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Article: Primary adenocarcinomas of the lung in nonsmokers show a distinct pattern of allelic imbalance

TitlePrimary adenocarcinomas of the lung in nonsmokers show a distinct pattern of allelic imbalance
Authors
Issue Date2002
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2002, v. 62 n. 15, p. 4464-4468 How to Cite?
AbstractLung cancer development in nonsmokers, particularly in females, has long been observed, but the genetic pathways of oncogenesis are still unclear. The purpose of this study was to identify important targets of chromosomal alteration involved in non-tobacco-related adenocarcinomas of lung. In this study, loci of recurrent allelic imbalance (AI) were identified by microsatellite analysis, focusing on tumors with low frequencies of AI (FAL) relative to the mean level. We reasoned that studying such tumors would facilitate the identification of essential genetic changes needed for the malignant phenotype, which could be masked by genomic instability and widespread nonspecific alterations, especially in tumors showing high FAL. Forty-two adenocarcinomas from nonsmokers (NT- ADs) were analyzed by a broad spectrum of 84 markers covering all nonacrocentric chromosomal arms. Using the mean AI frequency (40%) as the threshold, loci in 7q31, 8p23.2, 10p14-p15, 13q12.3, 16q24, 17p13.1-p13.3, 17q22, 19q13.3, and Xqll.2-ql2 showed recurrent AI in the low-FAL tumors, which suggested that essential targets of carcinogenesis may be present. To analyze whether loci, frequently altered in NT-ADs, were uniquely involved in these tumors, 43 loci were also studied in 29 adenocarcinomas from smokers. 2q, 6p, 10p, 13q, 16q, 17q, 19p, 19q, 20p, and 20q showed frequent aberrations in NT-ADs, whereas 1q, 2p, 3p, 3q, 7q, 8p, 9p, 9q, 10q, 11q, 13q, 14q, TP53, 17p, 18q, and 21q were commonly altered in both of the tumor groups. Further comparison of their low-FAL tumors showed that AI involving 16q24, 17q22, and 19q13.3 were significantly associated with NT-ADs; whereas those involving 7q31, 8p23.2, 1Op14-pI5, 13q12.3, and 17p13.1-p13.3 were observed in both. The findings suggest that oncogenesis in the lung of smokers and nonsmokers involve overlapping yet distinct genetic pathways, whereas the recurrent loci of alteration in NT-ADs may provide a basis for the further mapping of critical molecular targets in these pathways.
Persistent Identifierhttp://hdl.handle.net/10722/88445
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, MPen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorWang, Een_HK
dc.contributor.authorChiu, SWen_HK
dc.contributor.authorLam, CLen_HK
dc.contributor.authorChung, LPen_HK
dc.date.accessioned2010-09-06T09:43:28Z-
dc.date.available2010-09-06T09:43:28Z-
dc.date.issued2002en_HK
dc.identifier.citationCancer Research, 2002, v. 62 n. 15, p. 4464-4468en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88445-
dc.description.abstractLung cancer development in nonsmokers, particularly in females, has long been observed, but the genetic pathways of oncogenesis are still unclear. The purpose of this study was to identify important targets of chromosomal alteration involved in non-tobacco-related adenocarcinomas of lung. In this study, loci of recurrent allelic imbalance (AI) were identified by microsatellite analysis, focusing on tumors with low frequencies of AI (FAL) relative to the mean level. We reasoned that studying such tumors would facilitate the identification of essential genetic changes needed for the malignant phenotype, which could be masked by genomic instability and widespread nonspecific alterations, especially in tumors showing high FAL. Forty-two adenocarcinomas from nonsmokers (NT- ADs) were analyzed by a broad spectrum of 84 markers covering all nonacrocentric chromosomal arms. Using the mean AI frequency (40%) as the threshold, loci in 7q31, 8p23.2, 10p14-p15, 13q12.3, 16q24, 17p13.1-p13.3, 17q22, 19q13.3, and Xqll.2-ql2 showed recurrent AI in the low-FAL tumors, which suggested that essential targets of carcinogenesis may be present. To analyze whether loci, frequently altered in NT-ADs, were uniquely involved in these tumors, 43 loci were also studied in 29 adenocarcinomas from smokers. 2q, 6p, 10p, 13q, 16q, 17q, 19p, 19q, 20p, and 20q showed frequent aberrations in NT-ADs, whereas 1q, 2p, 3p, 3q, 7q, 8p, 9p, 9q, 10q, 11q, 13q, 14q, TP53, 17p, 18q, and 21q were commonly altered in both of the tumor groups. Further comparison of their low-FAL tumors showed that AI involving 16q24, 17q22, and 19q13.3 were significantly associated with NT-ADs; whereas those involving 7q31, 8p23.2, 1Op14-pI5, 13q12.3, and 17p13.1-p13.3 were observed in both. The findings suggest that oncogenesis in the lung of smokers and nonsmokers involve overlapping yet distinct genetic pathways, whereas the recurrent loci of alteration in NT-ADs may provide a basis for the further mapping of critical molecular targets in these pathways.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAdenocarcinoma - etiology - genetics - pathologyen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshAllelic Imbalanceen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLung Neoplasms - etiology - genetics - pathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMicrosatellite Repeatsen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNeoplasm Stagingen_HK
dc.subject.meshSmoking - adverse effects - geneticsen_HK
dc.titlePrimary adenocarcinomas of the lung in nonsmokers show a distinct pattern of allelic imbalanceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-5472&volume=62&spage=4464&epage=4468&date=2002&atitle=Primary+adenocarcinomas+of+the+lung+in+nonsmokers+show+a+distinct+pattern+of+allelic+imbalanceen_HK
dc.identifier.emailWong, MP: mwpik@hkucc.hku.hken_HK
dc.identifier.emailLam, CL: dcllam@hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.identifier.authorityLam, CL=rp01345en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid12154056-
dc.identifier.scopuseid_2-s2.0-0036682309en_HK
dc.identifier.hkuros76732en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036682309&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume62en_HK
dc.identifier.issue15en_HK
dc.identifier.spage4464en_HK
dc.identifier.epage4468en_HK
dc.identifier.isiWOS:000177105600045-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, MP=7403907887en_HK
dc.identifier.scopusauthoridLam, WK=7203021937en_HK
dc.identifier.scopusauthoridWang, E=7403414620en_HK
dc.identifier.scopusauthoridChiu, SW=12788356600en_HK
dc.identifier.scopusauthoridLam, CL=7201749615en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK

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