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Article: Distinct epidermal growth factor receptor and KRAS mutation patterns in non-small cell lung cancer patients with different tobacco exposure and clinicopathologic features

TitleDistinct epidermal growth factor receptor and KRAS mutation patterns in non-small cell lung cancer patients with different tobacco exposure and clinicopathologic features
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2006, v. 12 n. 5, p. 1647-1653 How to Cite?
AbstractPurpose: This study evaluated the mutational profile of epidermal growth factor receptor (EGFR) and KRAS in non-small cell lung cancers in Hong Kong and determined their relation with smoking history and other clinicopathologic features. Experimental Design: Mutational profile of exons 18 to 21 of EGFR and codons 12, 13, and 61 of KRAS were determined in 215 adenocarcinomas, 15 squamous cell (SCC), and 11 EBV-associated lymphoepithelioma-like carcinomas (LELC). Results: EGFR mutations were prevalent in adenocarcinomas (115 of 215), uncommon in LELC (1 of 11), and not found in SCC (P < 0.001). Among adenocarcinomas, mutations were associated with nonsmokers (83 of 111; P < 0.001), female gender (87 of 131; P < 0.001), and well-differentiated (55 of 86) compared with poorly differentiated (11 of 41) tumors (P < 0.001). Decreasing mutation rates with increasing direct tobacco exposure was observed, with 74.8% (83 of 111) in nonsmokers, 61.1% (11 of 18) in passive, 35.7% (10 of 28) in previous, and 19.0% (11 of 58) in current smokers. There were 53% amino acid substitutions, 43% in-frame deletions, and 4% insertions. Complex patterns with 13% double mutations, including five novel substitutions, were observed. For KRAS, mutations occurred in adenocarcinoma only (21 of 215) and were associated with smokers (11 of 58; P = 0.003), men (14 of 84; P = 0.009) and poorly differentiated (7 of 41) compared with well-differentiated (4 of 86) tumors (P = 0.037). EGFR and KRAS mutations occurred in mutually exclusive tumors. Regression analysis showed smoking history was the significant determinant for both mutations, whereas gender was a confounding factor. Conclusion: This study shows EGFR mutations are prevalent in lung adenocarcinoma and suggests that it plays an increasing oncogenic role with decreasing direct tobacco damage. © 2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/66445
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTam, IYSen_HK
dc.contributor.authorChung, LPen_HK
dc.contributor.authorSuen, WSen_HK
dc.contributor.authorWang, Een_HK
dc.contributor.authorWong, MCMen_HK
dc.contributor.authorHo, KKen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorChiu, SWen_HK
dc.contributor.authorGirard, Len_HK
dc.contributor.authorMinna, JDen_HK
dc.contributor.authorGazdar, AFen_HK
dc.contributor.authorWong, MPen_HK
dc.date.accessioned2010-09-06T05:46:25Z-
dc.date.available2010-09-06T05:46:25Z-
dc.date.issued2006en_HK
dc.identifier.citationClinical Cancer Research, 2006, v. 12 n. 5, p. 1647-1653en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/66445-
dc.description.abstractPurpose: This study evaluated the mutational profile of epidermal growth factor receptor (EGFR) and KRAS in non-small cell lung cancers in Hong Kong and determined their relation with smoking history and other clinicopathologic features. Experimental Design: Mutational profile of exons 18 to 21 of EGFR and codons 12, 13, and 61 of KRAS were determined in 215 adenocarcinomas, 15 squamous cell (SCC), and 11 EBV-associated lymphoepithelioma-like carcinomas (LELC). Results: EGFR mutations were prevalent in adenocarcinomas (115 of 215), uncommon in LELC (1 of 11), and not found in SCC (P < 0.001). Among adenocarcinomas, mutations were associated with nonsmokers (83 of 111; P < 0.001), female gender (87 of 131; P < 0.001), and well-differentiated (55 of 86) compared with poorly differentiated (11 of 41) tumors (P < 0.001). Decreasing mutation rates with increasing direct tobacco exposure was observed, with 74.8% (83 of 111) in nonsmokers, 61.1% (11 of 18) in passive, 35.7% (10 of 28) in previous, and 19.0% (11 of 58) in current smokers. There were 53% amino acid substitutions, 43% in-frame deletions, and 4% insertions. Complex patterns with 13% double mutations, including five novel substitutions, were observed. For KRAS, mutations occurred in adenocarcinoma only (21 of 215) and were associated with smokers (11 of 58; P = 0.003), men (14 of 84; P = 0.009) and poorly differentiated (7 of 41) compared with well-differentiated (4 of 86) tumors (P = 0.037). EGFR and KRAS mutations occurred in mutually exclusive tumors. Regression analysis showed smoking history was the significant determinant for both mutations, whereas gender was a confounding factor. Conclusion: This study shows EGFR mutations are prevalent in lung adenocarcinoma and suggests that it plays an increasing oncogenic role with decreasing direct tobacco damage. © 2006 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.en_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAdenocarcinoma - diagnosis - geneticsen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshAmino Acid Substitutionen_HK
dc.subject.meshCarcinoma, Non-Small-Cell Lung - diagnosis - geneticsen_HK
dc.subject.meshCarcinoma, Squamous Cell - diagnosis - geneticsen_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshDNA Mutational Analysisen_HK
dc.subject.meshExonsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshGenes, ras - geneticsen_HK
dc.subject.meshHerpesviridae Infections - complications - genetics - pathologyen_HK
dc.subject.meshHerpesvirus 4, Human - genetics - immunology - isolation & purificationen_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLung Neoplasms - diagnosis - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMutation - geneticsen_HK
dc.subject.meshReceptor, Epidermal Growth Factor - geneticsen_HK
dc.subject.meshSolitary Pulmonary Nodule - diagnosis - genetics - virologyen_HK
dc.subject.meshTobacco Smoke Pollutionen_HK
dc.titleDistinct epidermal growth factor receptor and KRAS mutation patterns in non-small cell lung cancer patients with different tobacco exposure and clinicopathologic featuresen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=12&issue=5&spage=1647&epage=53&date=2006&atitle=Distinct+epidermal+growth+factor+receptor+and+KRAS+mutation+patterns+in+non-small+cell+lung+cancer+patients+with+different+tobacco+exposure+and+clinicopathologic+featuresen_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.emailWong, MCM: mcmwong@hkucc.hku.hken_HK
dc.identifier.emailWong, MP: mwpik@hkucc.hku.hken_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.identifier.authorityWong, MCM=rp00024en_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-05-1981en_HK
dc.identifier.pmid16533793-
dc.identifier.scopuseid_2-s2.0-33645052711en_HK
dc.identifier.hkuros115288en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645052711&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1647en_HK
dc.identifier.epage1653en_HK
dc.identifier.isiWOS:000235988000034-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTam, IYS=8244035800en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK
dc.identifier.scopusauthoridSuen, WS=12786607600en_HK
dc.identifier.scopusauthoridWang, E=7403414620en_HK
dc.identifier.scopusauthoridWong, MCM=26029250900en_HK
dc.identifier.scopusauthoridHo, KK=12787864500en_HK
dc.identifier.scopusauthoridLam, WK=7203021937en_HK
dc.identifier.scopusauthoridChiu, SW=37044597800en_HK
dc.identifier.scopusauthoridGirard, L=7101715512en_HK
dc.identifier.scopusauthoridMinna, JD=35380041500en_HK
dc.identifier.scopusauthoridGazdar, AF=35372587300en_HK
dc.identifier.scopusauthoridWong, MP=7403907887en_HK

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