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Article: Minichromosome maintenance protein 7 expression in gestational trophoblastic disease: Correlation with Ki67, PCNA and clinicopathological parameters

TitleMinichromosome maintenance protein 7 expression in gestational trophoblastic disease: Correlation with Ki67, PCNA and clinicopathological parameters
Authors
KeywordsGestational trophoblastic disease
Ki67
MCM7
PCNA
Proliferation
Issue Date2003
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HIS
Citation
Histopathology, 2003, v. 43 n. 5, p. 485-490 How to Cite?
AbstractAims: To assess the proliferative activity of gestational trophoblastic disease (GTD) using one of the novel proliferation markers (MCM7) and to determine its prognostic value in hydatidiform mole (HM). Methods and results: Immunohistochemical staining for MCM7 was performed on 122 samples of paraffin-embedded trophoblastic tissues including 22 normal first-trimester placentas, 12 term placentas, 12 spontaneous miscarriages (SM), 21 partial moles (PM), 44 complete hydatidiform moles (CM), and 11 choriocarcinomas (CCA). The correlations between the proliferative indices assessed by MCM7, proliferating cell nuclear antigen (PCNA) and Ki67 (MIB1) immunoreactivity as well as clinical progress were assessed. MCM7 immunoreactivity was found predominantly in the nuclei of cytotrophoblast and intermediate trophoblast and decreased with placental maturation. MCM7 expression was highest in CCA, followed by CM, PM, normal first-trimester placenta, SM and term placenta. MCM7 index was significantly higher in PM and CM than in SM (P = 0.007, P < 0.001) but not between PM and CM themselves (P = 0.560). Eighteen of the 65 patients with HM developed persistent trophoblastic disease (PTD) requiring chemotherapy. There was no significant difference in MCM7 indices between the patients who developed PTD and those who did not (P = 0.312). MCM7 indices correlated well with Ki67 (P = 0.002) but not with PCNA (P = 0.054) indices. MCM7 indices demonstrated less variability than PCNA and Ki67 and may be a better proliferation marker than the latter two. Conclusions: We conclude that MCM7 is useful in differentiating molar and non-molar gestations but is not helpful in discriminating PM from CM or in predicting PTD.
Persistent Identifierhttp://hdl.handle.net/10722/67659
ISSN
2015 Impact Factor: 3.425
2015 SCImago Journal Rankings: 1.488
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXue, WCen_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-06T05:57:06Z-
dc.date.available2010-09-06T05:57:06Z-
dc.date.issued2003en_HK
dc.identifier.citationHistopathology, 2003, v. 43 n. 5, p. 485-490en_HK
dc.identifier.issn0309-0167en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67659-
dc.description.abstractAims: To assess the proliferative activity of gestational trophoblastic disease (GTD) using one of the novel proliferation markers (MCM7) and to determine its prognostic value in hydatidiform mole (HM). Methods and results: Immunohistochemical staining for MCM7 was performed on 122 samples of paraffin-embedded trophoblastic tissues including 22 normal first-trimester placentas, 12 term placentas, 12 spontaneous miscarriages (SM), 21 partial moles (PM), 44 complete hydatidiform moles (CM), and 11 choriocarcinomas (CCA). The correlations between the proliferative indices assessed by MCM7, proliferating cell nuclear antigen (PCNA) and Ki67 (MIB1) immunoreactivity as well as clinical progress were assessed. MCM7 immunoreactivity was found predominantly in the nuclei of cytotrophoblast and intermediate trophoblast and decreased with placental maturation. MCM7 expression was highest in CCA, followed by CM, PM, normal first-trimester placenta, SM and term placenta. MCM7 index was significantly higher in PM and CM than in SM (P = 0.007, P < 0.001) but not between PM and CM themselves (P = 0.560). Eighteen of the 65 patients with HM developed persistent trophoblastic disease (PTD) requiring chemotherapy. There was no significant difference in MCM7 indices between the patients who developed PTD and those who did not (P = 0.312). MCM7 indices correlated well with Ki67 (P = 0.002) but not with PCNA (P = 0.054) indices. MCM7 indices demonstrated less variability than PCNA and Ki67 and may be a better proliferation marker than the latter two. Conclusions: We conclude that MCM7 is useful in differentiating molar and non-molar gestations but is not helpful in discriminating PM from CM or in predicting PTD.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HISen_HK
dc.relation.ispartofHistopathologyen_HK
dc.rightsHistopathology. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectGestational trophoblastic diseaseen_HK
dc.subjectKi67en_HK
dc.subjectMCM7en_HK
dc.subjectPCNAen_HK
dc.subjectProliferationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGestational Trophoblastic Disease - metabolism - pathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshKi-67 Antigen - biosynthesisen_HK
dc.subject.meshPlacenta - metabolism - pathologyen_HK
dc.subject.meshPregnancyen_HK
dc.subject.meshPrognosisen_HK
dc.subject.meshProliferating Cell Nuclear Antigen - biosynthesisen_HK
dc.subject.meshTumor Markers, Biological - analysisen_HK
dc.titleMinichromosome maintenance protein 7 expression in gestational trophoblastic disease: Correlation with Ki67, PCNA and clinicopathological parametersen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0309-0167&volume=43&spage=485&epage=490&date=2003&atitle=Minichromosome+maintenance+protein+7+expression+in+gestational+trophoblastic+disease:+correlation+with+Ki67,+PCNA+and+clinicopathological+parametersen_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2559.2003.01728.xen_HK
dc.identifier.pmid14636275-
dc.identifier.scopuseid_2-s2.0-0344844595en_HK
dc.identifier.hkuros85073en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0344844595&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume43en_HK
dc.identifier.issue5en_HK
dc.identifier.spage485en_HK
dc.identifier.epage490en_HK
dc.identifier.isiWOS:000186237200008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridXue, WC=7103165268en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridChiu, PM=7103182596en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK

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