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Article: Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: Clinicopathological and karyotypic associations

TitleAberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: Clinicopathological and karyotypic associations
Authors
Keywordsp15 methylation
Therapy-related acute myeloid leukaemia/myelodysplasia
Issue Date2003
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJH
Citation
British Journal of Haematology, 2003, v. 120 n. 6, p. 1062-1065 How to Cite?
AbstractSeventeen patients with therapy-related myelodysplastic syndrome/acute myeloid leukaemia (t-MDS/AML) were examined for aberrant p15 gene methylation by methylation-specific polymerase chain reaction. Ten patients (58%) showed p15 methylation, which was significantly related to monosomy/deletion of chromosome 7q, but not to antecedent chemotherapy, blast count, leukaemic evolution or survival. In three of six patients with marrow samples obtained prior to the diagnosis of t-MDS/AML, p15 methylation predated disease development by up to 2 years. Bone marrow transplantation led to the disappearance of p15 methylation in one patient. These results showed that p15 methylation was an early event in the evolution of some t-MDS/AML patients.
Persistent Identifierhttp://hdl.handle.net/10722/77451
ISSN
2021 Impact Factor: 8.615
2020 SCImago Journal Rankings: 1.907
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAu, WYen_HK
dc.contributor.authorFung, Aen_HK
dc.contributor.authorMan, Cen_HK
dc.contributor.authorMa, SKen_HK
dc.contributor.authorWan, TSen_HK
dc.contributor.authorLiang, Ren_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:32:02Z-
dc.date.available2010-09-06T07:32:02Z-
dc.date.issued2003en_HK
dc.identifier.citationBritish Journal of Haematology, 2003, v. 120 n. 6, p. 1062-1065en_HK
dc.identifier.issn0007-1048en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77451-
dc.description.abstractSeventeen patients with therapy-related myelodysplastic syndrome/acute myeloid leukaemia (t-MDS/AML) were examined for aberrant p15 gene methylation by methylation-specific polymerase chain reaction. Ten patients (58%) showed p15 methylation, which was significantly related to monosomy/deletion of chromosome 7q, but not to antecedent chemotherapy, blast count, leukaemic evolution or survival. In three of six patients with marrow samples obtained prior to the diagnosis of t-MDS/AML, p15 methylation predated disease development by up to 2 years. Bone marrow transplantation led to the disappearance of p15 methylation in one patient. These results showed that p15 methylation was an early event in the evolution of some t-MDS/AML patients.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJHen_HK
dc.relation.ispartofBritish Journal of Haematologyen_HK
dc.subjectp15 methylation-
dc.subjectTherapy-related acute myeloid leukaemia/myelodysplasia-
dc.subject.meshAcute Diseaseen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshBone Marrow Transplantationen_HK
dc.subject.meshCell Cycle Proteinsen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p15en_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Myeloid - genetics - metabolism - therapyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMyelodysplastic Syndromes - genetics - metabolism - therapyen_HK
dc.subject.meshPolymerase Chain Reaction - methodsen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTranscription Factors - geneticsen_HK
dc.subject.meshTumor Suppressor Proteinsen_HK
dc.titleAberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: Clinicopathological and karyotypic associationsen_HK
dc.typeArticleen_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1046/j.1365-2141.2003.04194.xen_HK
dc.identifier.pmid12648079-
dc.identifier.scopuseid_2-s2.0-0037356973en_HK
dc.identifier.hkuros108947en_HK
dc.identifier.hkuros77791-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037356973&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume120en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1062en_HK
dc.identifier.epage1065en_HK
dc.identifier.isiWOS:000181633900020-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridAu, WY=7202383089en_HK
dc.identifier.scopusauthoridFung, A=7101926728en_HK
dc.identifier.scopusauthoridMan, C=7005722377en_HK
dc.identifier.scopusauthoridMa, SK=37020910400en_HK
dc.identifier.scopusauthoridWan, TS=25623981600en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.issnl0007-1048-

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