Oncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutation
about
MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinibThe T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATPAnalysis of the tyrosine kinome in melanoma reveals recurrent mutations in ERBB4.Primary concomitant EGFR T790M mutation predicted worse prognosis in non-small cell lung cancer patientsTherapeutic value of EGFR inhibition in CRC and NSCLC: 15 years of clinical evidenceHereditary lung cancer syndrome targets never smokers with germline EGFR gene T790M mutationsDetection of mutations in EGFR in circulating lung-cancer cellsHierarchical modeling of activation mechanisms in the ABL and EGFR kinase domains: thermodynamic and mechanistic catalysts of kinase activation by cancer mutations.Osimertinib in patients with advanced epidermal growth factor receptor T790M mutation-positive non-small cell lung cancer: rationale, evidence and place in therapyAmplification of EGFR T790M causes resistance to an irreversible EGFR inhibitorOncogenic JAK1 and JAK2-activating mutations resistant to ATP-competitive inhibitors.Germ-line mutations in epidermal growth factor receptor (EGFR) are rare but may contribute to oncogenesis: a novel germ-line mutation in EGFR detected in a patient with lung adenocarcinoma.Targeted inhibition of kinases in cancer therapyComprehensive genomic characterization of cutaneous malignant melanoma cell lines derived from metastatic lesions by whole-exome sequencing and SNP array profilingRational, biologically based treatment of EGFR-mutant non-small-cell lung cancer.Isoliquiritigenin induces apoptosis and inhibits xenograft tumor growth of human lung cancer cells by targeting both wild type and L858R/T790M mutant EGFR.Precision medicine clinical trials: defining new treatment strategies.Mechanisms of resistance to EGFR TKIs and development of a new generation of drugs in non-small-cell lung cancer.New strategies in overcoming acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in lung cancer.The role of epidermal growth factor receptor tyrosine kinase inhibitors in the treatment of advanced stage non-small cell lung cancerHomoharringtonine induces apoptosis and inhibits STAT3 via IL-6/JAK1/STAT3 signal pathway in Gefitinib-resistant lung cancer cells.MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibitionConverting cancer therapies into cures: lessons from infectious diseasesCrosstalk with cancer-associated fibroblasts induces resistance of non-small cell lung cancer cells to epidermal growth factor receptor tyrosine kinase inhibition.Signaling networks assembled by oncogenic EGFR and c-Met.Optimization of dosing for EGFR-mutant non-small cell lung cancer with evolutionary cancer modeling.Optimizing response to gefitinib in the treatment of non-small-cell lung cancer.Cancer as a moving target: understanding the composition and rebound growth kinetics of recurrent tumors.Monitoring EGFR T790M with plasma DNA from lung cancer patients in a prospective observational study.EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors.Modeling oncogene addiction using RNA interference.Dual MET-EGFR combinatorial inhibition against T790M-EGFR-mediated erlotinib-resistant lung cancer.Acquired resistance to epidermal growth factor receptor kinase inhibitors associated with a novel T854A mutation in a patient with EGFR-mutant lung adenocarcinomaEmerging paradigms in the development of resistance to tyrosine kinase inhibitors in lung cancer.Dual targeting of EGFR can overcome a major drug resistance mutation in mouse models of EGFR mutant lung cancer.The emergence of T790M mutation in EGFR-mutant lung adenocarcinoma patients having a history of acquired resistance to EGFR-TKI: focus on rebiopsy timing and long-term existence of T790M.Analysis of progression-free survival of first-line tyrosine kinase inhibitors in patients with non-small cell lung cancer harboring leu858Arg or exon 19 deletions.Contribution of KRAS mutations and c.2369C > T (p.T790M) EGFR to acquired resistance to EGFR-TKIs in EGFR mutant NSCLC: a study on circulating tumor DNA.Recent understanding of the molecular mechanisms for the efficacy and resistance of EGF receptor-specific tyrosine kinase inhibitors in non-small cell lung cancer.Other signalization targets.
