File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Cytogenetic and fluorescence in situ hybridization characterization of clonal chromosomal aberrations and CCND1 amplification in esophageal carcinomas

TitleCytogenetic and fluorescence in situ hybridization characterization of clonal chromosomal aberrations and CCND1 amplification in esophageal carcinomas
Authors
Issue Date2004
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2004, v. 148 n. 1, p. 21-28 How to Cite?
AbstractCytogenetic analyses of four squamous cell carcinomas (SCC) of the esophagus showed complex numerical and structural abnormalities. Chromosomal bands or regions preferentially involved were 11q13, 8q10, 21q10, 3p10∼p11, 1p11∼q11, 5p11∼q11, and 14p11∼q11. For the first time, to our knowledge, recurrent aberrations were identified in esophageal SCC, including homogenous staining region (hsr), isochromosomes i(3q) and i(21q), and ring chromosome. Losses of chromosomal material dominated over gains. Recurrent imbalances included under-representation of 4p13∼pter, 5q14∼qter, 9p22∼pter, 10p, 11p13∼pter, 12p13∼pter, 17p10∼pter, 18p11∼pter, 21p, and 22p, as well as over-representation of 1q25∼qter, 3q, 7q, and 8q. Interestingly, hsr at different chromosomal regions occurred in three of four cases. With the application of fluorescence in situ hybridization (FISH) and multicolor combined binary ratio labeling-FISH with specific DNA probes, it could be shown that in two cases the hsr was derived from chromosome 11 material and that the amplicon included CCND1. Our results, together with previous molecular genetic findings, indicate that CCND1might be a prime target in 11q13 amplification, and that amplification of this gene might be crucial in the tumorigenesis of esophageal SCC. These observed chromosomal aberrations and imbalances thus provide important information for further molecular genetic investigation of esophageal SCC. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/77705
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJin, Yen_HK
dc.contributor.authorJin, Cen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorZhang, Hen_HK
dc.contributor.authorStrombeck, Ben_HK
dc.contributor.authorYuen, APWen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:34:49Z-
dc.date.available2010-09-06T07:34:49Z-
dc.date.issued2004en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2004, v. 148 n. 1, p. 21-28en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77705-
dc.description.abstractCytogenetic analyses of four squamous cell carcinomas (SCC) of the esophagus showed complex numerical and structural abnormalities. Chromosomal bands or regions preferentially involved were 11q13, 8q10, 21q10, 3p10∼p11, 1p11∼q11, 5p11∼q11, and 14p11∼q11. For the first time, to our knowledge, recurrent aberrations were identified in esophageal SCC, including homogenous staining region (hsr), isochromosomes i(3q) and i(21q), and ring chromosome. Losses of chromosomal material dominated over gains. Recurrent imbalances included under-representation of 4p13∼pter, 5q14∼qter, 9p22∼pter, 10p, 11p13∼pter, 12p13∼pter, 17p10∼pter, 18p11∼pter, 21p, and 22p, as well as over-representation of 1q25∼qter, 3q, 7q, and 8q. Interestingly, hsr at different chromosomal regions occurred in three of four cases. With the application of fluorescence in situ hybridization (FISH) and multicolor combined binary ratio labeling-FISH with specific DNA probes, it could be shown that in two cases the hsr was derived from chromosome 11 material and that the amplicon included CCND1. Our results, together with previous molecular genetic findings, indicate that CCND1might be a prime target in 11q13 amplification, and that amplification of this gene might be crucial in the tumorigenesis of esophageal SCC. These observed chromosomal aberrations and imbalances thus provide important information for further molecular genetic investigation of esophageal SCC. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_HK
dc.relation.ispartofCancer Genetics and Cytogeneticsen_HK
dc.rightsCancer Genetics and Cytogenetics. Copyright © Elsevier Inc.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshCarcinoma, Squamous Cell - geneticsen_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshCyclin D1 - geneticsen_HK
dc.subject.meshEsophageal Neoplasms - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Amplificationen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescence - methodsen_HK
dc.subject.meshKaryotypingen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.titleCytogenetic and fluorescence in situ hybridization characterization of clonal chromosomal aberrations and CCND1 amplification in esophageal carcinomasen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=148&issue=1&spage=21&epage=28&date=2004&atitle=Cytogenetic+and+fluorescence+in+situ+hybridization+characterization+of+clonal+chromosomal+aberrations+and+CCND1+amplification+in+esophageal+carcinomasen_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL: ylkwong@hku.hken_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0165-4608(03)00213-9en_HK
dc.identifier.pmid14697637-
dc.identifier.scopuseid_2-s2.0-0347511688en_HK
dc.identifier.hkuros85615en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0347511688&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume148en_HK
dc.identifier.issue1en_HK
dc.identifier.spage21en_HK
dc.identifier.epage28en_HK
dc.identifier.isiWOS:000187804800004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridJin, Y=7404457413en_HK
dc.identifier.scopusauthoridJin, C=7401659093en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridZhang, H=14124271200en_HK
dc.identifier.scopusauthoridStrombeck, B=6701670678en_HK
dc.identifier.scopusauthoridYuen, APW=7006290111en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats