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Article: p21(WAF1/CIP1) expression in gestational trophoblastic disease: correlation with clinicopathological parameters, and Ki67 and p53 gene expression

Titlep21(WAF1/CIP1) expression in gestational trophoblastic disease: correlation with clinicopathological parameters, and Ki67 and p53 gene expression
Authors
KeywordsGestational trophoblastic disease
Ki67
p21(WAF1/CIP1)
p53
Issue Date1998
PublisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/
Citation
Journal Of Clinical Pathology, 1998, v. 51 n. 2, p. 159-162 How to Cite?
AbstractBackground--The p21(WAF1/CIP1) gene mediates growth arrest by inhibiting G 1 cyclin dependent kinases and has been considered as a downstream effector of the tumour suppressor gene p53. Aim--To analyse the role of p21(WAF1/CIP1) in gestational trophoblastic disease. Methods--The immunohistochemical expression of p21(WAF1/CIP1) gene was measured in 33 placentas, 28 partial hydatidiform moles, 54 complete hydatidiform moles, and 13 choriocarcinomas in paraffin wax embedded tissue. The results were correlated with p53 (DO7) and Ki67 (MIB1) immunoreactivity as well as clinical progress. Results--p21(WAF1/CIP1) immunoreactivity was found predominantly in the nuclei of the syncytiotrophoblasts. p21(WAF1/CIP1) protein expression correlated with gestational age in normal placentas (p = 0.0001) but not in hydatidiform moles (p = 0.89). Complete hydatidiform moles and choriocarcinomas had a significantly higher p21(WAF1/CIP1) expression compared with normal placentas and partial hydatiform moles (p < 0.001); there was no difference between placentas and partial hydatidiform moles. No correlation between p21(WAF1/CIP1) expression and either the proliferation (Ki67) index (p = 0.34) or p53 protein accumulation (p = 0.68) was demonstrated. There was no significant difference (p > 0.05) in p21(WAF1/CIP1) expression between the 17 patients who developed persistent gestational trophoblastic disease and those who did not. Conclusions--This study suggests that p21(WAF1/CIP1) expression in trophoblastic disease may be induced by a p53 independent pathway. The proliferative activity of gestational trophoblastic diseases might not be determined solely by the control of the cell cycle operated by p21(WAF1/CIP1). p21(WAF1/CIP1) expression is not an accurate prognostic indicator of gestational trophoblastic disease.
Persistent Identifierhttp://hdl.handle.net/10722/43590
ISSN
2015 Impact Factor: 2.912
2015 SCImago Journal Rankings: 1.260
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorShen, DHen_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorWong, LCen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2007-03-23T04:49:44Z-
dc.date.available2007-03-23T04:49:44Z-
dc.date.issued1998en_HK
dc.identifier.citationJournal Of Clinical Pathology, 1998, v. 51 n. 2, p. 159-162en_HK
dc.identifier.issn0021-9746en_HK
dc.identifier.urihttp://hdl.handle.net/10722/43590-
dc.description.abstractBackground--The p21(WAF1/CIP1) gene mediates growth arrest by inhibiting G 1 cyclin dependent kinases and has been considered as a downstream effector of the tumour suppressor gene p53. Aim--To analyse the role of p21(WAF1/CIP1) in gestational trophoblastic disease. Methods--The immunohistochemical expression of p21(WAF1/CIP1) gene was measured in 33 placentas, 28 partial hydatidiform moles, 54 complete hydatidiform moles, and 13 choriocarcinomas in paraffin wax embedded tissue. The results were correlated with p53 (DO7) and Ki67 (MIB1) immunoreactivity as well as clinical progress. Results--p21(WAF1/CIP1) immunoreactivity was found predominantly in the nuclei of the syncytiotrophoblasts. p21(WAF1/CIP1) protein expression correlated with gestational age in normal placentas (p = 0.0001) but not in hydatidiform moles (p = 0.89). Complete hydatidiform moles and choriocarcinomas had a significantly higher p21(WAF1/CIP1) expression compared with normal placentas and partial hydatiform moles (p < 0.001); there was no difference between placentas and partial hydatidiform moles. No correlation between p21(WAF1/CIP1) expression and either the proliferation (Ki67) index (p = 0.34) or p53 protein accumulation (p = 0.68) was demonstrated. There was no significant difference (p > 0.05) in p21(WAF1/CIP1) expression between the 17 patients who developed persistent gestational trophoblastic disease and those who did not. Conclusions--This study suggests that p21(WAF1/CIP1) expression in trophoblastic disease may be induced by a p53 independent pathway. The proliferative activity of gestational trophoblastic diseases might not be determined solely by the control of the cell cycle operated by p21(WAF1/CIP1). p21(WAF1/CIP1) expression is not an accurate prognostic indicator of gestational trophoblastic disease.en_HK
dc.format.extent951341 bytes-
dc.format.extent3013 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/en_HK
dc.relation.ispartofJournal of Clinical Pathologyen_HK
dc.rightsJournal of Clinical Pathology. Copyright © B M J Publishing Group.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectGestational trophoblastic diseaseen_HK
dc.subjectKi67en_HK
dc.subjectp21(WAF1/CIP1)en_HK
dc.subjectp53en_HK
dc.subject.meshTrophoblastic neoplasms - metabolism - pathologyen_HK
dc.subject.meshCyclins - metabolismen_HK
dc.subject.meshUterine neoplasms - metabolism - pathologyen_HK
dc.subject.meshNeoplasm proteins - metabolismen_HK
dc.subject.meshCyclin-dependent kinase inhibitor p21en_HK
dc.titlep21(WAF1/CIP1) expression in gestational trophoblastic disease: correlation with clinicopathological parameters, and Ki67 and p53 gene expressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9746&volume=51&issue=2&spage=159&epage=162&date=1998&atitle=p21WAF1/CIP1+expression+in+gestational+trophoblastic+disease:+correlation+with+clinicopathological+parameters,+and+Ki67+and+p53+gene+expressionen_HK
dc.identifier.emailCheung, ANY:anycheun@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US:uskhoo@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS:hysngan@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid9602692en_HK
dc.identifier.pmcidPMC500513-
dc.identifier.scopuseid_2-s2.0-0031596847en_HK
dc.identifier.hkuros33466-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031596847&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume51en_HK
dc.identifier.issue2en_HK
dc.identifier.spage159en_HK
dc.identifier.epage162en_HK
dc.identifier.isiWOS:000072479700016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridShen, DH=7401738584en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridWong, LC=7402092003en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK

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