rdf:type |
|
lifeskim:mentions |
umls-concept:C0007131,
umls-concept:C0027651,
umls-concept:C0034802,
umls-concept:C0332206,
umls-concept:C0449438,
umls-concept:C0851827,
umls-concept:C0871261,
umls-concept:C1554184,
umls-concept:C1701901,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
|
pubmed:issue |
12
|
pubmed:dateCreated |
2007-12-10
|
pubmed:abstractText |
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have demonstrated clinical benefit in patients with nonsmall cell lung cancer (NSCLC), particularly those with tumors that have EGFR-TK domain mutations. Moreover, the EGFR and cyclooxygenase (COX)-2 pathways are known to enhance the procarcinogenic effects of each other in different tumor types. Therefore, it was hypothesized that tumor EGFR mutation status may influence the effectiveness of simultaneous EGFR and COX-2 inhibition in patients with NSCLC.
|
pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2 Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/PTGS2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins E,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Quinazolines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/celecoxib,
http://linkedlifedata.com/resource/pubmed/chemical/erlotinib,
http://linkedlifedata.com/resource/pubmed/chemical/gefitinib
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0008-543X
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
110
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2775-84
|
pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17948911-Apoptosis,
pubmed-meshheading:17948911-Carcinoma, Non-Small-Cell Lung,
pubmed-meshheading:17948911-Cell Division,
pubmed-meshheading:17948911-Cell Survival,
pubmed-meshheading:17948911-Cyclooxygenase 2,
pubmed-meshheading:17948911-Cyclooxygenase 2 Inhibitors,
pubmed-meshheading:17948911-Genes, erbB-1,
pubmed-meshheading:17948911-Humans,
pubmed-meshheading:17948911-Lung Neoplasms,
pubmed-meshheading:17948911-Mutation,
pubmed-meshheading:17948911-Prostaglandins E,
pubmed-meshheading:17948911-Pyrazoles,
pubmed-meshheading:17948911-Quinazolines,
pubmed-meshheading:17948911-Receptor, Epidermal Growth Factor,
pubmed-meshheading:17948911-Sulfonamides,
pubmed-meshheading:17948911-Tumor Cells, Cultured
|
pubmed:year |
2007
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pubmed:articleTitle |
Response to dual blockade of epidermal growth factor receptor (EGFR) and cycloxygenase-2 in nonsmall cell lung cancer may be dependent on the EGFR mutational status of the tumor.
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pubmed:affiliation |
Division of Hematology/Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan 48201, USA. gadgeels@karmanos.org
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|