FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2206669969> ?p ?o ?g. }

• W2206669969 endingPage "200" @default.
• W2206669969 startingPage "199" @default.
• W2206669969 abstract "Somatic activating mutations in the gene encoding the epidermal growth factor receptor (EGFR) are found in a proportion of non–small-cell lung cancers (NSCLCs) and have been associated with sensitivity of lung tumors to the EGFR tyrosine kinase inhibitors (TKIs), gefitinib (Iressa; AstraZeneca, London, England) and erlotinib (Tarceva; Genentech, Inc., South San Francisco, CA).1Lynch TJ Bell DW Sordella R et al.Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib.N Engl J Med. 2004; 350: 2129-2139Crossref PubMed Scopus (9490) Google Scholar, 2Paez JG Janne PA Lee JC et al.EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.Science. 2004; 304: 1497-1500Crossref PubMed Scopus (8028) Google Scholar, 3Pao W Miller V Zakowski M et al.EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib.Proc Natl Acad Sci USA. 2004; 101: 13306-13311Crossref PubMed Scopus (3719) Google Scholar Such mutations occur in the exons (18–21) encoding the kinase domain of the protein; approximately 90% of such mutations occur as exon 19 deletions, which eliminate an LREA motif, or as exon 21 missense mutations, resulting in substitution of arginine for leucine at position 858 (L858R).4Pao W Miller VA EGFR mutations, small molecule kinase inhibitors, and non-small cell lung cancer: current knowledge and future directions.J Clin Oncol. 2006; 23: 2556-2568Crossref Scopus (540) Google Scholar These two types of mutations also appear to be the dominant mutations that predict sensitivity to treatment.5Greulich H Chen T-H Feng W et al.Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants.PLoS Med. 2006; e313Google Scholar Thus, testing tumors for drug-sensitive EGFR mutations can be relatively straightforward in the clinic, provided that adequate tissue specimen is available for analysis and that sensitive, reliable assays have been established.6Pan Q Pao W Ladanyi M Rapid PCR-based detection of epidermal growth factor receptor gene mutations in lung adenocarcinomas.J Mol Diagn. 2006; 7: 396-403Abstract Full Text Full Text PDF Scopus (217) Google Scholar Up to now, most research has focused on analysis of DNA from tumor specimens for EGFR mutations. However, in this issue of the Journal of Thoracic Oncology, Kimura and colleagues demonstrate that EGFR mutations can also be detected in DNA derived from the serum of lung cancer patients.7Kimura H Kasahara K Shibata K et al.EGFR mutation of tumor and serum in gefitinib-treated patients with chemotherapy-naive non–small-cell lung cancer.J Thorac Oncol. 2006; 1: 260-267Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar As part of a trial to evaluate the efficacy and safety of gefitinib monotherapy in chemotherapy-naive patients with advanced NSCLC, they collected serum from individuals before and 14 days after the initiation of gefitinib, and then performed sequencing analysis for EGFR mutations on DNA derived from the sera. Not only were mutations readily detectable but they were also more frequently observed in post-treatment samples from patients with a partial response or stable disease than in those patients with progressive disease. These results suggest that serum EGFR mutations could be useful as a biomarker for monitoring response to EGFR tyrosine kinase inhibitors during treatment. Detection of mutant DNA from the blood of lung cancer patients is not a new concept. For example, it has been previously shown that mutations in the KRAS oncogene, which occur in 15 to 30% of NSCLCs, can also be detected in the plasma of individuals whose tumors harbor such mutations.8Kimura T Holland WS Kawaguchi T et al.Mutant DNA in plasma of lung cancer patients.Ann NY Acad Sci. 2004; 1022: 55-60Crossref PubMed Scopus (48) Google Scholar In this previous study, serum analysis also appeared to show promise for monitoring patient response to therapy, as many patients had KRAS mutations before treatment that were not detectable after treatment (collected 16 weeks after treatment). KRAS mutations have also been detected in plasma or serum of patients with other types of cancer,9Kopreski MS Benko FA Kwee C et al.Detection of mutant K-ras DNA in plasma or serum of patients with colorectal cancer.Br J Cancer. 1997; 76: 1293-1299Crossref PubMed Scopus (153) Google Scholar and others have described finding amplifications, microsatellite alterations, gene rearrangements, and epigenetic alterations as well (reviewed in Johnson and Lo10Johnson PJ Lo YMD Plasma nucleic acids in the diagnosis and management of malignant disease.Clin Chem. 2002; 48: 1186-1193PubMed Google Scholar). Much work remains to be done before such tests can be used routinely in the clinic. Methods of DNA extraction and analysis from plasma and/or serum and tumor specimens need to be standardized; the reproducibility, sensitivity, and specificity of these tests need to be established in well-designed clinical trials; and the optimum time for posttreatment collection of blood remains to be determined—none of these were addressed by Kimura and colleagues. It will also be important to establish whether such tests can be used to detect early disease. More likely, though, serum analyses might be useful for detecting early recurrence in patients who have undergone resection and know their tumor mutation status. Moreover, because disease in most patients who initially respond to treatment with gefitinib or erlotinib eventually progresses on therapy, it will be interesting to determine whether markers of drug resistance, such as the T790M EGFR mutations,11Kobayashi S Boggon TJ Dayaram T et al.EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.N Engl J Med. 2006; 352: 786-792Crossref Scopus (3223) Google Scholar, 12Kwak EL Sordella R Bell DW et al.Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib.Proc Natl Acad Sci USA. 2006; 102: 7665-7670Crossref Scopus (826) Google Scholar, 13Pao W Miller VA Politi KA et al.Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain.PLoS Med. 2006; 2: e73Crossref Scopus (2906) Google Scholar can be detected before either clinical and/or radiographically documented progression." @default.
