Combined targeting of BRAF and CRAF or BRAF and PI3K effector pathways is required for efficacy in NRAS mutant tumors
about
Early steps in primary cilium assembly require EHD1/EHD3-dependent ciliary vesicle formationAnalysis of the genome to personalize therapy for melanomaMEK inhibitors and their potential in the treatment of advanced melanoma: the advantages of combination therapyMultiple Molecular Pathways in Melanomagenesis: Characterization of Therapeutic TargetsBeyond BRAF: where next for melanoma therapy?New treatments for metastatic melanomaEmerging phytochemicals for prevention of melanoma invasionCombined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo.Metformin and trametinib have synergistic effects on cell viability and tumor growth in NRAS mutant cancer.Routine multiplex mutational profiling of melanomas enables enrollment in genotype-driven therapeutic trialsA melanoma molecular disease modelCombinatorial drug screening and molecular profiling reveal diverse mechanisms of intrinsic and adaptive resistance to BRAF inhibition in V600E BRAF mutant melanomas.DNA methylation epigenotype and clinical features of NRAS-mutation(+) colorectal cancerRAF proteins exert both specific and compensatory functions during tumour progression of NRAS-driven melanoma.Correlation of somatic mutations and clinical outcome in melanoma patients treated with Carboplatin, Paclitaxel, and sorafenibElectrochemotherapy as an adjunct or alternative to other treatments for unresectable or in-transit melanoma.Molecular pathways: targeting NRAS in melanoma and acute myelogenous leukemia.NRAS mutations are rare in colorectal cancer.Phosphatidylinositol 3-kinase: the oncoprotein.Mitogen-activated protein kinase (MAPK) hyperactivation and enhanced NRAS expression drive acquired vemurafenib resistance in V600E BRAF melanoma cells.Mutant NRASQ61 shares signaling similarities across various cancer types--potential implications for future therapies.Targeted therapy for melanoma: a primer.Receptor tyrosine kinase pathway analysis sheds light on similarities between clear-cell sarcoma and metastatic melanoma.Driver mutations in melanoma: lessons learned from bench-to-bedside studiesComprehensive genomic characterization of cutaneous malignant melanoma cell lines derived from metastatic lesions by whole-exome sequencing and SNP array profilingTumor suppressors miR-143 and miR-145 and predicted target proteins API5, ERK5, K-RAS, and IRS-1 are differentially expressed in proximal and distal colon.Antitumor activity in RAS-driven tumors by blocking AKT and MEK.Clinically relevant genes and regulatory pathways associated with NRASQ61 mutations in melanoma through an integrative genomics approach.Prognostic parameters for the primary care of melanoma patients: what is really risky in melanoma?The current state of targeted therapy in melanoma: this time it's personalCombined Inhibition of MEK and Plk1 Has Synergistic Antitumor Activity in NRAS Mutant Melanoma.Disruption of the protein interaction between FAK and IGF-1R inhibits melanoma tumor growth.Sensitivity to the MEK inhibitor E6201 in melanoma cells is associated with mutant BRAF and wildtype PTEN statusAcyl protein thioesterase 1 and 2 (APT-1, APT-2) inhibitors palmostatin B, ML348 and ML349 have different effects on NRAS mutant melanoma cellsInhibition of Wee1, AKT, and CDK4 underlies the efficacy of the HSP90 inhibitor XL888 in an in vivo model of NRAS-mutant melanoma.Searching for the Chokehold of NRAS Mutant Melanoma.Ras-mutant cancer cells display B-Raf binding to Ras that activates extracellular signal-regulated kinase and is inhibited by protein kinase A phosphorylation.Identifying genotype-dependent efficacy of single and combined PI3K- and MAPK-pathway inhibition in cancer.Oncogene abnormalities in a series of primary melanomas of the sinonasal tract: NRAS mutations and cyclin D1 amplification are more frequent than KIT or BRAF mutations.miR-143 and miR-145 are downregulated in ulcerative colitis: putative regulators of inflammation and protooncogenes.
P2860
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P2860
Combined targeting of BRAF and CRAF or BRAF and PI3K effector pathways is required for efficacy in NRAS mutant tumors
description
2009 nî lūn-bûn
@nan
2009 թուականին հրատարակուած գիտական յօդուած
@hyw
2009 թվականին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@ast
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@en
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@nl
type
label
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@ast
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@en
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@nl
prefLabel
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@ast
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@en
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@nl
P2093
P2860
P1433
P1476
Combined targeting of BRAF and ...... efficacy in NRAS mutant tumors
@en
P2093
Bijay S Jaiswal
David P Davis
James E Cupp
Klaus P Hoeflich
Noelyn M Kljavin
Somasekar Seshagiri
Vasantharajan Janakiraman
Yuxin Liang
P2860
P356
10.1371/JOURNAL.PONE.0005717
P407
P577
2009-01-01T00:00:00Z