MEK1/2 inhibition elicits regression of autochthonous lung tumors induced by KRASG12D or BRAFV600E.
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Targeted therapies in development for non-small cell lung cancerTargeting RAF kinases for cancer therapy: BRAF-mutated melanoma and beyondContext-Dependent Effects of Amplified MAPK Signaling during Lung Adenocarcinoma Initiation and Progression.Small RNA combination therapy for lung cancerTP53 Silencing Bypasses Growth Arrest of BRAFV600E-Induced Lung Tumor Cells in a Two-Switch Model of Lung Tumorigenesis.The cholesterol-binding protein NPC2 restrains recruitment of stromal macrophage-lineage cells to early-stage lung tumours.PIK3CA(H1047R) Accelerates and Enhances KRAS(G12D)-Driven Lung Tumorigenesis.RAS signaling and anti-RAS therapy: lessons learned from genetically engineered mouse models, human cancer cells, and patient-related studies.Inflammation and Hras signaling control epithelial-mesenchymal transition during skin tumor progression.Mutationally activated PIK3CA(H1047R) cooperates with BRAF(V600E) to promote lung cancer progression.Ras effector mutant expression suggest a negative regulator inhibits lung tumor formation.Activity-Based Proteomics Reveals Heterogeneous Kinome and ATP-Binding Proteome Responses to MEK Inhibition in KRAS Mutant Lung Cancer.Diminished WNT -> β-catenin -> c-MYC signaling is a barrier for malignant progression of BRAFV600E-induced lung tumorsMouse models for lung cancerThe diagnostic utility of TP53 and CDKN2A to distinguish ovarian high-grade serous carcinoma from low-grade serous ovarian tumors.Emerging protein kinase inhibitors for non-small cell lung cancer.Type III or allosteric kinase inhibitors for the treatment of non-small cell lung cancer.Moving from histological subtyping to molecular characterization: new treatment opportunities in advanced non-small-cell lung cancer.Molecular Proteomic Characterization of a Pediatric Medulloblastoma Xenograft.Molecular heterogeneity of non-small cell lung carcinoma patient-derived xenografts closely reflect their primary tumors.Differential involvement of gp130 signalling pathways in modulating tobacco carcinogen-induced lung tumourigenesis.A CDK4/6 inhibitor enhances cytotoxicity of paclitaxel in lung adenocarcinoma cells harboring mutant KRAS as well as wild-type KRAS.What makes oncogenes mutually exclusive?Oncogene-induced senescence underlies the mutual exclusive nature of oncogenic KRAS and BRAF.Oncogene-dependent control of miRNA biogenesis and metastatic progression in a model of undifferentiated pleomorphic sarcoma.Ras Signaling Regulates Stem Cells and Amelogenesis in the Mouse Incisor.p53 loss does not permit escape from BrafV600E-induced senescence in a mouse model of lung cancer.Dabrafenib in combination with trametinib in the treatment of patients with BRAF V600-positive advanced or metastatic non-small cell lung cancer: clinical evidence and experience.
P2860
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P2860
MEK1/2 inhibition elicits regression of autochthonous lung tumors induced by KRASG12D or BRAFV600E.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
MEK1/2 inhibition elicits regr ...... uced by KRASG12D or BRAFV600E.
@en
MEK1/2 inhibition elicits regr ...... uced by KRASG12D or BRAFV600E.
@nl
type
label
MEK1/2 inhibition elicits regr ...... uced by KRASG12D or BRAFV600E.
@en
MEK1/2 inhibition elicits regr ...... uced by KRASG12D or BRAFV600E.
@nl
prefLabel
MEK1/2 inhibition elicits regr ...... uced by KRASG12D or BRAFV600E.
@en
MEK1/2 inhibition elicits regr ...... uced by KRASG12D or BRAFV600E.
@nl
P2093
P2860
P1433
P1476
MEK1/2 inhibition elicits regr ...... uced by KRASG12D or BRAFV600E.
@en
P2093
Alejandro Sweet-Cordero
Christy L Trejo
Joseph Juan
Martin McMahon
P2860
P304
P356
10.1158/0008-5472.CAN-11-3649
P407
P577
2012-04-17T00:00:00Z