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Article: Enhanced induction of prostatic dysplasia and carcinoma in Noble rat model by combination of neonatal estrogen exposure and hormonal treatments at adulthood.

TitleEnhanced induction of prostatic dysplasia and carcinoma in Noble rat model by combination of neonatal estrogen exposure and hormonal treatments at adulthood.
Authors
Issue Date2005
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/
Citation
International Journal Of Oncology., 2005, v. 27 n. 6, p. 1685-1695 How to Cite?
AbstractEstrogens have been implicated to play certain but yet undefined roles in the normal and neoplastic growth of prostate gland. Studies of perinatal exposure in rodents demonstrate that effects of perinatal estrogenization are permanent and carcinogenic in prostate gland. In the Noble (Nb) rat model, prostatic dysplasia and neoplastic lesions can be induced by a chronic treatment with both testosterone and estrogen at adulthood. However, by this conventional protocol, neoplastic lesions are mostly confined to the lateral (LP) and ventral (VP) prostates, while gross prostatic tumors are rarely induced. Based on these two experimental models, we developed a modified treatment protocol for the enhancement of prostate cancer induction in Nb rat model by combining neonatal estrogen exposure of male offspring followed by the hormonal treatment at adulthood (NeoE + T-E2). Using this modified protocol, we were able to induce more extensive development of neoplastic lesions in all three prostatic lobes and also gross tumors at relatively high incidence within 6-9 months. Western blottings and immunohistochemistry showed that ERalpha expression was increased in the hypertrophic peri-acinar and -ductal smooth muscle cells while ERbeta and AR expressions are markedly decreased in dysplastic and neoplastic lesions in NeoE + T-E2-treated prostates. Immunohistochemistry showed that expression of three tumor suppressors (BRCA2, PTEN, and Rap1) and tubulin-alpha are markedly decreased in dysplastic and neoplastic lesions. In addition, loss of expression of smooth muscle differentiation markers (desmin, alpha-actin, and vinculin) and defects of basement membranes were also seen in the reactive stroma. These results suggest that exposure to high levels of estrogens, either endogenous or exogenous, in early life could play a role in the development of prostate cancer in later life.
Persistent Identifierhttp://hdl.handle.net/10722/149650
ISSN
2015 Impact Factor: 3.018
2015 SCImago Journal Rankings: 1.270
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYuen, MTen_US
dc.contributor.authorLeung, LKen_US
dc.contributor.authorWang, Jen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorChan, FLen_US
dc.date.accessioned2012-06-26T05:56:33Z-
dc.date.available2012-06-26T05:56:33Z-
dc.date.issued2005en_US
dc.identifier.citationInternational Journal Of Oncology., 2005, v. 27 n. 6, p. 1685-1695en_US
dc.identifier.issn1019-6439en_US
dc.identifier.urihttp://hdl.handle.net/10722/149650-
dc.description.abstractEstrogens have been implicated to play certain but yet undefined roles in the normal and neoplastic growth of prostate gland. Studies of perinatal exposure in rodents demonstrate that effects of perinatal estrogenization are permanent and carcinogenic in prostate gland. In the Noble (Nb) rat model, prostatic dysplasia and neoplastic lesions can be induced by a chronic treatment with both testosterone and estrogen at adulthood. However, by this conventional protocol, neoplastic lesions are mostly confined to the lateral (LP) and ventral (VP) prostates, while gross prostatic tumors are rarely induced. Based on these two experimental models, we developed a modified treatment protocol for the enhancement of prostate cancer induction in Nb rat model by combining neonatal estrogen exposure of male offspring followed by the hormonal treatment at adulthood (NeoE + T-E2). Using this modified protocol, we were able to induce more extensive development of neoplastic lesions in all three prostatic lobes and also gross tumors at relatively high incidence within 6-9 months. Western blottings and immunohistochemistry showed that ERalpha expression was increased in the hypertrophic peri-acinar and -ductal smooth muscle cells while ERbeta and AR expressions are markedly decreased in dysplastic and neoplastic lesions in NeoE + T-E2-treated prostates. Immunohistochemistry showed that expression of three tumor suppressors (BRCA2, PTEN, and Rap1) and tubulin-alpha are markedly decreased in dysplastic and neoplastic lesions. In addition, loss of expression of smooth muscle differentiation markers (desmin, alpha-actin, and vinculin) and defects of basement membranes were also seen in the reactive stroma. These results suggest that exposure to high levels of estrogens, either endogenous or exogenous, in early life could play a role in the development of prostate cancer in later life.en_US
dc.languageengen_US
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/en_US
dc.relation.ispartofInternational journal of oncology.en_US
dc.subject.meshActins - Analysisen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshBrca2 Protein - Analysisen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshDesmin - Analysisen_US
dc.subject.meshDiethylstilbestrol - Administration & Dosage - Toxicityen_US
dc.subject.meshEstrogen Receptor Alpha - Analysisen_US
dc.subject.meshEstrogen Receptor Beta - Analysisen_US
dc.subject.meshEstrogens - Administration & Dosage - Toxicityen_US
dc.subject.meshEstrogens, Non-Steroidal - Administration & Dosage - Toxicityen_US
dc.subject.meshFemaleen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshInjections, Subcutaneousen_US
dc.subject.meshLaminin - Analysisen_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasms, Experimental - Chemically Induced - Metabolism - Pathologyen_US
dc.subject.meshPten Phosphohydrolase - Analysisen_US
dc.subject.meshPregnancyen_US
dc.subject.meshProstate - Chemistry - Drug Effects - Pathologyen_US
dc.subject.meshProstatic Neoplasms - Chemically Induced - Metabolism - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshReceptors, Androgen - Analysisen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTubulin - Analysisen_US
dc.subject.meshVinculin - Analysisen_US
dc.subject.meshRap1 Gtp-Binding Proteins - Analysisen_US
dc.titleEnhanced induction of prostatic dysplasia and carcinoma in Noble rat model by combination of neonatal estrogen exposure and hormonal treatments at adulthood.en_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.pmid16273225-
dc.identifier.scopuseid_2-s2.0-33644828568en_US
dc.identifier.hkuros113043-
dc.identifier.volume27en_US
dc.identifier.issue6en_US
dc.identifier.spage1685en_US
dc.identifier.epage1695en_US
dc.identifier.isiWOS:000233575100026-
dc.publisher.placeGreeceen_US
dc.identifier.scopusauthoridYuen, MT=7102031982en_US
dc.identifier.scopusauthoridLeung, LK=24172344900en_US
dc.identifier.scopusauthoridWang, J=36109297400en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridChan, FL=7202586505en_US

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