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dc.contributor.authorHendry, William J. IIIen_US
dc.contributor.authorZheng, Xinglongen_US
dc.contributor.authorLeavitt, Wendell W.en_US
dc.contributor.authorBranham, William S.en_US
dc.contributor.authorSheehan, Daniel M.en_US
dc.date.accessioned2012-01-24T17:49:05Z
dc.date.available2012-01-24T17:49:05Z
dc.date.issued1997-05-15en_US
dc.identifier9157983en_US
dc.identifierCA60250/ HD 28074en_US
dc.identifier2984705Ren_US
dc.identifier.citationCancer research. 1997 May 15; 57(10): 1903-8.en_US
dc.identifier.issn0008-5472en_US
dc.identifier.urihttp://cancerres.aacrjournals.org/content/57/10/1903.full.pdf+html
dc.identifier.urihttp://hdl.handle.net/10057/4155
dc.descriptionClick on the link below to access the article (may not be free).en_US
dc.description.abstractPrenatal exposure to the synthetic estrogen diethylstilbestrol (DES) causes morphogenetic alterations and neoplasia in the human reproductive tract. In the hamster, neonatal DES exposure alters early uterine morphogenesis and induces endometrial adenocarcinomas in adults. We now demonstrate that the preneoplastic stages of this phenomenon in the hamster reflect an abnormal uterotropic response to estrogen that is characterized by hyperplastic lesions in the endometrial epithelium and includes an immune and/or inflammatory component. Interestingly, biochemical and in situ analysis revealed that the hyperplastic epithelium is also an active site of cell death by apoptosis. To further probe the mechanism of this phenomenon, uteri from 7-day-old control or DES-exposed donors were transplanted into the cheek pouches of control or neonatally DES-exposed adult hosts, and both host groups were treated to provide high circulating levels of estradiol. Among the four ectopic scenarios, histopathological lesions (epithelial hyperplasia, dysplasia, and apoptosis), segregated almost exclusively to the two that consisted of neonatally DES-exposed uteri. The virtual absence of lesions in control uteri transplanted to DES hosts eliminated host systemic factors as causative agents. Therefore, we conclude that DES or its metabolites alter the cellular physiology and/or composition of the developing uterus (initiating event) in such a way that it thereafter responds abnormally to estrogenic stimulation (promoting event). These observations serve to further define a unique experimental system for probing: (a) various aspects of the clinical "DES Syndrome"; (b) how estrogen regulates normal uterine growth and morphogenesis; and (c) how this process can degenerate to the unregulated neoplastic state.en_US
dc.description.sponsorshipNCI NIH HHS/ NICHD NIH HHSen_US
dc.language.isoengen_US
dc.publisherAmerican Association for Cancer Researchen_US
dc.relation.ispartofseriesCancer researchen_US
dc.sourceNLMen_US
dc.subjectResearch Support, Non-U.S. Gov'ten_US
dc.subjectResearch Support, U.S. Gov't, Non-P.H.S.en_US
dc.subjectResearch Support, U.S. Gov't, P.H.S.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshApoptosis/drug effectsen_US
dc.subject.meshCheeken_US
dc.subject.meshCricetinaeen_US
dc.subject.meshDiethylstilbestrol/toxicityen_US
dc.subject.meshEndometrial Hyperplasia/chemically induceden_US
dc.subject.meshEstradiol/blooden_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMesocricetusen_US
dc.subject.meshPrecancerous Conditions/chemically induceden_US
dc.subject.meshPregnancyen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshUterine Neoplasms/chemically induceden_US
dc.subject.meshUterus/drug effectsen_US
dc.subject.meshEndometrial Hyperplasia/pathologyen_US
dc.subject.meshEstradiol/pharmacologyen_US
dc.subject.meshPrecancerous Conditions/pathologyen_US
dc.subject.meshUterine Neoplasms/pathologyen_US
dc.subject.meshUterus/pathologyen_US
dc.subject.meshUterus/transplantationen_US
dc.titleEndometrial hyperplasia and apoptosis following neonatal diethylstilbestrol exposure and subsequent estrogen stimulation in both host and transplanted hamster uterien_US
dc.typeArticleen_US
dc.description.versionpeer revieweden_US


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