rdf:type |
|
lifeskim:mentions |
umls-concept:C0024109,
umls-concept:C0026882,
umls-concept:C0031727,
umls-concept:C0036667,
umls-concept:C0086418,
umls-concept:C0087111,
umls-concept:C0312418,
umls-concept:C1326912,
umls-concept:C1414313,
umls-concept:C1514562,
umls-concept:C1515655,
umls-concept:C1880389,
umls-concept:C1883204,
umls-concept:C1883221
|
pubmed:issue |
6
|
pubmed:dateCreated |
2006-6-12
|
pubmed:abstractText |
To understand the role of human epidermal growth factor receptor (hEGFR) kinase domain mutations in lung tumorigenesis and response to EGFR-targeted therapies, we generated bitransgenic mice with inducible expression in type II pneumocytes of two common hEGFR mutants seen in human lung cancer. Both bitransgenic lines developed lung adenocarcinoma after sustained hEGFR mutant expression, confirming their oncogenic potential. Maintenance of these lung tumors was dependent on continued expression of the EGFR mutants. Treatment with small molecule inhibitors (erlotinib or HKI-272) as well as prolonged treatment with a humanized anti-hEGFR antibody (cetuximab) led to dramatic tumor regression. These data suggest that persistent EGFR signaling is required for tumor maintenance in human lung adenocarcinomas expressing EGFR mutants.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1535-6108
|
pubmed:author |
pubmed-author:Al-HashemRuqayyahR,
pubmed-author:AlbertMitchellM,
pubmed-author:BronsonRoderick TRT,
pubmed-author:ChirieacLucian RLR,
pubmed-author:JännePasi APA,
pubmed-author:JiHongbinH,
pubmed-author:JohnsonBruce EBE,
pubmed-author:KimWilliamW,
pubmed-author:KobayashiSusumuS,
pubmed-author:LiDananD,
pubmed-author:LiangChenC,
pubmed-author:MahmoodUmarU,
pubmed-author:McNamaraKateK,
pubmed-author:PaderaRobertR,
pubmed-author:ShapiroGeoffrey IGI,
pubmed-author:SharplessNorman ENE,
pubmed-author:ShimamuraTakeshiT,
pubmed-author:SunYangpingY,
pubmed-author:TenenDanielD,
pubmed-author:WeisslederRalphR,
pubmed-author:WongKwok-KinKK
|
pubmed:issnType |
Print
|
pubmed:volume |
9
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
485-95
|
pubmed:dateRevised |
2009-11-19
|
pubmed:meshHeading |
pubmed-meshheading:16730237-Adenocarcinoma,
pubmed-meshheading:16730237-Adenocarcinoma, Bronchiolo-Alveolar,
pubmed-meshheading:16730237-Animals,
pubmed-meshheading:16730237-Antibodies, Monoclonal,
pubmed-meshheading:16730237-Antineoplastic Agents,
pubmed-meshheading:16730237-Enzyme Activation,
pubmed-meshheading:16730237-Exons,
pubmed-meshheading:16730237-Humans,
pubmed-meshheading:16730237-Lung,
pubmed-meshheading:16730237-Lung Neoplasms,
pubmed-meshheading:16730237-Mice,
pubmed-meshheading:16730237-Mice, Transgenic,
pubmed-meshheading:16730237-Mutation,
pubmed-meshheading:16730237-Protein Structure, Tertiary,
pubmed-meshheading:16730237-Quinazolines,
pubmed-meshheading:16730237-Quinolines,
pubmed-meshheading:16730237-Receptor, Epidermal Growth Factor
|
pubmed:year |
2006
|
pubmed:articleTitle |
The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies.
|
pubmed:affiliation |
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|