BRAF V600E disrupts AZD6244-induced abrogation of negative feedback pathways between extracellular signal-regulated kinase and Raf proteins.
about
The RAF inhibitor PLX4032 inhibits ERK signaling and tumor cell proliferation in a V600E BRAF-selective mannerOptimal management of metastatic melanoma: current strategies and future directionsMechanism of MEK inhibition determines efficacy in mutant KRAS- versus BRAF-driven cancersTargeting the RAS oncogene.Microvesicle removal of anticancer drugs contributes to drug resistance in human pancreatic cancer cellsCombination treatment with MEK and AKT inhibitors is more effective than each drug alone in human non-small cell lung cancer in vitro and in vivoActivity of sorafenib in recurrent ovarian cancer and primary peritoneal carcinomatosis: a gynecologic oncology group trial.A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression.Survey of phosphorylation near drug binding sites in the Protein Data Bank (PDB) and their effects.High level of AKT activity is associated with resistance to MEK inhibitor AZD6244 (ARRY-142886)NFAT5-mediated expression of S100A4 contributes to proliferation and migration of renal carcinoma cells.Identification of common predictive markers of in vitro response to the Mek inhibitor selumetinib (AZD6244; ARRY-142886) in human breast cancer and non-small cell lung cancer cell lines.Identification of unique MEK-dependent genes in GNAQ mutant uveal melanoma involved in cell growth, tumor cell invasion, and MEK resistance.Dual-specificity MAP kinase phosphatases (MKPs): shaping the outcome of MAP kinase signalling.Resistance to chemotherapy and molecularly targeted therapies: rationale for combination therapy in malignant melanomaThe dual RAF/MEK inhibitor CH5126766/RO5126766 may be a potential therapy for RAS-mutated tumor cells.Phase II, open-label, randomized trial of the MEK1/2 inhibitor selumetinib as monotherapy versus temozolomide in patients with advanced melanoma.Oncogenic Kras promotes chemotherapy-induced growth factor shedding via ADAM17PTEN: Multiple Functions in Human Malignant TumorsEvaluation of efficacy of a new MEK inhibitor, RO4987655, in human tumor xenografts by [(18)F] FDG-PET imaging combined with proteomic approaches.Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: rationale and importance to inhibiting these pathways in human health.Combined PKC and MEK inhibition in uveal melanoma with GNAQ and GNA11 mutations.Epidermal growth factor receptor inhibition in lung cancer: the evolving role of individualized therapyTargeting drivers of melanoma with synthetic small molecules and phytochemicals.MEK1/2 Inhibitors: Molecular Activity and Resistance Mechanisms.Sprouty 2: a novel attenuator of B-cell receptor and MAPK-Erk signaling in CLL.Growth-inhibitory and antiangiogenic activity of the MEK inhibitor PD0325901 in malignant melanoma with or without BRAF mutationsRole of B-Raf(V600E) in differentiated thyroid cancer and preclinical validation of compounds against B-Raf(V600E).Overcoming IGF1R/IR resistance through inhibition of MEK signaling in colorectal cancer models.Synchronous BRAF(V600E) and MEK inhibition leads to superior control of murine melanoma by limiting MEK inhibitor induced skin toxicity.Differential induction of apoptosis in HER2 and EGFR addicted cancers following PI3K inhibition.Preclinical activity of the rational combination of selumetinib (AZD6244) in combination with vorinostat in KRAS-mutant colorectal cancer models.Dual-specificity phosphatase 5 controls the localized inhibition, propagation, and transforming potential of ERK signaling.Prospects for personalized medicine with inhibitors targeting the RAS and PI3K pathways.Network quantification of EGFR signaling unveils potential for targeted combination therapy.Emerging MEK inhibitors.Targeted cancer therapies in the twenty-first century: lessons from imatinib.Targeting the mitogen-activated protein kinase pathway: physiological feedback and drug response.Autoregulation of kinase dephosphorylation by ATP binding in AGC protein kinases.Robustness of signal transduction pathways.
P2860
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P2860
BRAF V600E disrupts AZD6244-induced abrogation of negative feedback pathways between extracellular signal-regulated kinase and Raf proteins.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
BRAF V600E disrupts AZD6244-in ...... lated kinase and Raf proteins.
@en
BRAF V600E disrupts AZD6244-in ...... lated kinase and Raf proteins.
@nl
type
label
BRAF V600E disrupts AZD6244-in ...... lated kinase and Raf proteins.
@en
BRAF V600E disrupts AZD6244-in ...... lated kinase and Raf proteins.
@nl
prefLabel
BRAF V600E disrupts AZD6244-in ...... lated kinase and Raf proteins.
@en
BRAF V600E disrupts AZD6244-in ...... lated kinase and Raf proteins.
@nl
P2093
P1433
P1476
BRAF V600E disrupts AZD6244-in ...... lated kinase and Raf proteins.
@en
P2093
Alex A Adjei
Bret B Friday
Chunrong Yu
Grace K Dy
Liang Wang
Paul D Smith
Stephen N Thibodeau
P304
P356
10.1158/0008-5472.CAN-08-1430
P407
P577
2008-08-01T00:00:00Z