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Article: Chromosomal aberrations of primary lung adenocarcinomas in nonsmokers

TitleChromosomal aberrations of primary lung adenocarcinomas in nonsmokers
Authors
KeywordsAdenocarcinoma
Chromosome aberration
Comparative genomic hybridization
Lung
Nonsmokers
Issue Date2003
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 2003, v. 97 n. 5, p. 1263-1270 How to Cite?
AbstractBACKGROUND. Lung carcinoma is a common malignancy, and tobacco carcinogenesis is the major cause. Studies on individual genes or loci have suggested, that in tumors from nonsmokers, different genetic alterations are present compared with tumors from smokers. It is possible that distinct genetic pathways may be involved. However, the targets remain largely unknown; and, to the authors' knowledge, molecular cytogenetics studies on lung carcinomas from nonsmokers have not been reported. METHODS. Comparative genomic hybridization (CGH) analysis was performed on primary lung adenocarcinoma samples from 32 patients who never smoked to identify loci of frequent aberrations. RESULTS. Different extents of aberration were found in 31 of the 32 samples studied. The most frequently altered locus was gain of 16p (59% of samples) followed by gain of 20q (44% of samples), with the minimal overlapping regions at 16p13.1-p13.2 and 20q13.2, respectively. Other over-represented loci with > 30% frequency were observed at 5p (34% of samples), 7p (41% of samples), 8q (31% of samples), 17q (34% of samples), and 19q (34% of samples); and high-level DNA amplifications were detected at 1q, 7p, 12q, 19q, and 20q. DNA under-representation was observed less commonly and included 8p (28% of samples), 9p (22% of samples), 13q (28% of samples), and 18q (38% of samples). CONCLUSIONS. The current study identified targets of frequent genetic aberration in primary adenocarcinomas from nonsmokers. Compared with reported CGH findings in the literature, the current findings suggest that DNA gain at 16p is the distinct aberration involved in these tumors. Other frequently altered loci involve commonly reported oncogenic and tumor suppressor loci, suggesting an overlap with the genetic pathways of tobacco-induced lung carcinogenesis. © 2003 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/88681
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, MPen_HK
dc.contributor.authorFung, LFen_HK
dc.contributor.authorWang, Een_HK
dc.contributor.authorChow, WSen_HK
dc.contributor.authorChiu, SWen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorHo, KKen_HK
dc.contributor.authorMa, ESKen_HK
dc.contributor.authorWan, TSKen_HK
dc.contributor.authorChung, LPen_HK
dc.date.accessioned2010-09-06T09:46:35Z-
dc.date.available2010-09-06T09:46:35Z-
dc.date.issued2003en_HK
dc.identifier.citationCancer, 2003, v. 97 n. 5, p. 1263-1270en_HK
dc.identifier.issn0008-543Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/88681-
dc.description.abstractBACKGROUND. Lung carcinoma is a common malignancy, and tobacco carcinogenesis is the major cause. Studies on individual genes or loci have suggested, that in tumors from nonsmokers, different genetic alterations are present compared with tumors from smokers. It is possible that distinct genetic pathways may be involved. However, the targets remain largely unknown; and, to the authors' knowledge, molecular cytogenetics studies on lung carcinomas from nonsmokers have not been reported. METHODS. Comparative genomic hybridization (CGH) analysis was performed on primary lung adenocarcinoma samples from 32 patients who never smoked to identify loci of frequent aberrations. RESULTS. Different extents of aberration were found in 31 of the 32 samples studied. The most frequently altered locus was gain of 16p (59% of samples) followed by gain of 20q (44% of samples), with the minimal overlapping regions at 16p13.1-p13.2 and 20q13.2, respectively. Other over-represented loci with > 30% frequency were observed at 5p (34% of samples), 7p (41% of samples), 8q (31% of samples), 17q (34% of samples), and 19q (34% of samples); and high-level DNA amplifications were detected at 1q, 7p, 12q, 19q, and 20q. DNA under-representation was observed less commonly and included 8p (28% of samples), 9p (22% of samples), 13q (28% of samples), and 18q (38% of samples). CONCLUSIONS. The current study identified targets of frequent genetic aberration in primary adenocarcinomas from nonsmokers. Compared with reported CGH findings in the literature, the current findings suggest that DNA gain at 16p is the distinct aberration involved in these tumors. Other frequently altered loci involve commonly reported oncogenic and tumor suppressor loci, suggesting an overlap with the genetic pathways of tobacco-induced lung carcinogenesis. © 2003 American Cancer Society.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_HK
dc.relation.ispartofCanceren_HK
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectAdenocarcinomaen_HK
dc.subjectChromosome aberrationen_HK
dc.subjectComparative genomic hybridizationen_HK
dc.subjectLungen_HK
dc.subjectNonsmokersen_HK
dc.subject.meshAdenocarcinoma - geneticsen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshChromosomes, Human, Pair 16 - geneticsen_HK
dc.subject.meshDNA, Neoplasm - analysisen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshLung Neoplasms - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNucleic Acid Hybridizationen_HK
dc.subject.meshSmoking - adverse effects - geneticsen_HK
dc.titleChromosomal aberrations of primary lung adenocarcinomas in nonsmokersen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-543X&volume=97&issue=5&spage=1263&epage=1270&date=2003&atitle=Chromosomal+aberrations+of+primary+lung+adenocarcinomas+in+nonsmokersen_HK
dc.identifier.emailWong, MP: mwpik@hkucc.hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/cncr.11183en_HK
dc.identifier.pmid12599234-
dc.identifier.scopuseid_2-s2.0-0037369201en_HK
dc.identifier.hkuros76746en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037369201&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume97en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1263en_HK
dc.identifier.epage1270en_HK
dc.identifier.isiWOS:000181190000017-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, MP=7403907887en_HK
dc.identifier.scopusauthoridFung, LF=35910298200en_HK
dc.identifier.scopusauthoridWang, E=7403414620en_HK
dc.identifier.scopusauthoridChow, WS=7402281124en_HK
dc.identifier.scopusauthoridChiu, SW=12788356600en_HK
dc.identifier.scopusauthoridLam, WK=7203021937en_HK
dc.identifier.scopusauthoridHo, KK=9536814400en_HK
dc.identifier.scopusauthoridMa, ESK=7202039934en_HK
dc.identifier.scopusauthoridWan, TSK=25623981600en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK

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