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Article: Epigenetic dysregulation of the DAP kinase/p14/HDM2/p53/Apaf-1 apoptosis pathway in acute leukaemias

TitleEpigenetic dysregulation of the DAP kinase/p14/HDM2/p53/Apaf-1 apoptosis pathway in acute leukaemias
Authors
Issue Date2008
PublisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/
Citation
Journal Of Clinical Pathology, 2008, v. 61 n. 7, p. 844-847 How to Cite?
AbstractBackground: Dysregulation of apoptosis is important in carcinogenesis. Aim and Methods: To analyse the potential inactivation of the DAP kinase/p14/HDM2/p53/Apaf-1 pathway by aberrant promoter methylation in acute leukaemias. Results: Of five leukaemic lines examined, p14 was unmethylated in Raji, HL60 and U937, but completely deleted in Jurkat and NB4. DAP kinase was totally methylated in Raji and NB4, but unmethylated in HL60, Jurkat and U937. Apaf-1 was unmethylated in all the lines. At diagnosis, DAP kinase methylation occurred in eight (25%) APL patients and none of the other AML patients (8/32 vs 0/50, p = 0.001). DAP kinase methylation was detected in four (16%) ALL patients. p14 and Apaf-1 methylation was not detected in any of the 32 cases of acute promyelocytic leukaemia (APL), 50 cases of other subtypes of acute myeloid leukaemia (AML), and 25 cases of acute lymphoblastic leukaemia. Conclusion: Among AML subtypes, DAP kinase is preferentially hypermethylated in APL.
Persistent Identifierhttp://hdl.handle.net/10722/59293
ISSN
2015 Impact Factor: 2.912
2015 SCImago Journal Rankings: 1.260
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorChan, WWLen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-05-31T03:47:09Z-
dc.date.available2010-05-31T03:47:09Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Clinical Pathology, 2008, v. 61 n. 7, p. 844-847en_HK
dc.identifier.issn0021-9746en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59293-
dc.description.abstractBackground: Dysregulation of apoptosis is important in carcinogenesis. Aim and Methods: To analyse the potential inactivation of the DAP kinase/p14/HDM2/p53/Apaf-1 pathway by aberrant promoter methylation in acute leukaemias. Results: Of five leukaemic lines examined, p14 was unmethylated in Raji, HL60 and U937, but completely deleted in Jurkat and NB4. DAP kinase was totally methylated in Raji and NB4, but unmethylated in HL60, Jurkat and U937. Apaf-1 was unmethylated in all the lines. At diagnosis, DAP kinase methylation occurred in eight (25%) APL patients and none of the other AML patients (8/32 vs 0/50, p = 0.001). DAP kinase methylation was detected in four (16%) ALL patients. p14 and Apaf-1 methylation was not detected in any of the 32 cases of acute promyelocytic leukaemia (APL), 50 cases of other subtypes of acute myeloid leukaemia (AML), and 25 cases of acute lymphoblastic leukaemia. Conclusion: Among AML subtypes, DAP kinase is preferentially hypermethylated in APL.en_HK
dc.languageengen_HK
dc.publisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/en_HK
dc.relation.ispartofJournal of Clinical Pathologyen_HK
dc.rightsJournal of Clinical Pathology. Copyright © B M J Publishing Group.en_HK
dc.titleEpigenetic dysregulation of the DAP kinase/p14/HDM2/p53/Apaf-1 apoptosis pathway in acute leukaemiasen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9746&volume=61&issue=7&spage=844&epage=7&date=2008&atitle=Epigenetic+dysregulation+of+the+DAP+kinase/p14/HDM2/p53/Apaf-1+apoptosis+pathway+in+acute+leukaemiasen_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1136/jcp.2007.047324en_HK
dc.identifier.scopuseid_2-s2.0-47049097078en_HK
dc.identifier.hkuros150361en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-47049097078&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume61en_HK
dc.identifier.issue7en_HK
dc.identifier.spage844en_HK
dc.identifier.epage847en_HK
dc.identifier.isiWOS:000257166400010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridChan, WWL=55040807500en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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