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Article: Roles of growth factors in mediating mesenchymal influence on the cytodifferentiation of the dunning prostatic adenocarcinoma

TitleRoles of growth factors in mediating mesenchymal influence on the cytodifferentiation of the dunning prostatic adenocarcinoma
Authors
Issue Date2000
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBI
Citation
Tumor Biology, 2000, v. 21 n. 1, p. 21-32 How to Cite?
AbstractEarlier studies have shown that seminal vesicle mesenchyme (SVM) has the ability to induce Dunning tumor (Dr) to undergo morphogenetic changes and cytodifferentiation. The aim of the present study was to investigate the roles of growth factors and their receptors in tumor-mesenchymal interactions. Small pieces of DT were combined with SVM (O-day neonatal SD rat) and the tissue recombinants (SVM + DT) were grafted under the renal capsule of male athymic nude mice and allowed to grow for 4 weeks. Histopathological examination confirmed that SVM can induce DT to express apparently more normal morphological features, with the formation of large tubules lined by highly differentiated columnar epithelial cells and the reappearance of a fibromuscular stroma. Using immunohistochemistry, the results demonstrated that the tissue recombinants typically exhibited an overexpression of EGF, EGF-R, bFGF, TGF-β 1 together with a concurrent downregulation of TGF-α, IGF-I, IGF-II, and VEGF receptors (flk-1, fit-1). The levels of these growth factors and their receptors in DT + SVM tissue recombinants were more similar to those of the normal prostate. These findings reaffirmed that SVM has the ability to reprogram DT toward a more normal direction on one hand, while implicating the importance of cytokines in mesenchyme-induced DT phenotypic changes under in vivo condition on the other hand. This study suggests that these factors and their receptors may be essential mediators in tumor-mesenchymal interactions.
Persistent Identifierhttp://hdl.handle.net/10722/149587
ISSN
2015 Impact Factor: 2.926
2015 SCImago Journal Rankings: 0.989
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLu, XFen_US
dc.contributor.authorTam, NCen_US
dc.contributor.authorWong, YCen_US
dc.date.accessioned2012-06-26T05:55:36Z-
dc.date.available2012-06-26T05:55:36Z-
dc.date.issued2000en_US
dc.identifier.citationTumor Biology, 2000, v. 21 n. 1, p. 21-32en_US
dc.identifier.issn1010-4283en_US
dc.identifier.urihttp://hdl.handle.net/10722/149587-
dc.description.abstractEarlier studies have shown that seminal vesicle mesenchyme (SVM) has the ability to induce Dunning tumor (Dr) to undergo morphogenetic changes and cytodifferentiation. The aim of the present study was to investigate the roles of growth factors and their receptors in tumor-mesenchymal interactions. Small pieces of DT were combined with SVM (O-day neonatal SD rat) and the tissue recombinants (SVM + DT) were grafted under the renal capsule of male athymic nude mice and allowed to grow for 4 weeks. Histopathological examination confirmed that SVM can induce DT to express apparently more normal morphological features, with the formation of large tubules lined by highly differentiated columnar epithelial cells and the reappearance of a fibromuscular stroma. Using immunohistochemistry, the results demonstrated that the tissue recombinants typically exhibited an overexpression of EGF, EGF-R, bFGF, TGF-β 1 together with a concurrent downregulation of TGF-α, IGF-I, IGF-II, and VEGF receptors (flk-1, fit-1). The levels of these growth factors and their receptors in DT + SVM tissue recombinants were more similar to those of the normal prostate. These findings reaffirmed that SVM has the ability to reprogram DT toward a more normal direction on one hand, while implicating the importance of cytokines in mesenchyme-induced DT phenotypic changes under in vivo condition on the other hand. This study suggests that these factors and their receptors may be essential mediators in tumor-mesenchymal interactions.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBIen_US
dc.relation.ispartofTumor Biologyen_US
dc.subject.meshAdenocarcinoma - Chemistry - Metabolism - Pathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Differentiationen_US
dc.subject.meshEndothelial Growth Factors - Metabolism - Physiologyen_US
dc.subject.meshEpidermal Growth Factor - Physiologyen_US
dc.subject.meshFibroblast Growth Factor 2 - Physiologyen_US
dc.subject.meshGrowth Substances - Physiologyen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshInsulin-Like Growth Factor I - Physiologyen_US
dc.subject.meshInsulin-Like Growth Factor Ii - Physiologyen_US
dc.subject.meshLymphokines - Metabolism - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMesoderm - Physiologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshProstatic Neoplasms - Chemistry - Metabolism - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptor Protein-Tyrosine Kinases - Physiologyen_US
dc.subject.meshReceptor, Epidermal Growth Factor - Physiologyen_US
dc.subject.meshReceptor, Igf Type 1 - Physiologyen_US
dc.subject.meshReceptors, Growth Factor - Physiologyen_US
dc.subject.meshReceptors, Vascular Endothelial Growth Factoren_US
dc.subject.meshTransforming Growth Factor Alpha - Physiologyen_US
dc.subject.meshTransforming Growth Factor Beta - Physiologyen_US
dc.subject.meshVascular Endothelial Growth Factor Aen_US
dc.subject.meshVascular Endothelial Growth Factorsen_US
dc.titleRoles of growth factors in mediating mesenchymal influence on the cytodifferentiation of the dunning prostatic adenocarcinomaen_US
dc.typeArticleen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid10601838-
dc.identifier.scopuseid_2-s2.0-0033982864en_US
dc.identifier.hkuros47686-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033982864&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume21en_US
dc.identifier.issue1en_US
dc.identifier.spage21en_US
dc.identifier.epage32en_US
dc.identifier.isiWOS:000084659500005-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridLu, XF=35215493700en_US
dc.identifier.scopusauthoridTam, NC=21646986100en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US

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