scholarly journals Comparable rate of EGFR kinase domain mutation in lung adenocarcinomas from Chinese male and female never-smokers

2010 ◽  
Vol 31 (5) ◽  
pp. 647-648 ◽  
Author(s):  
Yi-hua Sun ◽  
Rong Fang ◽  
Bin Gao ◽  
Xiang-kun Han ◽  
Jun-hua Zhang ◽  
...  
Keyword(s):  
Kinase Domain ◽  
Comparable Rate ◽  
Male And Female ◽  
Kinase Domain Mutation ◽  
Never Smokers ◽  
Lung Adenocarcinomas ◽  
Chinese Male ◽  
Egfr Kinase

scholarly journals EGFR kinase domain mutation positive lung cancers are sensitive to intrapleural perfusion with hyperthermic chemotherapy (IPHC) complete treatment

Oncotarget ◽  
2015 ◽  
Vol 7 (3) ◽  
pp. 3367-3378 ◽  
Author(s):  
Hongjuan Zhang ◽  
Cheng Zhan ◽  
Ji Ke ◽  
Zhiqiang Xue ◽  
Aiqun Zhang ◽  
...  
Keyword(s):  
Kinase Domain ◽  
Lung Cancers ◽  
Hyperthermic Chemotherapy ◽  
Complete Treatment ◽  
Kinase Domain Mutation ◽  
Egfr Kinase

scholarly journals Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas

2007 ◽  
Vol 117 (12) ◽  
pp. 3846-3856 ◽  
Author(s):  
Sizhi Paul Gao ◽  
Kevin G. Mark ◽  
Kenneth Leslie ◽  
William Pao ◽  
Noriko Motoi ◽  
...  
Keyword(s):  
Human Lung ◽  
Kinase Domain ◽  
Lung Adenocarcinomas ◽  
Egfr Kinase

scholarly journals Mutational Analysis of EGFR and Related Signaling Pathway Genes in Lung Adenocarcinomas Identifies a Novel Somatic Kinase Domain Mutation in FGFR4

PLoS ONE ◽  
2007 ◽  
Vol 2 (5) ◽  
pp. e426 ◽  
Author(s):  
Jenifer L. Marks ◽  
Michael D. McLellan ◽  
Maureen F. Zakowski ◽  
Alex E. Lash ◽  
Yumi Kasai ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mutational Analysis ◽  
Kinase Domain ◽  
Kinase Domain Mutation ◽  
Lung Adenocarcinomas

scholarly journals Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain

PLoS Medicine ◽  
2005 ◽  
Vol 2 (3) ◽  
pp. e73 ◽  
Author(s):  
William Pao ◽  
Vincent A Miller ◽  
Katerina A Politi ◽  
Gregory J Riely ◽  
Romel Somwar ◽  
...  
Keyword(s):  
Acquired Resistance ◽  
Kinase Domain ◽  
Lung Adenocarcinomas ◽  
Egfr Kinase

scholarly journals Absence of theERBB2 kinase domain mutation in lung adenocarcinomas in Korean patients

2005 ◽  
Vol 116 (4) ◽  
pp. 652-653 ◽  
Author(s):  
Jong Woo Lee ◽  
Young Hwa Soung ◽  
Su Young Kim ◽  
Won Sang Park ◽  
Suk Woo Nam ◽  
...  
Keyword(s):  
Kinase Domain ◽  
Korean Patients ◽  
Kinase Domain Mutation ◽  
Lung Adenocarcinomas

scholarly journals Structure–function analysis of oncogenic EGFR Kinase Domain Duplication reveals insights into activation and a potential approach for therapeutic targeting

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhenfang Du ◽  
Benjamin P. Brown ◽  
Soyeon Kim ◽  
Donna Ferguson ◽  
Dean C. Pavlick ◽  
...  
Keyword(s):  
Tandem Duplication ◽  
Function Analysis ◽  
Treatment Strategies ◽  
Kinase Domain ◽  
Time Resolved ◽  
Egfr Activation ◽  
Domain Duplication ◽  
Activation Mechanisms ◽  
Potential Therapeutic Intervention ◽  
Egfr Kinase

AbstractMechanistic understanding of oncogenic variants facilitates the development and optimization of treatment strategies. We recently identified in-frame, tandem duplication of EGFR exons 18 - 25, which causes EGFR Kinase Domain Duplication (EGFR-KDD). Here, we characterize the prevalence of ERBB family KDDs across multiple human cancers and evaluate the functional biochemistry of EGFR-KDD as it relates to pathogenesis and potential therapeutic intervention. We provide computational and experimental evidence that EGFR-KDD functions by forming asymmetric EGF-independent intra-molecular and EGF-dependent inter-molecular dimers. Time-resolved fluorescence microscopy and co-immunoprecipitation reveals EGFR-KDD can form ligand-dependent inter-molecular homo- and hetero-dimers/multimers. Furthermore, we show that inhibition of EGFR-KDD activity is maximally achieved by blocking both intra- and inter-molecular dimerization. Collectively, our findings define a previously unrecognized model of EGFR dimerization, providing important insights for the understanding of EGFR activation mechanisms and informing personalized treatment of patients with tumors harboring EGFR-KDD. Finally, we establish ERBB KDDs as recurrent oncogenic events in multiple cancers.

scholarly journals Lung Adenocarcinoma From East Asian Never-Smokers Is a Disease Largely Defined by Targetable Oncogenic Mutant Kinases

2010 ◽  
Vol 28 (30) ◽  
pp. 4616-4620 ◽  
Author(s):  
Yihua Sun ◽  
Yan Ren ◽  
Zhaoyuan Fang ◽  
Chenguang Li ◽  
Rong Fang ◽  
...  
Keyword(s):  
East Asian ◽  
Egfr Mutations ◽  
Driver Mutations ◽  
Single Institution ◽  
Pik3ca Mutations ◽  
Oncogenic Mutations ◽  
Oncogenic Driver ◽  
Never Smokers ◽  
Lung Adenocarcinomas ◽  
Concurrent Analysis

Purpose To determine the proportion of lung adenocarcinomas from East Asian never-smokers who harbor known oncogenic driver mutations. Patients and Methods In this surgical series, 52 resected lung adenocarcinomas from never-smokers (< 100 cigarettes in a lifetime) at a single institution (Fudan University, Shanghai, China) were analyzed concurrently for mutations in EGFR, KRAS, NRAS, HRAS, HER2, BRAF, ALK, PIK3CA, TP53 and LKB1. Results Forty-one tumors harbored EGFR mutations, three harbored EML4-ALK fusions, two harbored HER2 insertions, and one harbored a KRAS mutation. All mutations were mutually exclusive. Thus, 90% (47 of 52; 95% CI, 0.7896 to 0.9625) of lung adenocarcinomas from never-smokers were found to harbor well-known oncogenic mutations in just four genes. No BRAF, NRAS, HRAS, or LKB1 mutations were detected, while 15 had TP53 mutations. Four tumors contained PIK3CA mutations, always together with EGFR mutations. Conclusion To our knowledge, this study represents the first comprehensive and concurrent analysis of major recurrent oncogenic mutations found in a large cohort of lung adenocarcinomas from East Asian never-smokers. Since drugs are now available that target mutant EGFR, HER2, and ALK, respectively, this result indicates that prospective mutation testing in these patients should successfully assign a targeted therapy in the majority of cases.

Sign in / Sign up

Export Citation Format

Share Document