• W2206669969 created "2016-06-24" @default.
• W2206669969 creator A5062616992 @default.
• W2206669969 date "2006-03-01" @default.
• W2206669969 modified "2023-09-26" @default.
• W2206669969 title "Monitoring EGFR-Mutant Lung Cancers By Means of the Blood" @default.
• W2206669969 cites W1973312323 @default.
• W2206669969 cites W1977332018 @default.
• W2206669969 cites W2002937040 @default.
• W2206669969 cites W2003984225 @default.
• W2206669969 cites W2037873277 @default.
• W2206669969 cites W2043696829 @default.
• W2206669969 cites W2082856465 @default.
• W2206669969 cites W2124328824 @default.
• W2206669969 cites W2139236349 @default.
• W2206669969 cites W2161821474 @default.
• W2206669969 cites W2162698716 @default.
• W2206669969 cites W2169816570 @default.
• W2206669969 cites W86511531 @default.
• W2206669969 doi "https://doi.org/10.1016/s1556-0864(15)31566-5" @default.
• W2206669969 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17409855" @default.
• W2206669969 hasPublicationYear "2006" @default.
• W2206669969 type Work @default.
• W2206669969 sameAs 2206669969 @default.
• W2206669969 citedByCount "1" @default.
• W2206669969 countsByYear W22066699692017 @default.
• W2206669969 crossrefType "journal-article" @default.
• W2206669969 hasAuthorship W2206669969A5062616992 @default.
• W2206669969 hasBestOaLocation W22066699691 @default.
• W2206669969 hasConcept C104317684 @default.
• W2206669969 hasConcept C121608353 @default.
• W2206669969 hasConcept C126322002 @default.
• W2206669969 hasConcept C143998085 @default.
• W2206669969 hasConcept C170493617 @default.
• W2206669969 hasConcept C2776256026 @default.
• W2206669969 hasConcept C2778087573 @default.
• W2206669969 hasConcept C2779438470 @default.
• W2206669969 hasConcept C2780580887 @default.
• W2206669969 hasConcept C2780586478 @default.
• W2206669969 hasConcept C36823959 @default.
• W2206669969 hasConcept C42362537 @default.
• W2206669969 hasConcept C501734568 @default.
• W2206669969 hasConcept C502942594 @default.
• W2206669969 hasConcept C54355233 @default.
• W2206669969 hasConcept C71924100 @default.
• W2206669969 hasConcept C75563809 @default.
• W2206669969 hasConcept C86803240 @default.
• W2206669969 hasConceptScore W2206669969C104317684 @default.
• W2206669969 hasConceptScore W2206669969C121608353 @default.
• W2206669969 hasConceptScore W2206669969C126322002 @default.
• W2206669969 hasConceptScore W2206669969C143998085 @default.
• W2206669969 hasConceptScore W2206669969C170493617 @default.
• W2206669969 hasConceptScore W2206669969C2776256026 @default.
• W2206669969 hasConceptScore W2206669969C2778087573 @default.
• W2206669969 hasConceptScore W2206669969C2779438470 @default.
• W2206669969 hasConceptScore W2206669969C2780580887 @default.
• W2206669969 hasConceptScore W2206669969C2780586478 @default.
• W2206669969 hasConceptScore W2206669969C36823959 @default.
• W2206669969 hasConceptScore W2206669969C42362537 @default.
• W2206669969 hasConceptScore W2206669969C501734568 @default.
• W2206669969 hasConceptScore W2206669969C502942594 @default.
• W2206669969 hasConceptScore W2206669969C54355233 @default.
• W2206669969 hasConceptScore W2206669969C71924100 @default.
• W2206669969 hasConceptScore W2206669969C75563809 @default.
• W2206669969 hasConceptScore W2206669969C86803240 @default.
• W2206669969 hasIssue "3" @default.
• W2206669969 hasLocation W22066699691 @default.
• W2206669969 hasLocation W22066699692 @default.
• W2206669969 hasOpenAccess W2206669969 @default.
• W2206669969 hasPrimaryLocation W22066699691 @default.
• W2206669969 hasRelatedWork W2025029856 @default.
• W2206669969 hasRelatedWork W2049303357 @default.
• W2206669969 hasRelatedWork W2135761436 @default.
• W2206669969 hasRelatedWork W2160636733 @default.
• W2206669969 hasRelatedWork W2397917982 @default.
• W2206669969 hasRelatedWork W2416524679 @default.
• W2206669969 hasRelatedWork W2594832304 @default.
• W2206669969 hasRelatedWork W2888534976 @default.
• W2206669969 hasRelatedWork W2906574801 @default.
• W2206669969 hasRelatedWork W4287306528 @default.
• W2206669969 hasVolume "1" @default.
• W2206669969 isParatext "false" @default.
• W2206669969 isRetracted "false" @default.
• W2206669969 magId "2206669969" @default.
• W2206669969 workType "article" @default.