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Article: Analysis of cell cycle regulators: p161NK4A, pRb, and CDK4 in low- and high-grade meningiomas

TitleAnalysis of cell cycle regulators: p161NK4A, pRb, and CDK4 in low- and high-grade meningiomas
Authors
KeywordsMeningioma
Methylation
P16INK4A
Issue Date1998
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath
Citation
Human Pathology, 1998, v. 29 n. 11, p. 1200-1207 How to Cite?
AbstractAbnormalities in the p16INK4A, CDK4, and Rb genes, which regulate transition through G1 phase of the cell cycle, have been implicated in the progression of diverse types of cancer. To evaluate the involvement of p16INK4A, CDK4, and Rb in the tumorigenesis of meningiomas, the status of these genes or gene products were examined. The genetic alteration of the p16INK4A gene was examined by homozygous deletions and by mutation analysis. The methylation status of the p16INK4A was determined by Southern blotting. Neither homozygous deletions nor point mutations of the p16INK4A gene were observed in any of the 23 meningiomas. Partial rather than complete methylation of the p16INK4A gene at SacII or SmaI sites was shown in five (23.8%) meningiomas. The methylation status of the p16INK4A gene was not consistently associated with the expression of p16INK4A in meningiomas. These results suggest that the true relationship between methylation and expression of p16INK4A may be obscured in a complex manner by various mechanisms that regulate p16INK4A expression. Aberrant expressions of pRb and CDK4 were not observed in any of the meningiomas we examined, indicating that abnormalities of the pRb and CDK4 appear to be rare in meningiomas.
Persistent Identifierhttp://hdl.handle.net/10722/92178
ISSN
2015 Impact Factor: 2.791
2015 SCImago Journal Rankings: 1.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTse, JYMen_HK
dc.contributor.authorNg, HKen_HK
dc.contributor.authorLo, KWen_HK
dc.contributor.authorChong, EYYen_HK
dc.contributor.authorLam, PYPen_HK
dc.contributor.authorNg, EKOen_HK
dc.contributor.authorPoon, WSen_HK
dc.contributor.authorHuang, DPen_HK
dc.date.accessioned2010-09-17T10:38:22Z-
dc.date.available2010-09-17T10:38:22Z-
dc.date.issued1998en_HK
dc.identifier.citationHuman Pathology, 1998, v. 29 n. 11, p. 1200-1207en_HK
dc.identifier.issn0046-8177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92178-
dc.description.abstractAbnormalities in the p16INK4A, CDK4, and Rb genes, which regulate transition through G1 phase of the cell cycle, have been implicated in the progression of diverse types of cancer. To evaluate the involvement of p16INK4A, CDK4, and Rb in the tumorigenesis of meningiomas, the status of these genes or gene products were examined. The genetic alteration of the p16INK4A gene was examined by homozygous deletions and by mutation analysis. The methylation status of the p16INK4A was determined by Southern blotting. Neither homozygous deletions nor point mutations of the p16INK4A gene were observed in any of the 23 meningiomas. Partial rather than complete methylation of the p16INK4A gene at SacII or SmaI sites was shown in five (23.8%) meningiomas. The methylation status of the p16INK4A gene was not consistently associated with the expression of p16INK4A in meningiomas. These results suggest that the true relationship between methylation and expression of p16INK4A may be obscured in a complex manner by various mechanisms that regulate p16INK4A expression. Aberrant expressions of pRb and CDK4 were not observed in any of the meningiomas we examined, indicating that abnormalities of the pRb and CDK4 appear to be rare in meningiomas.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpathen_HK
dc.relation.ispartofHuman Pathologyen_HK
dc.subjectMeningiomaen_HK
dc.subjectMethylationen_HK
dc.subjectP16INK4Aen_HK
dc.titleAnalysis of cell cycle regulators: p161NK4A, pRb, and CDK4 in low- and high-grade meningiomasen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, EKO: ngko@hku.hken_HK
dc.identifier.authorityNg, EKO=rp01364en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid9824096-
dc.identifier.scopuseid_2-s2.0-0031728720en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031728720&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1200en_HK
dc.identifier.epage1207en_HK
dc.identifier.isiWOS:000076903000005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTse, JYM=36928242900en_HK
dc.identifier.scopusauthoridNg, HK=7401619354en_HK
dc.identifier.scopusauthoridLo, KW=7402101603en_HK
dc.identifier.scopusauthoridChong, EYY=7005870640en_HK
dc.identifier.scopusauthoridLam, PYP=24474907100en_HK
dc.identifier.scopusauthoridNg, EKO=21135553700en_HK
dc.identifier.scopusauthoridPoon, WS=7103025507en_HK
dc.identifier.scopusauthoridHuang, DP=7403891486en_HK

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