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Article: Infrequent Wnt inhibitory factor-1 (Wif-1) methylation in chronic lymphocytic leukemia

TitleInfrequent Wnt inhibitory factor-1 (Wif-1) methylation in chronic lymphocytic leukemia
Authors
KeywordsChinese
CLL
Methylation
Wif-1
Issue Date2006
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukres
Citation
Leukemia Research, 2006, v. 30 n. 9, p. 1135-1139 How to Cite?
AbstractThe Wnt pathway has been shown recently, to be activated in patients with chronic lymphocytic leukemia (CLL). This is the first study to examine the role of Wnt inhibitory factor-1 (Wif-1) methylation in the pathogenesis of haematolymphoid malignancies. Wif-1, a putative tumor suppressor, is a soluble negative regulator of the Wnt pathway activated in CLL. We studied the role of methylation of Wif-1 in 43 Chinese patients with CLL. At diagnosis, Wif-1 methylation was detected in 5/43 (11.6%) CLL marrow samples. Wif-1 methylation occurred more frequently in patients with advanced age (p = 0.059) but there was no correlation between Wif-1 methylation and sex, lymphocyte count and Rai stage at diagnosis. In conclusion, Wif-1 is infrequently methylated in CLL. Other factors leading to activation of the Wnt pathway warrant further study. © 2005 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76468
ISSN
2023 Impact Factor: 2.1
2023 SCImago Journal Rankings: 0.694
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.accessioned2010-09-06T07:21:33Z-
dc.date.available2010-09-06T07:21:33Z-
dc.date.issued2006en_HK
dc.identifier.citationLeukemia Research, 2006, v. 30 n. 9, p. 1135-1139en_HK
dc.identifier.issn0145-2126en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76468-
dc.description.abstractThe Wnt pathway has been shown recently, to be activated in patients with chronic lymphocytic leukemia (CLL). This is the first study to examine the role of Wnt inhibitory factor-1 (Wif-1) methylation in the pathogenesis of haematolymphoid malignancies. Wif-1, a putative tumor suppressor, is a soluble negative regulator of the Wnt pathway activated in CLL. We studied the role of methylation of Wif-1 in 43 Chinese patients with CLL. At diagnosis, Wif-1 methylation was detected in 5/43 (11.6%) CLL marrow samples. Wif-1 methylation occurred more frequently in patients with advanced age (p = 0.059) but there was no correlation between Wif-1 methylation and sex, lymphocyte count and Rai stage at diagnosis. In conclusion, Wif-1 is infrequently methylated in CLL. Other factors leading to activation of the Wnt pathway warrant further study. © 2005 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukresen_HK
dc.relation.ispartofLeukemia Researchen_HK
dc.subjectChinese-
dc.subjectCLL-
dc.subjectMethylation-
dc.subjectWif-1-
dc.subject.meshAdaptor Proteins, Signal Transducingen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshAsian Continental Ancestry Groupen_HK
dc.subject.meshCarrier Proteins - geneticsen_HK
dc.subject.meshChinaen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenes, Tumor Suppressoren_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Lymphocytic, Chronic, B-Cell - genetics - pathology - physiopathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshRepressor Proteins - geneticsen_HK
dc.subject.meshWnt Proteins - geneticsen_HK
dc.titleInfrequent Wnt inhibitory factor-1 (Wif-1) methylation in chronic lymphocytic leukemiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0145-2126&volume=30&issue=9&spage=1135&epage=9&date=2006&atitle=Infrequent+Wnt+inhibitory+factor-1+(Wif-1)+methylation+in+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.doi10.1016/j.leukres.2005.12.005en_HK
dc.identifier.pmid16427695en_HK
dc.identifier.scopuseid_2-s2.0-33745823867en_HK
dc.identifier.hkuros121976en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745823867&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1135en_HK
dc.identifier.epage1139en_HK
dc.identifier.isiWOS:000239620500015-
dc.publisher.placeUnited Kingdomen_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
dc.identifier.issnl0145-2126-

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