: MACC1 promotes the Warburg effect via activation of the PI3K/AKT signaling pathway RMEL3, a novel BRAFV600E-associated long noncoding RNA, is required for MAPK and PI3K signaling in melanoma.Activity-Based Proteomics Reveals Heterogeneous Kinome and ATP-Binding Proteome Responses to MEK Inhibition in KRAS Mutant Lung Cancer.VEGF blockade enhances the antitumor effect of BRAFV600E inhibition.Dependence On Glycolysis Sensitizes BRAF-mutated Melanomas For Increased Response To Targeted BRAF Inhibition.Oncogene-Selective Sensitivity to Synchronous Cell Death following Modulation of the Amino Acid Nutrient Cystine.Activity-Based Protein Profiling Shows Heterogeneous Signaling Adaptations to BRAF Inhibition.Emerging Approaches for Targeting Metabolic Vulnerabilities in Malignant Glioma.Phenformin Enhances the Efficacy of ERK Inhibition in NF1-Mutant Melanoma.The BRAF Inhibitor Vemurafenib Activates Mitochondrial Metabolism and Inhibits Hyperpolarized Pyruvate-Lactate Exchange in BRAF-Mutant Human Melanoma Cells.Glucose-independent Acetate Metabolism Promotes Melanoma Cell Survival and Tumor Growth.Hypoxia-Driven Mechanism of Vemurafenib Resistance in Melanoma MicroRNA 211 Functions as a Metabolic Switch in Human Melanoma Cells The transcription cofactor c-JUN mediates phenotype switching and BRAF inhibitor resistance in melanoma.Targeted agents and immunotherapies: optimizing outcomes in melanoma.

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Response of BRAF-mutant melanoma to BRAF inhibition is mediated by a network of transcriptional regulators of glycolysis.

http://www.wikidata.org/entity/Q33946905

description

2014 nî lūn-bûn

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2014 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2014 թվականի հունվարին հրատարակված գիտական հոդված

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2014年の論文

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Response of BRAF-mutant melano ...... onal regulators of glycolysis.

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Cancer Discovery

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Antoni Ribas

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Willy Hugo

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P2860

Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma

Understanding the Warburg effect: the metabolic requirements of cell proliferation

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

Improved survival with vemurafenib in melanoma with BRAF V600E mutation

Combined BRAF and MEK inhibition in melanoma with BRAF V600 mutations

Glucose deprivation contributes to the development of KRAS pathway mutations in tumor cells

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

Inhibition of Mutated, Activated BRAF in Metastatic Melanoma

Mutations of the BRAF gene in human cancer

Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre, open-label, phase 3 randomised controlled trial

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