Document Detail


Roles of growth factors in mediating mesenchymal influence on the cytodifferentiation of the Dunning prostatic adenocarcinoma.
MedLine Citation:
PMID:  10601838     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Earlier studies have shown that seminal vesicle mesenchyme (SVM) has the ability to induce Dunning tumor (DT) 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 (0-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-beta(1) together with a concurrent downregulation of TGF-alpha, IGF-I, IGF-II, and VEGF receptors (flk-1, flt-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.
Authors:
X F Lu; N C Tam; Y C Wong
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine     Volume:  21     ISSN:  1010-4283     ISO Abbreviation:  Tumour Biol.     Publication Date:    2000 Jan-Feb
Date Detail:
Created Date:  2000-02-18     Completed Date:  2000-02-18     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8409922     Medline TA:  Tumour Biol     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  21-32     Citation Subset:  IM    
Copyright Information:
Copyright 2000 S. Karger AG, Basel
Affiliation:
Department of Anatomy, Faculty of Medicine, University of Hong Kong, China.
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma / chemistry,  metabolism*,  pathology*
Animals
Cell Differentiation
Endothelial Growth Factors / metabolism,  physiology
Epidermal Growth Factor / physiology
Fibroblast Growth Factor 2 / physiology
Growth Substances / physiology*
Immunohistochemistry
Insulin-Like Growth Factor I / physiology
Insulin-Like Growth Factor II / physiology
Lymphokines / metabolism,  physiology
Male
Mesoderm / physiology*
Mice
Mice, Nude
Prostatic Neoplasms / chemistry,  metabolism*,  pathology*
Rats
Rats, Sprague-Dawley
Receptor Protein-Tyrosine Kinases / physiology
Receptor, Epidermal Growth Factor / physiology
Receptor, IGF Type 1 / physiology
Receptors, Growth Factor / physiology
Receptors, Vascular Endothelial Growth Factor
Transforming Growth Factor alpha / physiology
Transforming Growth Factor beta / physiology
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Chemical
Reg. No./Substance:
0/Endothelial Growth Factors; 0/Growth Substances; 0/Lymphokines; 0/Receptors, Growth Factor; 0/Transforming Growth Factor alpha; 0/Transforming Growth Factor beta; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; 103107-01-3/Fibroblast Growth Factor 2; 62229-50-9/Epidermal Growth Factor; 67763-96-6/Insulin-Like Growth Factor I; 67763-97-7/Insulin-Like Growth Factor II; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 2.7.10.1/Receptor, IGF Type 1; EC 2.7.10.1/Receptors, Vascular Endothelial Growth Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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