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Article: A dual colour dual fusion fluorescence in situ hybridisation study on the genesis of complex variant translocations in chronic myelogenous leukaemia

TitleA dual colour dual fusion fluorescence in situ hybridisation study on the genesis of complex variant translocations in chronic myelogenous leukaemia
Authors
Issue Date2008
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
Citation
Oncology Reports, 2008, v. 19 n. 5, p. 1181-1184 How to Cite?
AbstractComplex variant 9;22 translocations occur in a significant minority of chronic myelogenous leukaemia (CML) patients. Different mechanisms of their formation have been described. We report dual colour dual fusion fluorescence in situ hybridisation data in 12 Chinese CML patients with complex translocations. Three previously reported breakpoint hotspots in a third partner chromosome (14q32, 17q25, 1q2l) were observed. In 10/12 (83.3%) patients, the abnormality occurred as a single step 3-break event. Only a single abnormal clone harbouring the complex translocation was seen in this group. The remaining 2 cases in the chronic phase showed a 4-break mechanism (2/12,16.7%). Deletion of 5' ABL at der(9) was not observed in any of the 12 patients, however, the loss of 3' BCR was observed in 1 patient (1/12, 8.3%). Together with previous findings, these data suggest that these variant translocations occur more often as a 3-break single-step process with no reciprocal ABL-BCR fusion. On the other hand, a 4-break event is also regularly seen during the initial stages of leukaemogenesis, which likely predisposes to der(9) deletion. The observed difference in rates of der(9) deletion reported in a series of CML patients with variant translocations may be related to a difference in rates of a 4-break event.
Persistent Identifierhttp://hdl.handle.net/10722/88783
ISSN
2015 Impact Factor: 2.486
2015 SCImago Journal Rankings: 0.968
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSo, CCen_HK
dc.contributor.authorWan, TSKen_HK
dc.contributor.authorYip, SFen_HK
dc.contributor.authorChan, LCen_HK
dc.date.accessioned2010-09-06T09:47:56Z-
dc.date.available2010-09-06T09:47:56Z-
dc.date.issued2008en_HK
dc.identifier.citationOncology Reports, 2008, v. 19 n. 5, p. 1181-1184en_HK
dc.identifier.issn1021-335Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/88783-
dc.description.abstractComplex variant 9;22 translocations occur in a significant minority of chronic myelogenous leukaemia (CML) patients. Different mechanisms of their formation have been described. We report dual colour dual fusion fluorescence in situ hybridisation data in 12 Chinese CML patients with complex translocations. Three previously reported breakpoint hotspots in a third partner chromosome (14q32, 17q25, 1q2l) were observed. In 10/12 (83.3%) patients, the abnormality occurred as a single step 3-break event. Only a single abnormal clone harbouring the complex translocation was seen in this group. The remaining 2 cases in the chronic phase showed a 4-break mechanism (2/12,16.7%). Deletion of 5' ABL at der(9) was not observed in any of the 12 patients, however, the loss of 3' BCR was observed in 1 patient (1/12, 8.3%). Together with previous findings, these data suggest that these variant translocations occur more often as a 3-break single-step process with no reciprocal ABL-BCR fusion. On the other hand, a 4-break event is also regularly seen during the initial stages of leukaemogenesis, which likely predisposes to der(9) deletion. The observed difference in rates of der(9) deletion reported in a series of CML patients with variant translocations may be related to a difference in rates of a 4-break event.en_HK
dc.languageengen_HK
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htmen_HK
dc.relation.ispartofOncology Reportsen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshChinaen_HK
dc.subject.meshChromosome Bandingen_HK
dc.subject.meshChromosomes, Human, Pair 22en_HK
dc.subject.meshChromosomes, Human, Pair 9en_HK
dc.subject.meshCytogenetic Analysisen_HK
dc.subject.meshDNA Mutational Analysisen_HK
dc.subject.meshFluorescent Dyes - pharmacologyen_HK
dc.subject.meshFusion Proteins, bcr-abl - geneticsen_HK
dc.subject.meshGene Deletionen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescence - instrumentation - methodsen_HK
dc.subject.meshKaryotypingen_HK
dc.subject.meshLeukemia, Myelogenous, Chronic, BCR-ABL Positive - ethnology - geneticsen_HK
dc.subject.meshTranslocation, Geneticen_HK
dc.titleA dual colour dual fusion fluorescence in situ hybridisation study on the genesis of complex variant translocations in chronic myelogenous leukaemiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1021-335X&volume=19&issue=5&spage=1181&epage=1184&date=2008&atitle=A+dual+colour+dual+fusion+fluorescence+in+situ+hybridisation+study+on+the+genesis+of+complex+variant+translocations+in+chronic+myelogenous+leukaemiaen_HK
dc.identifier.emailSo, CC:scc@pathology.hku.hken_HK
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_HK
dc.identifier.authoritySo, CC=rp00391en_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3892/or.19.5.1181-
dc.identifier.pmid18425374-
dc.identifier.scopuseid_2-s2.0-47549114688en_HK
dc.identifier.hkuros150512en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-47549114688&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1181en_HK
dc.identifier.epage1184en_HK
dc.identifier.isiWOS:000255312000015-
dc.publisher.placeGreeceen_HK

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