Vemurafenib potently induces endoplasmic reticulum stress-mediated apoptosis in BRAFV600E melanoma cells. - Wikidata - wikimedia - TriplyDB

Vemurafenib potently induces endoplasmic reticulum stress-mediated apoptosis in BRAFV600E melanoma cells.

Vemurafenib potently induces endoplasmic reticulum stress-mediated apoptosis in BRAFV600E melanoma cells.

http://www.wikidata.org/entity/Q36974839

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Melanoma and the Unfolded Protein Response Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics Endoplasmic reticulum stress-mediated pathways to both apoptosis and autophagy: Significance for melanoma treatment Activated Ras as a Therapeutic Target: Constraints on Directly Targeting Ras Isoforms and Wild-Type versus Mutated Proteins Data Mining Approaches for Genomic Biomarker Development: Applications Using Drug Screening Data from the Cancer Genome Project and the Cancer Cell Line Encyclopedia Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer Novel anti-melanoma treatment: focus on immunotherapy.Endoplasmic reticulum stress mediates the anti-inflammatory effect of ethyl pyruvate in endothelial cells UPR, autophagy, and mitochondria crosstalk underlies the ER stress response Synergistic anti-tumor activity and inhibition of angiogenesis by cotargeting of oncogenic and death receptor pathways in human melanoma A strategy to combine pathway-targeted low toxicity drugs in ovarian cancer Mitochondrial oxidative stress is the Achille's heel of melanoma cells resistant to Braf-mutant inhibitor.Mitochondrial oxidative phosphorylation controls cancer cell's life and death decisions upon exposure to MAPK inhibitors.Dangerous liaisons: flirtations between oncogenic BRAF and GRP78 in drug-resistant melanomas.2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glucoside protects murine hearts against ischemia/reperfusion injury by activating Notch1/Hes1 signaling and attenuating endoplasmic reticulum stress.Reducing Smad3/ATF4 was essential for Sirt1 inhibiting ER stress-induced apoptosis in mice brown adipose tissue BRAF inhibitors amplify the pro-apoptotic activity of MEK inhibitors by inducing ER stress in NRAS-mutant melanoma.Signal Sequence Receptor 2 is required for survival of human melanoma cells as part of an unfolded protein response to endoplasmic reticulum stress.BET and BRAF inhibitors act synergistically against BRAF-mutant melanoma.Cobimetinib Plus Vemurafenib: A Review in BRAF (V600) Mutation-Positive Unresectable or Metastatic Melanoma.Combined activity of temozolomide and the mTOR inhibitor temsirolimus in metastatic melanoma involves DKK1.Key regulators of apoptosis execution as biomarker candidates in melanoma Targeting the hallmarks of cancer with therapy-induced endoplasmic reticulum (ER) stress.Activation of endoplasmic reticulum stress is involved in the activity of icariin against human lung adenocarcinoma cells.The nuclear translocation of ERK1/2 as an anticancer target.Cytotoxic mechanisms of panduratin A on A375 melanoma cells: A quantitative and temporal proteomics analysis.FOXO3-mediated up-regulation of Bim contributes to rhein-induced cancer cell apoptosis.Targeting ER stress-induced autophagy overcomes BRAF inhibitor resistance in melanoma.The plasma membrane Ca2+ pump PMCA4b inhibits the migratory and metastatic activity of BRAF mutant melanoma cells.Role Played by Signalling Pathways in Overcoming BRAF Inhibitor Resistance in Melanoma.Endoplasmic reticulum stress signaling and chemotherapy resistance in solid cancers.Critical role of reactive oxygen species (ROS) for synergistic enhancement of apoptosis by vemurafenib and the potassium channel inhibitor TRAM-34 in melanoma cells.The unfolded protein response impacts melanoma progression by enhancing FGF expression and can be antagonized by a chemical chaperone.Impaired NK cell recognition of vemurafenib-treated melanoma cells is overcome by simultaneous application of histone deacetylase inhibitors.The natural product mensacarcin induces mitochondrial toxicity and apoptosis in melanoma cells.Novel BRAF mutation in melanoma: A case report.ATF4 Targets RET for Degradation and Is a Candidate Tumor Suppressor Gene in Medullary Thyroid Cancer.Proteostasis trumps YAP in colon cancer.Glucose metabolism and NRF2 coordinate the antioxidant response in melanoma resistant to MAPK inhibitors.BH3-only proteins: possible proapoptotic triggers for melanoma therapy.

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P2860

Vemurafenib potently induces endoplasmic reticulum stress-mediated apoptosis in BRAFV600E melanoma cells.

http://www.wikidata.org/entity/Q36974839

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Vemurafenib potently induces e ...... s in BRAFV600E melanoma cells.

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Birgit Schittek

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Christian Busch

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Claus Garbe

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Dagmar Kulms

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Daniela Beck

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Friedegund Meier

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Heike Niessner

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Juan Lucio Iovanna

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Jürgen Eberle

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P2860

Endoplasmic reticulum stress: cell life and death decisions.

Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib

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

Improved survival with vemurafenib in melanoma with BRAF V600E mutation

p8 inhibits the growth of human pancreatic cancer cells and its expression is induced through pathways involved in growth inhibition and repressed by factors promoting cell growth

Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.

Inhibition of Mutated, Activated BRAF in Metastatic Melanoma

Mutations of the BRAF gene in human cancer

The HMG-I/Y-related protein p8 binds to p300 and Pax2 trans-activation domain-interacting protein to regulate the trans-activation activity of the Pax2A and Pax2B transcription factors on the glucagon gene promoter

Cloning and expression of the rat p8 cDNA, a new gene activated in pancreas during the acute phase of pancreatitis, pancreatic development, and regeneration, and which promotes cellular growth

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260

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6

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Dirk Schadendorf

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endoplasmic reticulum

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