Vemurafenib resistance reprograms melanoma cells towards glutamine dependence. - Wikidata - awgldk - TriplyDB

Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

http://www.wikidata.org/entity/Q35814876

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Retinoblastoma tumor suppressor functions shared by stem cell and cancer cell strategies Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis Metabolic rewiring in melanoma Head and Neck Squamous Cell Carcinoma Metabolism Draws on Glutaminolysis, and Stemness Is Specifically Regulated by Glutaminolysis via Aldehyde Dehydrogenase From Krebs to clinic: glutamine metabolism to cancer therapy.Regulation of glucose uptake in lymphoma cell lines by c-MYC- and PI3K-dependent signaling pathways and impact of glycolytic pathways on cell viability.Attacking the supply wagons to starve cancer cells to death.Clinical development of cancer therapeutics that target metabolism.IKKβ promotes metabolic adaptation to glutamine deprivation via phosphorylation and inhibition of PFKFB3.Translation reprogramming is an evolutionarily conserved driver of phenotypic plasticity and therapeutic resistance in melanoma.Dependence On Glycolysis Sensitizes BRAF-mutated Melanomas For Increased Response To Targeted BRAF Inhibition.Tumor-associated mutant p53 promotes cancer cell survival upon glutamine deprivation through p21 induction.A tale of two glutaminases: homologous enzymes with distinct roles in tumorigenesis.Blockage of glutaminolysis enhances the sensitivity of ovarian cancer cells to PI3K/mTOR inhibition involvement of STAT3 signaling.Targeting growth hormone receptor in human melanoma cells attenuates tumor progression and epithelial mesenchymal transition via suppression of multiple oncogenic pathways.Melanoma Therapeutic Strategies that Select against Resistance by Exploiting MYC-Driven Evolutionary Convergence.Degradation of AMPK-α1 sensitizes BRAF inhibitor-resistant melanoma cells to arginine deprivation.Growth Hormone Receptor Knockdown Sensitizes Human Melanoma Cells to Chemotherapy by Attenuating Expression of ABC Drug Efflux Pumps.Targeting Glutamine Metabolism for Cancer Treatment.Structure-function analysis and therapeutic efficacy of antibodies to fungal melanin for melanoma radioimmunotherapy.Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanoma.Participation of xCT in melanoma cell proliferation in vitro and tumorigenesis in vivo

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Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

http://www.wikidata.org/entity/Q35814876

description

2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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2015年论文

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name

Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

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Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

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type

label

Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

@ast

Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

@en

prefLabel

Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

@ast

Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

@en

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S12967-015-0581-2

P1433

Journal of Translational Medicine

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Vemurafenib resistance reprograms melanoma cells towards glutamine dependence.

@en

P2093

Gatien Moriceau

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

Jenny E Hernandez-Davies

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

Jun Wu

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

Kimberly R Rosales

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

Mei Kong

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

Michael A Reid

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

Min Pan

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

Roger S Lo

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

Thai Q Tran

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

Xazmin H Lowman

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

P2860

Tunable-combinatorial mechanisms of acquired resistance limit the efficacy of BRAF/MEK cotargeting but result in melanoma drug addiction.

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

Safety and efficacy of vemurafenib in BRAF(V600E) and BRAF(V600K) mutation-positive melanoma (BRIM-3): extended follow-up of a phase 3, randomised, open-label study

Structural basis for the allosteric inhibitory mechanism of human kidney-type glutaminase (KGA) and its regulation by Raf-Mek-Erk signaling in cancer cell metabolism

Structural Basis for the Active Site Inhibition Mechanism of Human Kidney-Type Glutaminase (KGA)

Improved overall survival in melanoma with combined dabrafenib and trametinib.

Mutations of the BRAF gene in human cancer

Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B cells

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2015-07-03T00:00:00Z

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