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Article: Low frequency of FLT3 gene internal tandem duplication and activating loop mutation in therapy-related acute myelocyticleukemia and myelodysplastic syndrome

TitleLow frequency of FLT3 gene internal tandem duplication and activating loop mutation in therapy-related acute myelocyticleukemia and myelodysplastic syndrome
Authors
Issue Date2004
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2004, v. 149 n. 2, p. 169-172 How to Cite?
AbstractFLT3 gene internal tandem duplication (ITD) and activating loop mutations (D835) were determined in 22 cases of therapy-related acute myelocytic leukemia/myelodysplastic syndrome (t-AML/MDS) and 102 cases of de novo AML/MDS. In t-AML/MDS, FLT3 ITD was absent, and D835 was found in only one case of therapy-related acute promyelocytic leukemia (APL). In de novo AML/MDS, however, FLT3 ITD and D835 were significantly more frequent (28 of 102 cases, P=0.024) and were associated with high peripheral blood and marrow blast counts. Our results suggest that different pathogenetic pathways might be involved in t-AML/MDS and de novo AML/MDS. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78342
ISSN
2012 Impact Factor: 1.929
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAu, WYen_HK
dc.contributor.authorFung, ATen_HK
dc.contributor.authorMa, ESen_HK
dc.contributor.authorLiang, RHen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:41:49Z-
dc.date.available2010-09-06T07:41:49Z-
dc.date.issued2004en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2004, v. 149 n. 2, p. 169-172en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78342-
dc.description.abstractFLT3 gene internal tandem duplication (ITD) and activating loop mutations (D835) were determined in 22 cases of therapy-related acute myelocytic leukemia/myelodysplastic syndrome (t-AML/MDS) and 102 cases of de novo AML/MDS. In t-AML/MDS, FLT3 ITD was absent, and D835 was found in only one case of therapy-related acute promyelocytic leukemia (APL). In de novo AML/MDS, however, FLT3 ITD and D835 were significantly more frequent (28 of 102 cases, P=0.024) and were associated with high peripheral blood and marrow blast counts. Our results suggest that different pathogenetic pathways might be involved in t-AML/MDS and de novo AML/MDS. © 2004 Elsevier 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.meshAgeden_HK
dc.subject.meshChilden_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Duplicationen_HK
dc.subject.meshGene Frequencyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Myeloid, Acute - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMutationen_HK
dc.subject.meshMyelodysplastic Syndromes - geneticsen_HK
dc.subject.meshProto-Oncogene Proteins - geneticsen_HK
dc.subject.meshReceptor Protein-Tyrosine Kinases - geneticsen_HK
dc.subject.meshfms-Like Tyrosine Kinase 3en_HK
dc.titleLow frequency of FLT3 gene internal tandem duplication and activating loop mutation in therapy-related acute myelocyticleukemia and myelodysplastic syndromeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=149&issue=2&spage=169&epage=172 &date=2004&atitle=Low+frequency+of+FLT3+gene+internal+tandem+duplication+and+activating+loop+mutation+in+therapy-related+acute+myelocyticleukemia+and+myelodysplastic+syndromeen_HK
dc.identifier.emailLiang, RH:rliang@hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.authorityLiang, RH=rp00345en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cancergencyto.2003.07.007en_HK
dc.identifier.pmid15036894en_HK
dc.identifier.scopuseid_2-s2.0-1442299812en_HK
dc.identifier.hkuros87387en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1442299812&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume149en_HK
dc.identifier.issue2en_HK
dc.identifier.spage169en_HK
dc.identifier.epage172en_HK
dc.identifier.isiWOS:000220343100012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridAu, WY=7202383089en_HK
dc.identifier.scopusauthoridFung, AT=7101926728en_HK
dc.identifier.scopusauthoridMa, ES=7202039934en_HK
dc.identifier.scopusauthoridLiang, RH=26643224900en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.issnl0165-4608-

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