Long-Term ERK Inhibition in KRAS-Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression. - Test2 - elhamkhani - TriplyDB

Long-Term ERK Inhibition in KRAS-Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression.

Long-Term ERK Inhibition in KRAS-Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression.

http://www.wikidata.org/entity/Q27853310

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KRAS Mutant Pancreatic Cancer: No Lone Path to an Effective Treatment CIViC database KRAS-dependent suppression of MYC enhances the sensitivity of cancer cells to cytotoxic agents.MYC Deregulation in Primary Human Cancers.Interaction of tRNA with MEK2 in pancreatic cancer cells Periostin promotes tumor angiogenesis in pancreatic cancer via Erk/VEGF signaling Oncogenic KRAS-associated gene signature defines co-targeting of CDK4/6 and MEK as a viable therapeutic strategy in colorectal cancer.The G protein-coupled receptor GPR31 promotes membrane association of KRAS.Targeting ERK enhances the cytotoxic effect of the novel PI3K and mTOR dual inhibitor VS-5584 in preclinical models of pancreatic cancer ERK/MAPK Signaling Drives Overexpression of the Rac-GEF, PREX1, in BRAF- and NRAS-Mutant Melanoma.Protein Kinase CK2α Maintains Extracellular Signal-regulated Kinase (ERK) Activity in a CK2α Kinase-independent Manner to Promote Resistance to Inhibitors of RAF and MEK but Not ERK in BRAF Mutant Melanoma The Atypical Kinase RIOK1 Promotes Tumor Growth and Invasive Behavior.Enhanced dependency of KRAS-mutant colorectal cancer cells on RAD51-dependent homologous recombination repair identified from genetic interactions in Saccharomyces cerevisiae.Genetic alterations affecting GTPases and T-cell receptor signaling in peripheral T-cell lymphomas.Strategies for monitoring and combating resistance to combination kinase inhibitors for cancer therapy.Constitutive IRAK4 Activation Underlies Poor Prognosis and Chemoresistance in Pancreatic Ductal Adenocarcinoma.Signaling pathway profiling using reverse-phase protein array and its clinical applications.Non-canonical PI3K-Cdc42-Pak-Mek-Erk Signaling Promotes Immune-Complex-Induced Apoptosis in Human Neutrophils.A screen for inducers of bHLH activity identifies pitavastatin as a regulator of p21, Rb phosphorylation and E2F target gene expression in pancreatic cancer.Fructose-1,6-bisphosphatase Inhibits ERK Activation and Bypasses Gemcitabine Resistance in Pancreatic Cancer by Blocking IQGAP1-MAPK Interaction.Key roles of EMT for adaptive resistance to MEK inhibitor in KRAS mutant lung cancer.Inhibition of mTORC2 component RICTOR impairs tumor growth in pancreatic cancer models.Phosphorylation of the C-Raf N-region promotes Raf dimerization.Evaluation of the selectivity and sensitivity of isoform- and mutation-specific RAS antibodies.Cucurbitacin B and SCH772984 exhibit synergistic anti-pancreatic cancer activities by suppressing EGFR, PI3K/Akt/mTOR, STAT3 and ERK signaling.STK38L kinase ablation promotes loss of cell viability in a subset of KRAS-dependent pancreatic cancer cell lines.Nrf2 promotes mutant K-ras/p53-driven pancreatic carcinogenesis.A Molecular Cascade Modulates MAP1B and Confers Resistance to mTOR Inhibition in Human Glioblastoma.KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer.Oncogenic RAS-induced downregulation of ATG12 is required for survival of malignant intestinal epithelial cells.Synthetic Lethal Vulnerabilities in KRAS-Mutant Cancers.β-Catenin mRNA Silencing and MEK Inhibition Display Synergistic Efficacy in Preclinical Tumor Models.Deletion of sphingosine kinase 1 inhibits liver tumorigenesis in diethylnitrosamine-treated mice.Development of MK-8353, an orally administered ERK1/2 inhibitor, in patients with advanced solid tumors.Phosphoinositide 3-Kinase Signaling Pathway in Pancreatic Ductal Adenocarcinoma Progression, Pathogenesis, and Therapeutics.E47 Governs the MYC-CDKN1B/p27KIP1-RB Network to Growth Arrest PDA Cells Independent of CDKN2A/p16INK4A and Wild-Type p53.FBP1 loss contributes to BET inhibitors resistance by undermining c-Myc expression in pancreatic ductal adenocarcinoma Acquired resistance to BRAFi reverses senescence-like phenotype in mutant BRAF melanoma

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Long-Term ERK Inhibition in KRAS-Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression.

http://www.wikidata.org/entity/Q27853310

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2016 nî lūn-bûn

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2016 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2016年の論文

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

Mechanism of MEK inhibition determines efficacy in mutant KRAS- versus BRAF-driven cancers

Inhibition of PI3Kβ signaling with AZD8186 inhibits growth of PTEN-deficient breast and prostate tumors alone and in combination with docetaxel.

Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence

Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K

COT drives resistance to RAF inhibition through MAP kinase pathway reactivation

Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer

KRAS and YAP1 converge to regulate EMT and tumor survival

Protein microarrays: meeting analytical challenges for clinical applications.

Aging, cellular senescence, and cancer

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