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Article: The Influence of Mesenchyme of Neonatal Seminal Vesicle and Embryonic Urogenital Sinus on the Morphologic and Functional Cytodifferentiation of Dunning Prostatic Adenocarcinoma: Roles of Growth Factors and Proto-oncogenes

TitleThe Influence of Mesenchyme of Neonatal Seminal Vesicle and Embryonic Urogenital Sinus on the Morphologic and Functional Cytodifferentiation of Dunning Prostatic Adenocarcinoma: Roles of Growth Factors and Proto-oncogenes
Authors
KeywordsBasic fibroblast growth factor (bFGF)
Dunning tumor
Epidermal growth factor (EGF)
Epidermal growth factor receptor (EGFr)
Seminal vesicle mesenchyme (SVM)
Transforming growth factor-beta (TGF-β, c-fos, c-jun, epigenetic factors, tumor-stromal interactions
Urogenital sinus mesenchyme (UGM)
Issue Date1997
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/urolonco
Citation
Urologic Oncology, 1997, v. 3 n. 3, p. 85-93 How to Cite?
AbstractPrevious studies have demonstrated that male genital tract mesenchymes can induce morphogenetic changes in the rat prostatic. Dunning tumor (DT). However, the mechanism of these cellular interactions remains unknown. The aims of this paper are: (1) to examine the influence of neonatal seminal vesicle mesenchyme (SVM) and embryonic urogenital sinus mesenchyme (UGM) on the growth, and morphologic and functional cytodifferentiation of DT: (2) to investigate the possible role of growth factors and receptors including epidermal growth factor and its receptor, basic fibroblast growth factor and transforming growth factor-beta, and two proto-oncogenes, c-fos and c-jun, in these tumor-mesenchymal interactions. Combination of mesenchymes (SVM or UGM) with DT enhanced the growth and induced an apparently more normal morphologic cytodifferentiation in vivo with formation of large tubules lined by highly differentiated columnar epithelial cells and reappearance of fibromuscular stroma. The SDS-PAGE analysis has shown that the DT + UGM enlarged and small tubules secreted proteins different from those of parental DT, demonstrating that mesenchymes can also modulate the functional expression of DT. Interestingly, our immunohistochemical data demonstrate that all the selected growth factors, receptors, and proto-oncogenes are upregulated in the mesenchyme-induced DT epithelial cells, suggesting that these cellular regulators may be closely associated with the mesenchymal induction on the DT phenotypic changes in vivo. This finding implicates the potential role of these growth factors, receptors, and proto-oncogenes in the epigenetic pathway of prostate carcinogenesis via tumor-stromal interactions.
Persistent Identifierhttp://hdl.handle.net/10722/67783
ISSN
2015 Impact Factor: 2.921
2015 SCImago Journal Rankings: 1.069
References

 

DC FieldValueLanguage
dc.contributor.authorTam, NNCen_HK
dc.contributor.authorWang, YZen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-06T05:58:12Z-
dc.date.available2010-09-06T05:58:12Z-
dc.date.issued1997en_HK
dc.identifier.citationUrologic Oncology, 1997, v. 3 n. 3, p. 85-93en_HK
dc.identifier.issn1078-1439en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67783-
dc.description.abstractPrevious studies have demonstrated that male genital tract mesenchymes can induce morphogenetic changes in the rat prostatic. Dunning tumor (DT). However, the mechanism of these cellular interactions remains unknown. The aims of this paper are: (1) to examine the influence of neonatal seminal vesicle mesenchyme (SVM) and embryonic urogenital sinus mesenchyme (UGM) on the growth, and morphologic and functional cytodifferentiation of DT: (2) to investigate the possible role of growth factors and receptors including epidermal growth factor and its receptor, basic fibroblast growth factor and transforming growth factor-beta, and two proto-oncogenes, c-fos and c-jun, in these tumor-mesenchymal interactions. Combination of mesenchymes (SVM or UGM) with DT enhanced the growth and induced an apparently more normal morphologic cytodifferentiation in vivo with formation of large tubules lined by highly differentiated columnar epithelial cells and reappearance of fibromuscular stroma. The SDS-PAGE analysis has shown that the DT + UGM enlarged and small tubules secreted proteins different from those of parental DT, demonstrating that mesenchymes can also modulate the functional expression of DT. Interestingly, our immunohistochemical data demonstrate that all the selected growth factors, receptors, and proto-oncogenes are upregulated in the mesenchyme-induced DT epithelial cells, suggesting that these cellular regulators may be closely associated with the mesenchymal induction on the DT phenotypic changes in vivo. This finding implicates the potential role of these growth factors, receptors, and proto-oncogenes in the epigenetic pathway of prostate carcinogenesis via tumor-stromal interactions.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/uroloncoen_HK
dc.relation.ispartofUrologic Oncologyen_HK
dc.subjectBasic fibroblast growth factor (bFGF)en_HK
dc.subjectDunning tumoren_HK
dc.subjectEpidermal growth factor (EGF)en_HK
dc.subjectEpidermal growth factor receptor (EGFr)en_HK
dc.subjectSeminal vesicle mesenchyme (SVM)en_HK
dc.subjectTransforming growth factor-beta (TGF-β, c-fos, c-jun, epigenetic factors, tumor-stromal interactionsen_HK
dc.subjectUrogenital sinus mesenchyme (UGM)en_HK
dc.titleThe Influence of Mesenchyme of Neonatal Seminal Vesicle and Embryonic Urogenital Sinus on the Morphologic and Functional Cytodifferentiation of Dunning Prostatic Adenocarcinoma: Roles of Growth Factors and Proto-oncogenesen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S1078-1439(97)00040-9en_HK
dc.identifier.pmid21227091-
dc.identifier.scopuseid_2-s2.0-0344835785en_HK
dc.identifier.hkuros29803en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0344835785&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue3en_HK
dc.identifier.spage85en_HK
dc.identifier.epage93en_HK
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTam, NNC=7101712624en_HK
dc.identifier.scopusauthoridWang, YZ=8581934500en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK

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