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Article: Adverse prognostic impact of CDKN2B hyper-methylation in acute promyelocytic leukemia

TitleAdverse prognostic impact of CDKN2B hyper-methylation in acute promyelocytic leukemia
Authors
Issue Date2006
PublisherInforma Healthcare. The Journal's web site is located at http://informahealthcare.com/loi/lal
Citation
Leukemia And Lymphoma, 2006, v. 47 n. 5, p. 815-825 How to Cite?
AbstractThe use of all-trans retinoic acid (ATRA) has markedly improved the survival of patients with acute promyelocytic leukemia (APL), making it potentially curable. However, the identification of prognostic markers predictive of durable remission remains an important aspect in risk-adjusted treatment algorithms. High presentation leucocyte count has been found to correlate with inferior disease-free-survival (DFS). However, recent studies have also shown aberrant promoter methylation of the CDKN2B (alias p15) gene to be a negative prognostic factor. Promoter methylation results in the formation of a repressor complex, leading to chromatin compaction and suppression of gene expression and is, therefore, an alternative mechanism of gene inactivation. CDKN2B, a cyclin-dependent kinase inhibitor, is a tumor suppressor gene inhibiting cell cycle progression. The CpG island inside the CDKN2B promoter is hyper-methylated in ∼50-60% of APL patients. CDKN2B methylation correlates negatively with DFS. As methylation-induced inactivation of CDKN2B pre-disposes to unchecked cellular proliferation, CDKN2B hyper-methylation is also associated with high presentation leucocyte count. Multivariate analysis in several studies, however, has shown that the negative prognostic impact of CDKN2B methylation is independent of its association with high leucocyte counts. Therefore, CDKN2B methylation is a potential prognostic factor that may be incorporated into a risk-stratified therapeutic strategy, which aims at achieving a cure with optimal amounts of treatment. © 2006 Taylor & Francis.
Persistent Identifierhttp://hdl.handle.net/10722/162985
ISSN
2015 Impact Factor: 3.093
2015 SCImago Journal Rankings: 1.202
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_US
dc.contributor.authorKwong, YLen_US
dc.date.accessioned2012-09-05T05:26:15Z-
dc.date.available2012-09-05T05:26:15Z-
dc.date.issued2006en_US
dc.identifier.citationLeukemia And Lymphoma, 2006, v. 47 n. 5, p. 815-825en_US
dc.identifier.issn1042-8194en_US
dc.identifier.urihttp://hdl.handle.net/10722/162985-
dc.description.abstractThe use of all-trans retinoic acid (ATRA) has markedly improved the survival of patients with acute promyelocytic leukemia (APL), making it potentially curable. However, the identification of prognostic markers predictive of durable remission remains an important aspect in risk-adjusted treatment algorithms. High presentation leucocyte count has been found to correlate with inferior disease-free-survival (DFS). However, recent studies have also shown aberrant promoter methylation of the CDKN2B (alias p15) gene to be a negative prognostic factor. Promoter methylation results in the formation of a repressor complex, leading to chromatin compaction and suppression of gene expression and is, therefore, an alternative mechanism of gene inactivation. CDKN2B, a cyclin-dependent kinase inhibitor, is a tumor suppressor gene inhibiting cell cycle progression. The CpG island inside the CDKN2B promoter is hyper-methylated in ∼50-60% of APL patients. CDKN2B methylation correlates negatively with DFS. As methylation-induced inactivation of CDKN2B pre-disposes to unchecked cellular proliferation, CDKN2B hyper-methylation is also associated with high presentation leucocyte count. Multivariate analysis in several studies, however, has shown that the negative prognostic impact of CDKN2B methylation is independent of its association with high leucocyte counts. Therefore, CDKN2B methylation is a potential prognostic factor that may be incorporated into a risk-stratified therapeutic strategy, which aims at achieving a cure with optimal amounts of treatment. © 2006 Taylor & Francis.en_US
dc.languageengen_US
dc.publisherInforma Healthcare. The Journal's web site is located at http://informahealthcare.com/loi/lalen_US
dc.relation.ispartofLeukemia and Lymphomaen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P15 - Geneticsen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshLeukemia, Promyelocytic, Acute - Diagnosis - Drug Therapy - Geneticsen_US
dc.subject.meshPrognosisen_US
dc.subject.meshPromoter Regions, Genetic - Geneticsen_US
dc.subject.meshRisk Assessmenten_US
dc.titleAdverse prognostic impact of CDKN2B hyper-methylation in acute promyelocytic leukemiaen_US
dc.typeArticleen_US
dc.identifier.emailChim, CS:jcschim@hku.hken_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.authorityChim, CS=rp00408en_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1080/10428190500513827en_US
dc.identifier.pmid16753865-
dc.identifier.scopuseid_2-s2.0-33744920104en_US
dc.identifier.hkuros121952-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33744920104&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume47en_US
dc.identifier.issue5en_US
dc.identifier.spage815en_US
dc.identifier.epage825en_US
dc.identifier.isiWOS:000238200600009-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChim, CS=7004597253en_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US
dc.identifier.citeulike679159-

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