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Article: Characterization of additional genetic events in childhood acute lymphoblastic leukemia with TEL/AML1 gene fusion: A molecular cytogenetics study

TitleCharacterization of additional genetic events in childhood acute lymphoblastic leukemia with TEL/AML1 gene fusion: A molecular cytogenetics study
Authors
KeywordsAML1 amplification
Childhood ALL
Molecular cytogenetics
TEL/AML1 fusion
Issue Date2001
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leu
Citation
Leukemia, 2001, v. 15 n. 9, p. 1442-1447 How to Cite?
AbstractTEL/AML1 gene fusion that results from a cryptic t(12;21) is the most common genetic aberration in childhood B-lineage acute lymphoblastic leukemia (ALL). While the translocation may initiate the leukemic process, critical secondary genetic events are currently believed to be pivotal for leukemogenesis. We investigated 12 cases of childhood ALL with TEL/AML1 gene fusion by fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH) and documented additional or secondary genetic changes in seven patients (58%). Three patients showed extra copies of chromosome 21 including a case in which the trisomy 21 (+21) clone was distinct from the one harboring TEL/AML1 gene fusion. Interestingly, one patient without +21 showed amplification of the AML1 gene on chromosome 21q, supporting the contention that AML1 amplification may be an important additional genetic event. Gene expression study by semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR) in two of these four patients showed an increase in AML1 transcripts that paralleled the increase in gene copy number. Deletion of the normal TEL allele was detected in two patients, with one of them showing loss of chromosome 12 together with duplication of the der(12)t(12;21). Finally, one patient showed duplication of the fusion signal. Our findings confirm that additional or secondary genetic changes including AML1 amplification are commonly encountered in childhood ALL with TEL/AML1 gene fusion, which are envisaged to play significant roles in disease progression.
Persistent Identifierhttp://hdl.handle.net/10722/148221
ISSN
2015 Impact Factor: 12.104
2015 SCImago Journal Rankings: 5.142
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMa, SKen_HK
dc.contributor.authorWan, TSKen_HK
dc.contributor.authorCheuk, ATCen_HK
dc.contributor.authorFung, LFen_HK
dc.contributor.authorChan, GCFen_HK
dc.contributor.authorChan, SYen_HK
dc.contributor.authorHa, SYen_HK
dc.contributor.authorChan, LCen_HK
dc.date.accessioned2012-05-29T06:11:35Z-
dc.date.available2012-05-29T06:11:35Z-
dc.date.issued2001en_HK
dc.identifier.citationLeukemia, 2001, v. 15 n. 9, p. 1442-1447en_HK
dc.identifier.issn0887-6924en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148221-
dc.description.abstractTEL/AML1 gene fusion that results from a cryptic t(12;21) is the most common genetic aberration in childhood B-lineage acute lymphoblastic leukemia (ALL). While the translocation may initiate the leukemic process, critical secondary genetic events are currently believed to be pivotal for leukemogenesis. We investigated 12 cases of childhood ALL with TEL/AML1 gene fusion by fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH) and documented additional or secondary genetic changes in seven patients (58%). Three patients showed extra copies of chromosome 21 including a case in which the trisomy 21 (+21) clone was distinct from the one harboring TEL/AML1 gene fusion. Interestingly, one patient without +21 showed amplification of the AML1 gene on chromosome 21q, supporting the contention that AML1 amplification may be an important additional genetic event. Gene expression study by semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR) in two of these four patients showed an increase in AML1 transcripts that paralleled the increase in gene copy number. Deletion of the normal TEL allele was detected in two patients, with one of them showing loss of chromosome 12 together with duplication of the der(12)t(12;21). Finally, one patient showed duplication of the fusion signal. Our findings confirm that additional or secondary genetic changes including AML1 amplification are commonly encountered in childhood ALL with TEL/AML1 gene fusion, which are envisaged to play significant roles in disease progression.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leuen_HK
dc.relation.ispartofLeukemiaen_HK
dc.subjectAML1 amplificationen_HK
dc.subjectChildhood ALLen_HK
dc.subjectMolecular cytogeneticsen_HK
dc.subjectTEL/AML1 fusionen_HK
dc.subject.meshAdolescenten_US
dc.subject.meshArtificial Gene Fusionen_US
dc.subject.meshChilden_US
dc.subject.meshChild, Preschoolen_US
dc.subject.meshCohort Studiesen_US
dc.subject.meshCore Binding Factor Alpha 2 Subuniten_US
dc.subject.meshDna-Binding Proteins - Geneticsen_US
dc.subject.meshDown Syndrome - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunophenotypingen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshKaryotypingen_US
dc.subject.meshMaleen_US
dc.subject.meshPrecursor Cell Lymphoblastic Leukemia-Lymphoma - Geneticsen_US
dc.subject.meshProto-Oncogene Proteinsen_US
dc.subject.meshProto-Oncogene Proteins C-Etsen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTranscription Factors - Geneticsen_US
dc.titleCharacterization of additional genetic events in childhood acute lymphoblastic leukemia with TEL/AML1 gene fusion: A molecular cytogenetics studyen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, GCF:gcfchan@hkucc.hku.hken_HK
dc.identifier.emailChan, SY:sychan@hkucc.hku.hken_HK
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_HK
dc.identifier.authorityChan, GCF=rp00431en_HK
dc.identifier.authorityChan, SY=rp00356en_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.leu.2402202en_HK
dc.identifier.pmid11516105-
dc.identifier.scopuseid_2-s2.0-0034854751en_HK
dc.identifier.hkuros63382-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034854751&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1442en_HK
dc.identifier.epage1447en_HK
dc.identifier.isiWOS:000170639900015-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMa, SK=9042504200en_HK
dc.identifier.scopusauthoridWan, TSK=25623981600en_HK
dc.identifier.scopusauthoridCheuk, ATC=25646034500en_HK
dc.identifier.scopusauthoridFung, LF=35910298200en_HK
dc.identifier.scopusauthoridChan, GCF=16160154400en_HK
dc.identifier.scopusauthoridChan, SY=7404255082en_HK
dc.identifier.scopusauthoridHa, SY=7202501115en_HK
dc.identifier.scopusauthoridChan, LC=7403540707en_HK

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