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Article: Trisomy 21 and other chromosomal abnormalities in acute promyelocytic leukemia

TitleTrisomy 21 and other chromosomal abnormalities in acute promyelocytic leukemia
Authors
Issue Date2003
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2003, v. 140 n. 2, p. 170-173 How to Cite?
AbstractWe describe a case of acute promyelocytic leukemia (APL) with t(15;17)(q22;q12) and trisomy 21 as an additional change in a patient who died at relapse after achieving complete remission (CR) for the duration of 20 months. A survey of 42 cases of APL with cytogenetic study performed at our institution over the past 10 years showed 12 cases (28.6%) having chromosomal changes in addition to t(15;17). Trisomy 8 and trisomy 21 as additional changes were noted in 4 and 2 cases, respectively, with one patient showing both trisomies simultaneously. Two cases showed t(15;17) in hyperdiploid clones. Among the 10 patients with follow-up data, all eventually relapsed and none achieved continuous complete remission 1. Survival analysis performed in APL patients with adequate follow-up data showed no significant difference in overall and disease free survival between those with and without additional cytogenetic changes. After excluding cases with one induction death, the overall survival was significantly in favor of the group without additional cytogenetic abnormalities (P = 0.022). Late relapses may therefore be significantly more common in APL patients with additional cytogenetic abnormalities, and may not be reflected by analysis focused at three-year survival only. As APL is now considered a curable disease, any confirmed long-term survival impact of additional cytogenetic changes is expected to have important management implications. © 2003 Elsevier Science Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/88782
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWan, TSKen_HK
dc.contributor.authorMa, SKen_HK
dc.contributor.authorAu, WYen_HK
dc.contributor.authorLiu, HSYen_HK
dc.contributor.authorChan, JCWen_HK
dc.contributor.authorChan, LCen_HK
dc.date.accessioned2010-09-06T09:47:55Z-
dc.date.available2010-09-06T09:47:55Z-
dc.date.issued2003en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2003, v. 140 n. 2, p. 170-173en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88782-
dc.description.abstractWe describe a case of acute promyelocytic leukemia (APL) with t(15;17)(q22;q12) and trisomy 21 as an additional change in a patient who died at relapse after achieving complete remission (CR) for the duration of 20 months. A survey of 42 cases of APL with cytogenetic study performed at our institution over the past 10 years showed 12 cases (28.6%) having chromosomal changes in addition to t(15;17). Trisomy 8 and trisomy 21 as additional changes were noted in 4 and 2 cases, respectively, with one patient showing both trisomies simultaneously. Two cases showed t(15;17) in hyperdiploid clones. Among the 10 patients with follow-up data, all eventually relapsed and none achieved continuous complete remission 1. Survival analysis performed in APL patients with adequate follow-up data showed no significant difference in overall and disease free survival between those with and without additional cytogenetic changes. After excluding cases with one induction death, the overall survival was significantly in favor of the group without additional cytogenetic abnormalities (P = 0.022). Late relapses may therefore be significantly more common in APL patients with additional cytogenetic abnormalities, and may not be reflected by analysis focused at three-year survival only. As APL is now considered a curable disease, any confirmed long-term survival impact of additional cytogenetic changes is expected to have important management implications. © 2003 Elsevier Science Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_HK
dc.relation.ispartofCancer Genetics and Cytogeneticsen_HK
dc.rightsCancer Genetics and Cytogenetics. Copyright © Elsevier Inc.en_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAntineoplastic Agents - therapeutic useen_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshChromosome Bandingen_HK
dc.subject.meshChromosomes, Human, Pair 15 - ultrastructureen_HK
dc.subject.meshChromosomes, Human, Pair 17 - ultrastructureen_HK
dc.subject.meshChromosomes, Human, Pair 21en_HK
dc.subject.meshDeath, Suddenen_HK
dc.subject.meshFatal Outcomeen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHong Kong - epidemiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Promyelocytic, Acute - drug therapy - genetics - mortalityen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPulmonary Embolism - etiologyen_HK
dc.subject.meshRemission Inductionen_HK
dc.subject.meshRetrospective Studiesen_HK
dc.subject.meshSurvival Analysisen_HK
dc.subject.meshTranslocation, Geneticen_HK
dc.subject.meshTretinoin - therapeutic useen_HK
dc.subject.meshTrisomyen_HK
dc.titleTrisomy 21 and other chromosomal abnormalities in acute promyelocytic leukemiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=140&issue=2&spage=170&epage=173&date=2003&atitle=Trisomy+21+and+other+chromosomal+abnormalities+in+acute+promyelocytic+leukemiaen_HK
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0165-4608(02)00684-2en_HK
dc.identifier.pmid12645658-
dc.identifier.scopuseid_2-s2.0-0037438881en_HK
dc.identifier.hkuros76747en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037438881&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume140en_HK
dc.identifier.issue2en_HK
dc.identifier.spage170en_HK
dc.identifier.epage173en_HK
dc.identifier.isiWOS:000180762100014-
dc.publisher.placeUnited Statesen_HK

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