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Article: Serial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxide

TitleSerial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxide
Authors
Au, WYFung, ATMa, ESChan, CHWong, KFChim, CSLiang, RHKwong, YL
KeywordsAcute promyelocytic leukaemia
CDKN2A
CDKN2B
Methylation
Issue Date2005
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJH
Citation
British Journal Of Haematology, 2005, v. 131 n. 5, p. 632-635 How to Cite?
DOI: http://dx.doi.org/10.1111/j.1365-2141.2005.05818.x
AbstractNinety consecutive patients with acute promyelocytic leukaemia were investigated for promoter methylation of CDKN2B (alias p15) and CDKN2A (alias p16) in disease relapse and progression. CDKN2B methylation was significantly more frequent at first relapse (30/36, 83%) than at presentation (48/77, 62%) (P = 0·025), while CDKN2A methylation appeared unaffected. Both acquisition and loss of CDKN2B methylation happened at relapse, with acquisition more frequent. No significant increase in CDKN2B and CDKN2A methylation occurred at more advanced relapses. At first or subsequent relapses, owing to highly effective salvage by arsenic trioxide, CDKN2B methylation did not impact on event-free survival or overall survival. © 2005 Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/77104
ISSN
0007-1048
2023 Impact Factor: 5.1
2023 SCImago Journal Rankings: 1.574
ISI Accession Number ID
WOS:000233988000009
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorAu, WYen_HK
dc.contributor.authorFung, ATen_HK
dc.contributor.authorMa, ESen_HK
dc.contributor.authorChan, CHen_HK
dc.contributor.authorWong, KFen_HK
dc.contributor.authorChim, CSen_HK
dc.contributor.authorLiang, RHen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:28:18Z-
dc.date.available2010-09-06T07:28:18Z-
dc.date.issued2005en_HK
dc.identifier.citationBritish Journal Of Haematology, 2005, v. 131 n. 5, p. 632-635en_HK
dc.identifier.issn0007-1048en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77104-
dc.description.abstractNinety consecutive patients with acute promyelocytic leukaemia were investigated for promoter methylation of CDKN2B (alias p15) and CDKN2A (alias p16) in disease relapse and progression. CDKN2B methylation was significantly more frequent at first relapse (30/36, 83%) than at presentation (48/77, 62%) (P = 0·025), while CDKN2A methylation appeared unaffected. Both acquisition and loss of CDKN2B methylation happened at relapse, with acquisition more frequent. No significant increase in CDKN2B and CDKN2A methylation occurred at more advanced relapses. At first or subsequent relapses, owing to highly effective salvage by arsenic trioxide, CDKN2B methylation did not impact on event-free survival or overall survival. © 2005 Blackwell Publishing Ltd.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.rightsBritish Journal of Haematology. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectAcute promyelocytic leukaemiaen_HK
dc.subjectCDKN2Aen_HK
dc.subjectCDKN2Ben_HK
dc.subjectMethylationen_HK
dc.titleSerial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxideen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1048&volume=131&issue=5&spage=632&epage=5&date=2005&atitle=Serial+studies+of+methylation+of+CDKN2B+and+CDKN2A+in+relapsed+acute+promyelocytic+leukaemia+treated+with+arsenic+trioxideen_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.emailLiang, RH:rliang@hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.identifier.authorityLiang, RH=rp00345en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2141.2005.05818.xen_HK
dc.identifier.scopuseid_2-s2.0-33644795400en_HK
dc.identifier.hkuros119554en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33644795400&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume131en_HK
dc.identifier.issue5en_HK
dc.identifier.spage632en_HK
dc.identifier.epage635en_HK
dc.identifier.isiWOS:000233988000009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridAu, WY=7202383089en_HK
dc.identifier.scopusauthoridFung, AT=7101926728en_HK
dc.identifier.scopusauthoridMa, ES=7202039934en_HK
dc.identifier.scopusauthoridChan, CH=9940314800en_HK
dc.identifier.scopusauthoridWong, KF=7404759860en_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridLiang, RH=26643224900en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.citeulike401339-
dc.identifier.issnl0007-1048-

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