Optimization of dosing for EGFR-mutant non-small cell lung cancer with evolutionary cancer modeling.
about
EGFR-mutant lung adenocarcinomas treated first-line with the novel EGFR inhibitor, XL647, can subsequently retain moderate sensitivity to erlotinibOncogenic kinase fusions: an evolving arena with innovative clinical opportunitiesMolecular testing guideline for selection of lung cancer patients for EGFR and ALK tyrosine kinase inhibitors: guideline from the College of American Pathologists, International Association for the Study of Lung Cancer, and Association for MolecularEGFR mutations as a prognostic and predictive marker in non-small-cell lung cancerManagement of acquired resistance to epidermal growth factor receptor kinase inhibitors in patients with advanced non-small cell lung cancerPersonalized cancer medicine: molecular diagnostics, predictive biomarkers, and drug resistanceCancer evolution: mathematical models and computational inferenceA high-content image-based method for quantitatively studying context-dependent cell population dynamicsMechanisms of resistance to crizotinib in patients with ALK gene rearranged non-small cell lung cancer.Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers.Discovery of a mutant-selective covalent inhibitor of EGFR that overcomes T790M-mediated resistance in NSCLC.The predictive role of pretreatment epidermal growth factor receptor T790M mutation on the progression-free survival of tyrosine-kinase inhibitor-treated non-small cell lung cancer patients: a meta-analysis.AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancerUnravelling signal escape through maintained EGFR activation in advanced non-small cell lung cancer (NSCLC): new treatment optionsALK and crizotinib: after the honeymoon…what else? Resistance mechanisms and new therapies to overcome itFitness conferred by BCR-ABL kinase domain mutations determines the risk of pre-existing resistance in chronic myeloid leukemiaNonheritable cellular variability accelerates the evolutionary processes of cancerGefitinib inhibits invasive phenotype and epithelial-mesenchymal transition in drug-resistant NSCLC cells with MET amplificationDose-Dependent Mutation Rates Determine Optimum Erlotinib Dosing Strategies for EGFR Mutant Non-Small Cell Lung Cancer PatientsLeveraging Hypoxia-Activated Prodrugs to Prevent Drug Resistance in Solid TumorsTargeting nucleophosmin 1 represents a rational strategy for radiation sensitization.Predicting disease progression from short biomarker series using expert advice algorithmEpidermal growth factor receptor (EGFR) mutations in lung cancer: preclinical and clinical data.Clinical outcome according to the level of preexisting epidermal growth factor receptor T790M mutation in patients with lung cancer harboring sensitive epidermal growth factor receptor mutations.Modeling Tumor Clonal Evolution for Drug Combinations DesignRational design of non-resistant targeted cancer therapiesRoutine genetic testing of lung cancer specimens derived from surgery, bronchoscopy and fluid aspiration by next generation sequencing.Meta-analysis of the impact of de novo and acquired EGFR T790M mutations on the prognosis of patients with non-small cell lung cancer receiving EGFR-TKIs.The quest to overcome resistance to EGFR-targeted therapies in cancer.Dynamic monitoring of EGFR mutations in circulating cell-free DNA for EGFR-mutant metastatic patients with lung cancer: Early detection of drug resistance and prognostic significanceEvolution of acquired resistance to anti-cancer therapy.Quantitative proteomics in lung cancer.Acquired resistance of EGFR-mutant lung adenocarcinomas to afatinib plus cetuximab is associated with activation of mTORC1.The level of serum carcinoembryonic antigen is a surrogate marker for the efficacy of EGFR-TKIs but is not an indication of acquired resistance to EGFR-TKIs in NSCLC patients with EGFR mutationsmReverse epithelial-mesenchymal transition contributes to the regain of drug sensitivity in tyrosine kinase inhibitor-resistant non-small cell lung cancer cells.Drug resistance to molecular targeted therapy and its consequences for treatment decisions in non-small-cell lung cancer.Intratumor heterogeneity alters most effective drugs in designed combinations.Evolutionary dynamics of carcinogenesis and why targeted therapy does not work.Efficacy analysis of tyrosine kinase inhibitors on rare non-small cell lung cancer patients harboring complex EGFR mutations
P2860
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P2860
Optimization of dosing for EGFR-mutant non-small cell lung cancer with evolutionary cancer modeling.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年学术文章
@wuu
2011年学术文章
@zh-cn
2011年学术文章
@zh-hans
2011年学术文章
@zh-my
2011年学术文章
@zh-sg
2011年學術文章
@yue
2011年學術文章
@zh
2011年學術文章
@zh-hant
name
Optimization of dosing for EGF ...... evolutionary cancer modeling.
@ast
Optimization of dosing for EGF ...... evolutionary cancer modeling.
@en
type
label
Optimization of dosing for EGF ...... evolutionary cancer modeling.
@ast
Optimization of dosing for EGF ...... evolutionary cancer modeling.
@en
prefLabel
Optimization of dosing for EGF ...... evolutionary cancer modeling.
@ast
Optimization of dosing for EGF ...... evolutionary cancer modeling.
@en
P2093
P2860
P50
P1476
Optimization of dosing for EGF ...... evolutionary cancer modeling.
@en
P2093
Agnes Viale
Akira Inoue
Franziska Michor
Geoffrey R Oxnard
Jasmine Foo
Katherine Hutchinson
Katherine R Amato
Maria Arcila
Martin L Sos
P2860
P304
P356
10.1126/SCITRANSLMED.3002356
P407
P577
2011-07-01T00:00:00Z