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Article: Nasopharyngeal carcinomas frequently lack the p16/MTS1 tumor suppressor protein but consistently express the retinoblastoma gene product

TitleNasopharyngeal carcinomas frequently lack the p16/MTS1 tumor suppressor protein but consistently express the retinoblastoma gene product
Authors
Issue Date1998
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 1998, v. 152 n. 4, p. 865-869 How to Cite?
AbstractThe p16/MTS1 gene is altered by deletion, mutation, or hypermethylation in a wide variety of human cancers. As a result of deficient p16 protein, these cancers lack a critical mechanism for halting G1/S cell cycle progression. In the current study, 59 cases of nasopharyngeal carcinoma were evaluated for expression of the p16 rumor suppressor protein by immunohistochemical analysis of paraffin-embedded tissue. There was no detectable p16 in 38/59 cases (64%), which implies a very high rate of p16 inactivation in this type of cancer. On the other hand, the retinoblastoma gene product, which also regulates the G1 to S phase transition of the cell cycle, was consistently expressed in nasopharyngeal carcinomas by immunohistochemical analysis. These results implicate p16 inactivation but not Rb alteration in the stepwise progression of nasopharyngeal carcinogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/49410
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGulley, MLen_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorSchneider, BGen_HK
dc.contributor.authorAmin, MBen_HK
dc.contributor.authorRo, JYen_HK
dc.contributor.authorGeradts, Jen_HK
dc.date.accessioned2008-06-12T06:41:53Z-
dc.date.available2008-06-12T06:41:53Z-
dc.date.issued1998en_HK
dc.identifier.citationAmerican Journal Of Pathology, 1998, v. 152 n. 4, p. 865-869en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49410-
dc.description.abstractThe p16/MTS1 gene is altered by deletion, mutation, or hypermethylation in a wide variety of human cancers. As a result of deficient p16 protein, these cancers lack a critical mechanism for halting G1/S cell cycle progression. In the current study, 59 cases of nasopharyngeal carcinoma were evaluated for expression of the p16 rumor suppressor protein by immunohistochemical analysis of paraffin-embedded tissue. There was no detectable p16 in 38/59 cases (64%), which implies a very high rate of p16 inactivation in this type of cancer. On the other hand, the retinoblastoma gene product, which also regulates the G1 to S phase transition of the cell cycle, was consistently expressed in nasopharyngeal carcinomas by immunohistochemical analysis. These results implicate p16 inactivation but not Rb alteration in the stepwise progression of nasopharyngeal carcinogenesis.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCarcinoma, Squamous Cell - metabolismen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p16 - metabolismen_HK
dc.subject.meshNasopharyngeal Neoplasms - metabolismen_HK
dc.subject.meshRetinoblastoma Protein - metabolismen_HK
dc.subject.meshHerpesvirus 4, Human - isolation & purificationen_HK
dc.titleNasopharyngeal carcinomas frequently lack the p16/MTS1 tumor suppressor protein but consistently express the retinoblastoma gene producten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9440&volume=152&issue=4&spage=865&epage=869&date=1998&atitle=Nasopharyngeal+carcinomas+frequently+lack+the+p16/MTS1+tumor+suppressor+protein+but+consistently+express+the+retinoblastoma+gene+producten_HK
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid9546345-
dc.identifier.pmcidPMC1858242-
dc.identifier.scopuseid_2-s2.0-0031919421en_HK
dc.identifier.hkuros34031-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031919421&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume152en_HK
dc.identifier.issue4en_HK
dc.identifier.spage865en_HK
dc.identifier.epage869en_HK
dc.identifier.isiWOS:000072924700003-
dc.publisher.placeUnited Statesen_HK

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