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Article: Frequent DAP kinase but not p14 or Apaf-1 hypermethylation in B-cell chronic lymphocytic leukemia

TitleFrequent DAP kinase but not p14 or Apaf-1 hypermethylation in B-cell chronic lymphocytic leukemia
Authors
Issue Date2006
PublisherSpringer Japan. The Journal's web site is located at http://link.springer.de/link/service/journals/10038/index.htm
Citation
Journal Of Human Genetics, 2006, v. 51 n. 9, p. 832-838 How to Cite?
AbstractDysregulation of apoptosis, and thus the p14/DAP kinase/HDM2/p53/Apaf-1 pathway, is potentially important in carcinogenesis. Chronic lymphocytic leukemia (CLL), uncommon in the Chinese, is a disease characterized by impaired apoptosis, of the neoplastic lymphocytes. Hypermethylation of p14, DAP kinase and Apaf-1 was studied by methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) alleles in 50 diagnostic marrow samples from patients with CLL. Chinese CLL patients had an indolent course similar to Caucasians with median overall survival (OS) of 96 months, which was adversely affected by advanced Rai stage (projected 5-year OS = 72% and 39% for Rai ≤ 2 and Rai > 2; P = 0.01). DAP kinase was methylated in 18 (36%) patients while p14 and Apaf-1 were completely unmethylated in all the primary CLL samples. There was no correlation between DAP kinase hypermethylation and age, sex, poor-risk karyotype, lymphocyte count and Rai stage at diagnosis. Projected OS for patients with and without DAP kinase hypermethylation were 59 and 57% (P = 0.91). DAP kinase, but not p14 and Apaf-1, of the DAP kinase/p14/HDM2/p53/Apaf-1 pathway is frequently hypermethylated in CLL, but not of prognostic significance. Moreover Chinese patients with CLL share a similarly indolent clinical course, and this is the first comprehensive study on p14, DAP kinase and Apaf-1 hypermethylation in CLL. © The Japan Society of Human Genetics and Springer-Verlag 2006.
Persistent Identifierhttp://hdl.handle.net/10722/78122
ISSN
2015 Impact Factor: 2.487
2015 SCImago Journal Rankings: 1.416
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorFung, TKen_HK
dc.contributor.authorWong, KFen_HK
dc.contributor.authorLau, JSen_HK
dc.contributor.authorLiang, Ren_HK
dc.date.accessioned2010-09-06T07:39:24Z-
dc.date.available2010-09-06T07:39:24Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Human Genetics, 2006, v. 51 n. 9, p. 832-838en_HK
dc.identifier.issn1434-5161en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78122-
dc.description.abstractDysregulation of apoptosis, and thus the p14/DAP kinase/HDM2/p53/Apaf-1 pathway, is potentially important in carcinogenesis. Chronic lymphocytic leukemia (CLL), uncommon in the Chinese, is a disease characterized by impaired apoptosis, of the neoplastic lymphocytes. Hypermethylation of p14, DAP kinase and Apaf-1 was studied by methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) alleles in 50 diagnostic marrow samples from patients with CLL. Chinese CLL patients had an indolent course similar to Caucasians with median overall survival (OS) of 96 months, which was adversely affected by advanced Rai stage (projected 5-year OS = 72% and 39% for Rai ≤ 2 and Rai > 2; P = 0.01). DAP kinase was methylated in 18 (36%) patients while p14 and Apaf-1 were completely unmethylated in all the primary CLL samples. There was no correlation between DAP kinase hypermethylation and age, sex, poor-risk karyotype, lymphocyte count and Rai stage at diagnosis. Projected OS for patients with and without DAP kinase hypermethylation were 59 and 57% (P = 0.91). DAP kinase, but not p14 and Apaf-1, of the DAP kinase/p14/HDM2/p53/Apaf-1 pathway is frequently hypermethylated in CLL, but not of prognostic significance. Moreover Chinese patients with CLL share a similarly indolent clinical course, and this is the first comprehensive study on p14, DAP kinase and Apaf-1 hypermethylation in CLL. © The Japan Society of Human Genetics and Springer-Verlag 2006.en_HK
dc.languageengen_HK
dc.publisherSpringer Japan. The Journal's web site is located at http://link.springer.de/link/service/journals/10038/index.htmen_HK
dc.relation.ispartofJournal of Human Geneticsen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshApoptosis Regulatory Proteins - geneticsen_HK
dc.subject.meshApoptotic Protease-Activating Factor 1en_HK
dc.subject.meshAsian Continental Ancestry Group - geneticsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCalcium-Calmodulin-Dependent Protein Kinases - geneticsen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA, Neoplasm - chemistry - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteins - geneticsen_HK
dc.subject.meshLeukemia, Lymphocytic, Chronic, B-Cell - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshProteins - geneticsen_HK
dc.subject.meshProto-Oncogene Proteins c-mdm2 - geneticsen_HK
dc.subject.meshTumor Suppressor Protein p14ARF - geneticsen_HK
dc.titleFrequent DAP kinase but not p14 or Apaf-1 hypermethylation in B-cell chronic lymphocytic leukemiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1434-5161&volume=9&spage=832&epage=8&date=2006&atitle=Frequent+DAP+kinase+but+not+p14+or+Apaf-1+hypermethylation+in+B-cell+chronic+lymphocytic+leukemiaen_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10038-006-0029-xen_HK
dc.identifier.pmid16897188-
dc.identifier.scopuseid_2-s2.0-33748657136en_HK
dc.identifier.hkuros121951en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33748657136&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume51en_HK
dc.identifier.issue9en_HK
dc.identifier.spage832en_HK
dc.identifier.epage838en_HK
dc.identifier.isiWOS:000240469700015-
dc.publisher.placeJapanen_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridFung, TK=7102715924en_HK
dc.identifier.scopusauthoridWong, KF=7404759860en_HK
dc.identifier.scopusauthoridLau, JS=36903981300en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK

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