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Article: Loss of Programmed cell death 4 (Pdcd4) associates with the progression of ovarian cancer

TitleLoss of Programmed cell death 4 (Pdcd4) associates with the progression of ovarian cancer
Authors
Wei, NLiu, SSLeung, THYTam, KFLiao, XYCheung, ANYChan, KKLNgan, HYS
Issue Date2009
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.molecular-cancer.com
Citation
Molecular Cancer, 2009, v. 8, p. 70 How to Cite?
DOI: http://dx.doi.org/10.1186/1476-4598-8-70
AbstractBackground: Programmed cell death 4 (Pdcd4) is a novel tumour suppressor and originally identified as a neoplastic transformation inhibitor. The aim of this study was to investigate the expression, prognostic significance and potential function of Pdcd4 in ovarian cancer. Results: The expression of Pdcd4 was examined in 30 normal ovarian tissues, 16 borderline and 93 malignant ovarian tissues. A continuous down regulation of Pdcd4 expression in the sequence of normal, borderline and malignant tissues was observed. The expressions of Pdcd4 in both ovarian borderline tissues and carcinomas were significantly lower than the expression in normal ovarian tissues (p < 0.001). Furthermore, patients with lower Pdcd4 expressions were found to have shorter disease-free survival (p = 0.037). The expression of Pdcd4 was also assessed by immunohistochemical analysis in 13 ovarian normal tissues and 44 carcinomas. Different subcellular localization of Pdcd4 was observed in normal compared to malignant cells. Predominant nuclear localization of Pdcd4 was found in normal ovarian tissues while ovarian carcinomas showed mainly cytoplasmic localization of Pdcd4. Conclusion: Our study demonstrated that the loss of Pdcd4 was a common abnormality at molecular level in ovarian cancer and it might be a potential prognostic factor in ovarian cancer patients. © 2009 Wei et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/87313
ISSN
1476-4598
2023 Impact Factor: 27.7
2023 SCImago Journal Rankings: 8.222
ISI Accession Number ID
WOS:000269950900001
Funding AgencyGrant Number
Wong Check She Charitable Foundation
Department of Obstetrics and Gynaecology
University of Hong Kong
Funding Information:

This research was jointly funded by the Wong Check She Charitable Foundation and the Research Fund from the Department of Obstetrics and Gynaecology, the University of Hong Kong.

References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorWei, Nen_HK
dc.contributor.authorLiu, SSen_HK
dc.contributor.authorLeung, THYen_HK
dc.contributor.authorTam, KFen_HK
dc.contributor.authorLiao, XYen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorChan, KKLen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-09-06T09:28:04Z-
dc.date.available2010-09-06T09:28:04Z-
dc.date.issued2009en_HK
dc.identifier.citationMolecular Cancer, 2009, v. 8, p. 70en_HK
dc.identifier.issn1476-4598en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87313-
dc.description.abstractBackground: Programmed cell death 4 (Pdcd4) is a novel tumour suppressor and originally identified as a neoplastic transformation inhibitor. The aim of this study was to investigate the expression, prognostic significance and potential function of Pdcd4 in ovarian cancer. Results: The expression of Pdcd4 was examined in 30 normal ovarian tissues, 16 borderline and 93 malignant ovarian tissues. A continuous down regulation of Pdcd4 expression in the sequence of normal, borderline and malignant tissues was observed. The expressions of Pdcd4 in both ovarian borderline tissues and carcinomas were significantly lower than the expression in normal ovarian tissues (p < 0.001). Furthermore, patients with lower Pdcd4 expressions were found to have shorter disease-free survival (p = 0.037). The expression of Pdcd4 was also assessed by immunohistochemical analysis in 13 ovarian normal tissues and 44 carcinomas. Different subcellular localization of Pdcd4 was observed in normal compared to malignant cells. Predominant nuclear localization of Pdcd4 was found in normal ovarian tissues while ovarian carcinomas showed mainly cytoplasmic localization of Pdcd4. Conclusion: Our study demonstrated that the loss of Pdcd4 was a common abnormality at molecular level in ovarian cancer and it might be a potential prognostic factor in ovarian cancer patients. © 2009 Wei et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.molecular-cancer.comen_HK
dc.relation.ispartofMolecular Canceren_HK
dc.rightsMolecular Cancer. Copyright © BioMed Central Ltd.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshApoptosis Regulatory Proteins - genetics - metabolismen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshDisease Progressionen_HK
dc.subject.meshDisease-Free Survivalen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNeoplasm Stagingen_HK
dc.subject.meshOvarian Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshOvary - cytology - metabolismen_HK
dc.subject.meshRNA-Binding Proteins - genetics - metabolismen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.titleLoss of Programmed cell death 4 (Pdcd4) associates with the progression of ovarian canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1476-4598&volume=8&spage=70&epage=&date=2009&atitle=Loss+of+programmed+cell+death+4+(Pdcd4)+associates+with+the+progression+of+ovarian+cancer+en_HK
dc.identifier.emailLiu, SS:stephasl@hku.hken_HK
dc.identifier.emailCheung, ANY:anycheun@hkucc.hku.hken_HK
dc.identifier.emailChan, KKL:kklchan@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS:hysngan@hkucc.hku.hken_HK
dc.identifier.authorityLiu, SS=rp00372en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityChan, KKL=rp00499en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1186/1476-4598-8-70en_HK
dc.identifier.pmid19728867-
dc.identifier.scopuseid_2-s2.0-70350087561en_HK
dc.identifier.hkuros166505en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350087561&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.spage70en_HK
dc.identifier.epage70en_HK
dc.identifier.isiWOS:000269950900001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWei, N=23101332300en_HK
dc.identifier.scopusauthoridLiu, SS=37102450400en_HK
dc.identifier.scopusauthoridLeung, THY=7202110922en_HK
dc.identifier.scopusauthoridTam, KF=35622901400en_HK
dc.identifier.scopusauthoridLiao, XY=7202134156en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridChan, KKL=8655666700en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.citeulike5719396-
dc.identifier.issnl1476-4598-

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