P2860
Q24646295-1860D3D9-B1D8-4F47-9ECF-F5436152F8F7Q24649549-7C207407-FC05-43FB-8BDF-97C00CD42F8BQ27851483-D0A7774A-D671-4966-82F9-074DB761D506Q27852993-557F03EF-B53F-46B5-A130-F8FB81EA7F97Q28071772-BE67DF30-D9A1-4EE5-9B97-B57697EA5A6CQ28384015-34EE5DA3-EAD6-4EFB-824E-D95FDF75EEFFQ29615033-20AFC3E9-B5D7-49EA-8C6F-D58EE16188AFQ30157152-11E44921-FD77-413F-9FAB-21C3EA0C36A2Q33757134-A837BE3E-F1F4-4CBE-9B56-3A66B33322B7Q33810574-BB416F06-46B1-45FD-9C48-011A06670B69Q33843072-6CE22207-BCD9-4F56-A4DC-E60F05B3FBF4Q33901617-CF124323-5E40-4B9E-B8FD-A6F281C4B236Q34683348-754FC63C-91F4-4B4E-A93F-7A8784BF7A66Q34737562-5BDD4FA8-78BC-4E2D-BD8A-C8B90CE79D14Q34773458-6BA13516-E42E-4D7A-AF69-12E64BBE4855Q34774462-60ED87B6-FAE9-4BED-9B2B-618D5135BA51Q34794577-80C89311-0C4E-48E1-BAA3-C3A0C928470FQ35043706-E1A10794-FD5C-434C-8BE4-5328B4A454B5Q35196345-544808C5-CF87-4C33-ADFE-FD18D80850C0Q35667688-537C3BA0-9A9F-4A4D-8AE6-4C6A2B61E7C5Q35844693-53BF25C3-4AF5-496F-8DE0-990AF0C2E522Q36265149-9D105B45-4FBE-4D5C-8B77-9829F2835012Q36301709-71E7D61E-A83E-4AEB-8922-66DCB8B34E9EQ36365503-CEB65EAB-FF0F-43E2-B68E-9F6E21020D63Q36392991-62D45426-3266-40F4-885E-1D9BB04B1254Q36406541-1B7D8816-B8FC-4364-B225-EE55021746F2Q36441490-F5899702-245B-4FA1-B46E-13AF588CAB55Q36595762-BD91FCD9-094A-4C7D-A034-F86660B9FC55Q36622073-6468C73F-EFF1-40D0-AEFD-9E483D8F66C8Q36687288-28109D5F-9D9F-4393-9D71-DAA2FCEFD01CQ36840172-FEF0D47C-1AD9-4A2B-90E8-38BD6C72EFE5Q36882696-848C3759-8496-4859-8BA1-AC74570FA424Q37000611-BA310E34-F477-47C1-BE09-C11D84E007F2Q37249366-F7177415-5999-4766-9468-616FA74CCC31Q37363050-3F766CED-83D9-48D6-97F6-B62EEC40CF7EQ37565381-2D625365-372C-4CF1-AB9F-2D3BE73E3EA9Q37702099-A3B4FC42-1134-4B72-A093-6285107696DBQ37706672-B8CF0824-5E5D-4583-A3B0-534158DD1723Q38023942-3D75A1A4-87B5-4F09-AC6C-C720E705B1C6Q38073157-68D0DD19-2F6F-444A-895A-D639101041FB
P2860
Oncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutation
description
2007 nî lūn-bûn
@nan
2007 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
Oncogenic activity of epiderma ...... T790M drug resistance mutation
@ast
Oncogenic activity of epiderma ...... T790M drug resistance mutation
@en
type
label
Oncogenic activity of epiderma ...... T790M drug resistance mutation
@ast
Oncogenic activity of epiderma ...... T790M drug resistance mutation
@en
prefLabel
Oncogenic activity of epiderma ...... T790M drug resistance mutation
@ast
Oncogenic activity of epiderma ...... T790M drug resistance mutation
@en
P2093
P2860
P1433
P1476
Oncogenic activity of epiderma ...... T790M drug resistance mutation
@en
P2093
Daniel A Haber
Daphne W Bell
Ianthe Bryant
Jeffrey Settleman
Lindsey Ulkus
Miguel N Rivera
Nadia Godin-Heymann
P2860
P304
P356
10.1158/0008-5472.CAN-06-4625
P407
P577
2007-08-01T00:00:00Z