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Article: Translocation (3;5)(q21;q34) in erythroleukemia: A molecular and in situ hybridization study

TitleTranslocation (3;5)(q21;q34) in erythroleukemia: A molecular and in situ hybridization study
Authors
Issue Date1998
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 1998, v. 103 n. 1, p. 15-19 How to Cite?
AbstractTranslocation (3;5) is an uncommon karyotypic aberration in acute myeloid leukemia (AML). With the exception of M3, t(3;5) has been reported in every other subtype of AML, being most frequently associated with AML M6. Although a variety of breakpoints have been described, it has been suggested that the breakpoints in t(3;5) of all the reported cases should be assigned to 3q25.1 and 5q34. Recently, the breakpoints in three pediatric cases of AML M2 with t(3;5) were cloned and shown to involve the myelodysplasia/myeloid leukemia factor I (MLF1) gene on 3q25.1 and the nucleophosmin (NPM) gene on 5q34, generating a chimeric NPM/MLF1 transcript. An adult case of indolent erythroleukemia was found on karyotypic analysis to have t(3;5)(q21;q34). In about 60% of cells, the translocation was unbalanced, resulting in loss of the der(3) chromosome, implying that the critical leukemogenic sequence might reside on the der(5) chromosome. Molecular analysis of this case, however, failed to show rearrangement of the NPM gene and an MLF1/NPM transcript. A review of other reported cases of AML M6 with t(3;5) showed that the commonest breakpoint on chromosome 3 was also assigned to 3q21, as in our case. The considerable clinical, pathologic, cytogenetic and molecular differences observed in AML with t(3;5) suggest that these cases might be heterogeneous.
Persistent Identifierhttp://hdl.handle.net/10722/162252
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwong, YLen_US
dc.date.accessioned2012-09-05T05:18:24Z-
dc.date.available2012-09-05T05:18:24Z-
dc.date.issued1998en_US
dc.identifier.citationCancer Genetics And Cytogenetics, 1998, v. 103 n. 1, p. 15-19en_US
dc.identifier.issn0165-4608en_US
dc.identifier.urihttp://hdl.handle.net/10722/162252-
dc.description.abstractTranslocation (3;5) is an uncommon karyotypic aberration in acute myeloid leukemia (AML). With the exception of M3, t(3;5) has been reported in every other subtype of AML, being most frequently associated with AML M6. Although a variety of breakpoints have been described, it has been suggested that the breakpoints in t(3;5) of all the reported cases should be assigned to 3q25.1 and 5q34. Recently, the breakpoints in three pediatric cases of AML M2 with t(3;5) were cloned and shown to involve the myelodysplasia/myeloid leukemia factor I (MLF1) gene on 3q25.1 and the nucleophosmin (NPM) gene on 5q34, generating a chimeric NPM/MLF1 transcript. An adult case of indolent erythroleukemia was found on karyotypic analysis to have t(3;5)(q21;q34). In about 60% of cells, the translocation was unbalanced, resulting in loss of the der(3) chromosome, implying that the critical leukemogenic sequence might reside on the der(5) chromosome. Molecular analysis of this case, however, failed to show rearrangement of the NPM gene and an MLF1/NPM transcript. A review of other reported cases of AML M6 with t(3;5) showed that the commonest breakpoint on chromosome 3 was also assigned to 3q21, as in our case. The considerable clinical, pathologic, cytogenetic and molecular differences observed in AML with t(3;5) suggest that these cases might be heterogeneous.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_US
dc.relation.ispartofCancer Genetics and Cytogeneticsen_US
dc.rightsCancer Genetics and Cytogenetics. Copyright © Elsevier Inc.-
dc.subject.meshAgeden_US
dc.subject.meshBlotting, Southernen_US
dc.subject.meshChromosomes, Human, Pair 3 - Geneticsen_US
dc.subject.meshChromosomes, Human, Pair 5 - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshKaryotypingen_US
dc.subject.meshLeukemia, Erythroblastic, Acute - Genetics - Metabolism - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshPolymorphism, Restriction Fragment Lengthen_US
dc.subject.meshTranslocation, Genetic - Geneticsen_US
dc.titleTranslocation (3;5)(q21;q34) in erythroleukemia: A molecular and in situ hybridization studyen_US
dc.typeArticleen_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0165-4608(97)00366-Xen_US
dc.identifier.pmid9595039-
dc.identifier.scopuseid_2-s2.0-0032078826en_US
dc.identifier.hkuros41944-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032078826&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume103en_US
dc.identifier.issue1en_US
dc.identifier.spage15en_US
dc.identifier.epage19en_US
dc.identifier.isiWOS:000073410600004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US

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