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Article: Id helix-loop-helix proteins are differentially expressed in gestational trophoblastic disease

TitleId helix-loop-helix proteins are differentially expressed in gestational trophoblastic disease
Authors
KeywordsApoptosis
Gestational trophoblastic disease
Id proteins
Proliferation
Issue Date2005
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HIS
Citation
Histopathology, 2005, v. 47 n. 3, p. 303-309 How to Cite?
AbstractAims: To assess the expression of Id proteins in trophoblastic tissues and to correlate this with clinical parameters, proliferative and apoptotic indices as well as to related oncogene expression. Methods and results: Immunohistochemistry for Id1, Id2, Id3 and Id4 was performed on 83 trophoblastic tissues including 17 normal first-trimester placentas, seven term placentas, 47 hydatidiform moles (HM), and 12 spontaneous miscarriages. The four Id proteins were predominantly expressed in the villous and implantation site intermediate trophoblast. Expression of Id1 in HM was significantly higher than that in normal placenta (P = 0.0006) and spontaneous miscarriage (P = 0.0001) but did not correlate with subsequent development of gestational trophoblastic neoplasia (GTN). Id1 expression correlated with the proliferation index as assessed by MCM7 (P = 0.003) and Ki67 (P = 0.017) and with the apoptotic activity assessed by TUNEL (P = 0.001) and M30 CytoDeath antibody (P = 0.013). Moreover, the expression of Id1 correlated with the expression of p53 (P = 0.004), P21 WAF1/CIP1 (P = 0.003) but not with p16 (P = 0.107). Conclusions: Id proteins may play a role in the regulation of proliferative and apoptotic activity in trophoblastic tissue and are potentially useful in differentiating molar and non-molar gestation, but are not helpful in predicting GTN. © 2005 Blackwell Publishing Limited.
Persistent Identifierhttp://hdl.handle.net/10722/67664
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.authorFeng, HCen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-06T05:57:09Z-
dc.date.available2010-09-06T05:57:09Z-
dc.date.issued2005en_HK
dc.identifier.citationHistopathology, 2005, v. 47 n. 3, p. 303-309en_HK
dc.identifier.issn0309-0167en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67664-
dc.description.abstractAims: To assess the expression of Id proteins in trophoblastic tissues and to correlate this with clinical parameters, proliferative and apoptotic indices as well as to related oncogene expression. Methods and results: Immunohistochemistry for Id1, Id2, Id3 and Id4 was performed on 83 trophoblastic tissues including 17 normal first-trimester placentas, seven term placentas, 47 hydatidiform moles (HM), and 12 spontaneous miscarriages. The four Id proteins were predominantly expressed in the villous and implantation site intermediate trophoblast. Expression of Id1 in HM was significantly higher than that in normal placenta (P = 0.0006) and spontaneous miscarriage (P = 0.0001) but did not correlate with subsequent development of gestational trophoblastic neoplasia (GTN). Id1 expression correlated with the proliferation index as assessed by MCM7 (P = 0.003) and Ki67 (P = 0.017) and with the apoptotic activity assessed by TUNEL (P = 0.001) and M30 CytoDeath antibody (P = 0.013). Moreover, the expression of Id1 correlated with the expression of p53 (P = 0.004), P21 WAF1/CIP1 (P = 0.003) but not with p16 (P = 0.107). Conclusions: Id proteins may play a role in the regulation of proliferative and apoptotic activity in trophoblastic tissue and are potentially useful in differentiating molar and non-molar gestation, but are not helpful in predicting GTN. © 2005 Blackwell Publishing Limited.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.subjectApoptosisen_HK
dc.subjectGestational trophoblastic diseaseen_HK
dc.subjectId proteinsen_HK
dc.subjectProliferationen_HK
dc.subject.meshCell Cycle Proteins - analysisen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p21en_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHelix-Loop-Helix Motifsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHydatidiform Mole - metabolism - pathologyen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshInhibitor of Differentiation Protein 1en_HK
dc.subject.meshPlacenta - chemistryen_HK
dc.subject.meshPregnancyen_HK
dc.subject.meshRepressor Proteins - biosynthesisen_HK
dc.subject.meshTranscription Factors - biosynthesisen_HK
dc.subject.meshTrophoblasts - chemistry - pathologyen_HK
dc.subject.meshTumor Suppressor Protein p53 - analysisen_HK
dc.titleId helix-loop-helix proteins are differentially expressed in gestational trophoblastic diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0309-0167&volume=47&issue=3&spage=303&epage=9&date=2005&atitle=Id+helix-loop-helix+proteins+are+differentially+expressed+in+gestational+trophoblastic+disease.en_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2559.2005.02190.xen_HK
dc.identifier.pmid16115231-
dc.identifier.scopuseid_2-s2.0-24144431605en_HK
dc.identifier.hkuros101217en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-24144431605&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume47en_HK
dc.identifier.issue3en_HK
dc.identifier.spage303en_HK
dc.identifier.epage309en_HK
dc.identifier.isiWOS:000231394800008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridXue, WC=7103165268en_HK
dc.identifier.scopusauthoridFeng, HC=7401736336en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridChiu, PM=7103182596en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.citeulike308567-

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