EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib
about
Recent advances of novel targeted therapy in non-small cell lung cancerProfiling critical cancer gene mutations in clinical tumor samplesKRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinibTranslatability scoring in drug development: eight case studiesLung cancer incidence in never smokersSingle-walled carbon nanotube-induced mitotic disruptionPotential pulmonary effects of engineered carbon nanotubes: in vitro genotoxic effectsDynamic profiling of the post-translational modifications and interaction partners of epidermal growth factor receptor signaling after stimulation by epidermal growth factor using Extended Range Proteomic Analysis (ERPA)Lyn, a Src family kinase, regulates activation of epidermal growth factor receptors in lung adenocarcinoma cellsPerturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanismsEpithelial membrane protein-1 is a biomarker of gefitinib resistance.Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752Epidemiology of lung cancerIntratumoral epiregulin is a marker of advanced disease in non-small cell lung cancer patients and confers invasive properties on EGFR-mutant cellsEGFR-mutant lung adenocarcinomas treated first-line with the novel EGFR inhibitor, XL647, can subsequently retain moderate sensitivity to erlotinibMolecular biology of lung cancer: clinical implicationsMolecular epidemiology of EGFR and KRAS mutations in 3,026 lung adenocarcinomas: higher susceptibility of women to smoking-related KRAS-mutant cancersRetroviral oncogenes: a historical primerEnhancing diagnosis, prognosis, and therapeutic outcome prediction of gliomas using genomicsImpact of epidermal growth factor receptor and KRAS mutations on clinical outcomes in previously untreated non-small cell lung cancer patients: results of an online tumor registry of clinical trialsLung cancer: epidemiology, etiology, and preventionCirculating tumor cells: approaches to isolation and characterizationPhosphorylated epidermal growth factor receptor on tumor-associated endothelial cells is a primary target for therapy with tyrosine kinase inhibitorsMET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinibSomatic mutations affect key pathways in lung adenocarcinomaSomatic mutations of the epidermal growth factor receptor and non-small-cell lung cancerThe T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATPBIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer modelsEGFR targeted therapy in non-small cell lung cancer: potential role of cetuximabEpidermal growth factor receptor tyrosine kinase inhibitors for the treatment of non-small-cell lung cancer: results and open issuesMutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomasErbB receptors: from oncogenes to targeted cancer therapiesMucinous differentiation correlates with absence of EGFR mutation and presence of KRAS mutation in lung adenocarcinomas with bronchioloalveolar featuresAcquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domainEGFR inhibition in non-small cell lung cancer: resistance, once again, rears its ugly headGene mutations in lung cancer: promising predictive factors for the success of molecular therapyOncogenic transformation by inhibitor-sensitive and -resistant EGFR mutantsWhen clinical trials are compromised: a perspective from a patient advocateAcquired gefitinib-resistant mutation of EGFR in a chemonaive lung adenocarcinoma harboring gefitinib-sensitive mutation L858RMetaplastic breast carcinomas exhibit EGFR, but not HER2, gene amplification and overexpression: immunohistochemical and chromogenic in situ hybridization analysis.
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P2860
EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib
description
2004 nî lūn-bûn
@nan
2004 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2004年の論文
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2004年学术文章
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2004年学术文章
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2004年学术文章
@zh-hans
2004年学术文章
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2004年学术文章
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2004年學術文章
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name
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@ast
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@en
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@nl
type
label
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@ast
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@en
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@nl
prefLabel
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@ast
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@en
EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@nl
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EGF receptor gene mutations ar ...... ors to gefitinib and erlotinib
@en
P2093
Bhuvanesh Singh
Doris Kupfer
Inderpal Sarkaria
Jennifer Doherty
Maureen Zakowski
Richard Wilson
Robert Heelan
Vincent Miller
P2860
P304
P3181
P356
10.1073/PNAS.0405220101
P407
P577
2004-09-07T00:00:00Z