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Article: Pathogenesis of jumping translocations: A molecular cytogenetics study

TitlePathogenesis of jumping translocations: A molecular cytogenetics study
Authors
Issue Date2004
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukres
Citation
Leukemia Research, 2004, v. 28 n. 10, p. 1075-1079 How to Cite?
AbstractBackground/aims: Jumping translocations are rare cytogenetic aberrations in haematological malignancies, the pathogenesis of which remains to be fully characterised. We investigated the mechanism of formation of jumping translocations in a case of adult common acute lymphoblastic leukaemia (ALL) positive for the Ph translocation. Methods: Interphase and metaphase fluorescence in situ hybridisation (FISH) was performed using several probe systems. Results were correlated with findings on conventional cytogenetics. Granulocytes, T-cells and leukaemic B-cells in peripheral blood were sorted by immunomagnetic method and the terminal restriction fragment (TRF) length of these cellular populations was determined by Southern blot analysis. Results: Duplicated BCR-ABL fusion signals were found on a dic(14;22)der(22)t(9;22) chromosome. Clonal jumping translocations, existing as evolutionary changes, involved the donor chromosomal segment distal to 1q12 jumping onto the telomere ends of 11q, 15p, 19p and 20p. Telomere length was decreased in the neoplastic B-cell population and contributed to the formation of the dicentric chromosome that showed absence of telomere repeats at fusion ends. Subsequent pericentromeric heterochromatin decondensation of chromosome 1q occurred, and this donor segment was randomly fused to the shortened telomere ends of non-homologous chromosomes. Conclusions: Both telomere shortening and pericentromeric heterochromatin decondensation contribute to the formation of jumping translocations, which is most probably a multi-stage process. © 2004 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/148541
ISSN
2015 Impact Factor: 2.606
2015 SCImago Journal Rankings: 1.043
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWan, TSKen_US
dc.contributor.authorMa, SKen_US
dc.contributor.authorChow, EYDen_US
dc.contributor.authorLi, YHen_US
dc.contributor.authorLin, SYen_US
dc.contributor.authorChan, LCen_US
dc.date.accessioned2012-05-29T06:13:37Z-
dc.date.available2012-05-29T06:13:37Z-
dc.date.issued2004en_US
dc.identifier.citationLeukemia Research, 2004, v. 28 n. 10, p. 1075-1079en_US
dc.identifier.issn0145-2126en_US
dc.identifier.urihttp://hdl.handle.net/10722/148541-
dc.description.abstractBackground/aims: Jumping translocations are rare cytogenetic aberrations in haematological malignancies, the pathogenesis of which remains to be fully characterised. We investigated the mechanism of formation of jumping translocations in a case of adult common acute lymphoblastic leukaemia (ALL) positive for the Ph translocation. Methods: Interphase and metaphase fluorescence in situ hybridisation (FISH) was performed using several probe systems. Results were correlated with findings on conventional cytogenetics. Granulocytes, T-cells and leukaemic B-cells in peripheral blood were sorted by immunomagnetic method and the terminal restriction fragment (TRF) length of these cellular populations was determined by Southern blot analysis. Results: Duplicated BCR-ABL fusion signals were found on a dic(14;22)der(22)t(9;22) chromosome. Clonal jumping translocations, existing as evolutionary changes, involved the donor chromosomal segment distal to 1q12 jumping onto the telomere ends of 11q, 15p, 19p and 20p. Telomere length was decreased in the neoplastic B-cell population and contributed to the formation of the dicentric chromosome that showed absence of telomere repeats at fusion ends. Subsequent pericentromeric heterochromatin decondensation of chromosome 1q occurred, and this donor segment was randomly fused to the shortened telomere ends of non-homologous chromosomes. Conclusions: Both telomere shortening and pericentromeric heterochromatin decondensation contribute to the formation of jumping translocations, which is most probably a multi-stage process. © 2004 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukresen_US
dc.relation.ispartofLeukemia Researchen_US
dc.subject.meshAntigens, Cd - Biosynthesisen_US
dc.subject.meshAntigens, Differentiation, Myelomonocytic - Biosynthesisen_US
dc.subject.meshBlotting, Southernen_US
dc.subject.meshChromosome Aberrationsen_US
dc.subject.meshChromosomes, Human, Pair 14 - Geneticsen_US
dc.subject.meshChromosomes, Human, Pair 22 - Geneticsen_US
dc.subject.meshChromosomes, Human, Pair 9 - Geneticsen_US
dc.subject.meshCytogenetic Analysis - Methodsen_US
dc.subject.meshFatal Outcomeen_US
dc.subject.meshFusion Proteins, Bcr-Abl - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridization, Fluorescence - Methodsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPolymorphism, Restriction Fragment Lengthen_US
dc.subject.meshPrecursor Cell Lymphoblastic Leukemia-Lymphoma - Diagnosis - Geneticsen_US
dc.subject.meshSensitivity And Specificityen_US
dc.subject.meshSignal Transduction - Geneticsen_US
dc.subject.meshTelomere - Geneticsen_US
dc.subject.meshTranslocation, Genetic - Geneticsen_US
dc.titlePathogenesis of jumping translocations: A molecular cytogenetics studyen_US
dc.typeArticleen_US
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_US
dc.identifier.authorityChan, LC=rp00373en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.leukres.2004.01.021en_US
dc.identifier.pmid15289020en_US
dc.identifier.scopuseid_2-s2.0-3843134061en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3843134061&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume28en_US
dc.identifier.issue10en_US
dc.identifier.spage1075en_US
dc.identifier.epage1079en_US
dc.identifier.isiWOS:000223429800012-
dc.publisher.placeUnited Kingdomen_US

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