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Article: Increased chromosome 20 copy number detected by fluorescence in situ hybridization (FISH) in malignant melanoma

TitleIncreased chromosome 20 copy number detected by fluorescence in situ hybridization (FISH) in malignant melanoma
Authors
Issue Date1997
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250
Citation
Genes Chromosomes And Cancer, 1997, v. 19 n. 4, p. 278-285 How to Cite?
AbstractDNA amplification is an important mechanism of tumor progression that allows cancer cells to up-regulate the expression of critical genes such as oncogenes and genes conferring drug resistance. Recent studies using comparative genomic hybridization (CGH) revealed increased DNA copies of 20q sequences in 7 melanoma cell lines and 8 archival metastatic melanoma lesions. To evaluate chromosome 20 abnormalities in more detail and to resolve discrepancies between karyotype and CGH findings, we performed FISH analysis of metaphase cells in 13 melanoma cell lines (including the 7 lines used for CGH) and 9 primary melanoma specimens by using a whole chromosome paint specific for chromosome 20. All 13 cell lines (100%) and 8/9 primary tumors (89%) showed extra copies of chromosome 20 relative to tumor ploidy. Additionally, 6/14 cell lines (43%) and 2/8 primary tumors (25%) showed translocated chromosome 20 material previously undetected by standard cytogenetics. Cytologic evidence for gene amplification was also found in one cell line, which contained an add(20)(p 13), with additional DNA being derived from 20q sequences. These data suggest that overrepresentation of a gene or genes important for melanoma pathogenesis resides on the long arm of chromosome 20.
Persistent Identifierhttp://hdl.handle.net/10722/150729
ISSN
2015 Impact Factor: 3.96
2015 SCImago Journal Rankings: 2.210
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBarks, JHen_US
dc.contributor.authorThompson, FHen_US
dc.contributor.authorTaetle, Ren_US
dc.contributor.authorYang, JMen_US
dc.contributor.authorStone, JFen_US
dc.contributor.authorWymer, JAen_US
dc.contributor.authorKhavari, Ren_US
dc.contributor.authorGuan, XYen_US
dc.contributor.authorTrent, JMen_US
dc.contributor.authorPinkel, Den_US
dc.contributor.authorNelson, MAen_US
dc.date.accessioned2012-06-26T06:09:19Z-
dc.date.available2012-06-26T06:09:19Z-
dc.date.issued1997en_US
dc.identifier.citationGenes Chromosomes And Cancer, 1997, v. 19 n. 4, p. 278-285en_US
dc.identifier.issn1045-2257en_US
dc.identifier.urihttp://hdl.handle.net/10722/150729-
dc.description.abstractDNA amplification is an important mechanism of tumor progression that allows cancer cells to up-regulate the expression of critical genes such as oncogenes and genes conferring drug resistance. Recent studies using comparative genomic hybridization (CGH) revealed increased DNA copies of 20q sequences in 7 melanoma cell lines and 8 archival metastatic melanoma lesions. To evaluate chromosome 20 abnormalities in more detail and to resolve discrepancies between karyotype and CGH findings, we performed FISH analysis of metaphase cells in 13 melanoma cell lines (including the 7 lines used for CGH) and 9 primary melanoma specimens by using a whole chromosome paint specific for chromosome 20. All 13 cell lines (100%) and 8/9 primary tumors (89%) showed extra copies of chromosome 20 relative to tumor ploidy. Additionally, 6/14 cell lines (43%) and 2/8 primary tumors (25%) showed translocated chromosome 20 material previously undetected by standard cytogenetics. Cytologic evidence for gene amplification was also found in one cell line, which contained an add(20)(p 13), with additional DNA being derived from 20q sequences. These data suggest that overrepresentation of a gene or genes important for melanoma pathogenesis resides on the long arm of chromosome 20.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/38250en_US
dc.relation.ispartofGenes Chromosomes and Canceren_US
dc.subject.meshChromosome Aberrationsen_US
dc.subject.meshChromosome Deletionen_US
dc.subject.meshChromosomes, Human, Pair 20 - Geneticsen_US
dc.subject.meshGene Amplificationen_US
dc.subject.meshGenetic Markersen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshKaryotypingen_US
dc.subject.meshMelanoma - Genetics - Pathologyen_US
dc.subject.meshMetaphaseen_US
dc.subject.meshPloidiesen_US
dc.subject.meshTranslocation, Geneticen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleIncreased chromosome 20 copy number detected by fluorescence in situ hybridization (FISH) in malignant melanomaen_US
dc.typeArticleen_US
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_US
dc.identifier.authorityGuan, XY=rp00454en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/(SICI)1098-2264(199708)19:4<278::AID-GCC11>3.0.CO;2-Cen_US
dc.identifier.pmid9258664-
dc.identifier.scopuseid_2-s2.0-0030836424en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030836424&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume19en_US
dc.identifier.issue4en_US
dc.identifier.spage278en_US
dc.identifier.epage285en_US
dc.identifier.isiWOS:A1997XN87300011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBarks, JH=7003536764en_US
dc.identifier.scopusauthoridThompson, FH=7202217465en_US
dc.identifier.scopusauthoridTaetle, R=7006711648en_US
dc.identifier.scopusauthoridYang, JM=12445064900en_US
dc.identifier.scopusauthoridStone, JF=7403061421en_US
dc.identifier.scopusauthoridWymer, JA=8665972800en_US
dc.identifier.scopusauthoridKhavari, R=6507147389en_US
dc.identifier.scopusauthoridGuan, XY=7201463221en_US
dc.identifier.scopusauthoridTrent, JM=7201692482en_US
dc.identifier.scopusauthoridPinkel, D=35392644900en_US
dc.identifier.scopusauthoridNelson, MA=7403461044en_US

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