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Article: Gain of 9p in the pathogenesis of polycythemia vera

TitleGain of 9p in the pathogenesis of polycythemia vera
Authors
Issue Date1998
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, 1998, v. 22 n. 4, p. 321-324 How to Cite?
AbstractPolycythemia vera (PV) is a clonal stem cell disorder characterized by excessive erythrocyte production, resulting in absolute erythrocytosis. No specific structural chromosomal abnormalities have been reported in PV to date. We have observed two cases of PV with an extra i(9)(p10) as the sole anomaly, and FISH analysis using a 9p-specific chromosome microdissection probe showed that two other PV patients previously identified as having an add(18p) and an add(lp) as the primary changes actually carried a der(18)t(9;18)(p12;p11.2) and a der(1)t(1;9)(p12;p12), respectively. The same FISH assay was employed to evaluate domain signals on interphase cells of 15 more cases of PV with normal karyotypes and five normal controls. Two patients were observed with a significant increase in the percentage of cells with three domain signals. Our results strongly indicate that an additional i(9)(p10) is a new and recurrent primary chromosome anomaly in PV, and, in consideration of trisomy 9 being one of the most common anomalies in PV, amplification of a gene or genes on 9p, but not on 9q, may play a crucial role in the pathogenesis of PV.
Persistent Identifierhttp://hdl.handle.net/10722/150737
ISSN
2015 Impact Factor: 3.96
2015 SCImago Journal Rankings: 2.210
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Zen_US
dc.contributor.authorNotohamiprodjo, Men_US
dc.contributor.authorGuan, XYen_US
dc.contributor.authorPaietta, Een_US
dc.contributor.authorBlackwell, Sen_US
dc.contributor.authorStout, Ken_US
dc.contributor.authorTurner, Aen_US
dc.contributor.authorRichkind, Ken_US
dc.contributor.authorTrent, JMen_US
dc.contributor.authorLamb, Aen_US
dc.contributor.authorSandberg, AAen_US
dc.date.accessioned2012-06-26T06:09:27Z-
dc.date.available2012-06-26T06:09:27Z-
dc.date.issued1998en_US
dc.identifier.citationGenes Chromosomes And Cancer, 1998, v. 22 n. 4, p. 321-324en_US
dc.identifier.issn1045-2257en_US
dc.identifier.urihttp://hdl.handle.net/10722/150737-
dc.description.abstractPolycythemia vera (PV) is a clonal stem cell disorder characterized by excessive erythrocyte production, resulting in absolute erythrocytosis. No specific structural chromosomal abnormalities have been reported in PV to date. We have observed two cases of PV with an extra i(9)(p10) as the sole anomaly, and FISH analysis using a 9p-specific chromosome microdissection probe showed that two other PV patients previously identified as having an add(18p) and an add(lp) as the primary changes actually carried a der(18)t(9;18)(p12;p11.2) and a der(1)t(1;9)(p12;p12), respectively. The same FISH assay was employed to evaluate domain signals on interphase cells of 15 more cases of PV with normal karyotypes and five normal controls. Two patients were observed with a significant increase in the percentage of cells with three domain signals. Our results strongly indicate that an additional i(9)(p10) is a new and recurrent primary chromosome anomaly in PV, and, in consideration of trisomy 9 being one of the most common anomalies in PV, amplification of a gene or genes on 9p, but not on 9q, may play a crucial role in the pathogenesis of PV.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.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshChromosome Bandingen_US
dc.subject.meshChromosomes, Human, Pair 9 - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Amplificationen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshKaryotypingen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPolycythemia Vera - Genetics - Pathologyen_US
dc.titleGain of 9p in the pathogenesis of polycythemia veraen_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(199808)22:4<321::AID-GCC8>3.0.CO;2-Xen_US
dc.identifier.pmid9669670-
dc.identifier.scopuseid_2-s2.0-0031798991en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031798991&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume22en_US
dc.identifier.issue4en_US
dc.identifier.spage321en_US
dc.identifier.epage324en_US
dc.identifier.isiWOS:000074537100008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChen, Z=7409491627en_US
dc.identifier.scopusauthoridNotohamiprodjo, M=6508174023en_US
dc.identifier.scopusauthoridGuan, XY=7201463221en_US
dc.identifier.scopusauthoridPaietta, E=7004993241en_US
dc.identifier.scopusauthoridBlackwell, S=7005821095en_US
dc.identifier.scopusauthoridStout, K=35618930900en_US
dc.identifier.scopusauthoridTurner, A=7401819886en_US
dc.identifier.scopusauthoridRichkind, K=6604058699en_US
dc.identifier.scopusauthoridTrent, JM=7201692482en_US
dc.identifier.scopusauthoridLamb, A=7102445668en_US
dc.identifier.scopusauthoridSandberg, AA=7202853810en_US

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