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Article: Induction of high incidence of mammary tumour in female Noble rats with a combination of 17β-oestradiol and testosterone

TitleInduction of high incidence of mammary tumour in female Noble rats with a combination of 17β-oestradiol and testosterone
Authors
Issue Date1999
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 1999, v. 20 n. 6, p. 1069-1078 How to Cite?
AbstractBreast cancer is the most common cancer and the second most frequent cause of cancer death in women. Despite extensive research, the precise mechanisms of breast carcinogenesis remain unclear. One of the reasons for this is due, at least in part, to a lack of a suitable animal model which can closely mimic the breast carcinogenesis in normal situations without using chemical carcinogens. We have developed an animal model of mammary gland carcinogenesis using a combination of oestradiol and testosterone, and succeeded in inducing a high percentage of female Noble rats to develop mammary cancer in a relatively short time (~ 6 months). The results showed that androgens might work as a promoter to shorten the latency time of mammary gland carcinogenesis. Histopathological examination revealed that hyperplasia and dysplasia were first observed 2 months after treatment, in situ carcinoma after 3 months, and fully developed carcinoma of various forms including cribriform, papillary and camedo types were observed from 5 to 6 months after hormone implantation. Animals implanted with oestrogen or testosterone alone also developed mammary cancers, though with a lower overall incidence than the two hormones combined. They ranged from well differentiated to poorly differentiated forms with predominantly infiltrating ductal carcinoma. We have also observed a case of secondary cancer in the uterus. In addition to the high incidence of carcinoma, there was also a peculiar unexplained ipsilateral correlation between the site of hormonal implantation and the location of tumours, and the highest incidence of carcinogenesis was found to be in thoracic mammary gland. The study showed that both oestrogens and androgens are important in mammary cancer development. The animal model would prove to be a useful model for analysis of the mechanism(s) of hormonal carcinogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/149580
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 1.074
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXie, Ben_US
dc.contributor.authorTsao, SWen_US
dc.contributor.authorWong, YCen_US
dc.date.accessioned2012-06-26T05:55:33Z-
dc.date.available2012-06-26T05:55:33Z-
dc.date.issued1999en_US
dc.identifier.citationCarcinogenesis, 1999, v. 20 n. 6, p. 1069-1078en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://hdl.handle.net/10722/149580-
dc.description.abstractBreast cancer is the most common cancer and the second most frequent cause of cancer death in women. Despite extensive research, the precise mechanisms of breast carcinogenesis remain unclear. One of the reasons for this is due, at least in part, to a lack of a suitable animal model which can closely mimic the breast carcinogenesis in normal situations without using chemical carcinogens. We have developed an animal model of mammary gland carcinogenesis using a combination of oestradiol and testosterone, and succeeded in inducing a high percentage of female Noble rats to develop mammary cancer in a relatively short time (~ 6 months). The results showed that androgens might work as a promoter to shorten the latency time of mammary gland carcinogenesis. Histopathological examination revealed that hyperplasia and dysplasia were first observed 2 months after treatment, in situ carcinoma after 3 months, and fully developed carcinoma of various forms including cribriform, papillary and camedo types were observed from 5 to 6 months after hormone implantation. Animals implanted with oestrogen or testosterone alone also developed mammary cancers, though with a lower overall incidence than the two hormones combined. They ranged from well differentiated to poorly differentiated forms with predominantly infiltrating ductal carcinoma. We have also observed a case of secondary cancer in the uterus. In addition to the high incidence of carcinoma, there was also a peculiar unexplained ipsilateral correlation between the site of hormonal implantation and the location of tumours, and the highest incidence of carcinogenesis was found to be in thoracic mammary gland. The study showed that both oestrogens and androgens are important in mammary cancer development. The animal model would prove to be a useful model for analysis of the mechanism(s) of hormonal carcinogenesis.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_US
dc.relation.ispartofCarcinogenesisen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBody Weighten_US
dc.subject.meshCocarcinogenesisen_US
dc.subject.meshEstradiol - Blood - Toxicityen_US
dc.subject.meshFemaleen_US
dc.subject.meshIncidenceen_US
dc.subject.meshMammary Neoplasms, Experimental - Chemically Induced - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshTestosterone - Blood - Toxicityen_US
dc.titleInduction of high incidence of mammary tumour in female Noble rats with a combination of 17β-oestradiol and testosteroneen_US
dc.typeArticleen_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.authorityTsao, SW=rp00399en_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/carcin/20.6.1069en_US
dc.identifier.pmid10357790-
dc.identifier.scopuseid_2-s2.0-0033059603en_US
dc.identifier.hkuros46301-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033059603&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume20en_US
dc.identifier.issue6en_US
dc.identifier.spage1069en_US
dc.identifier.epage1078en_US
dc.identifier.isiWOS:000080798500023-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridXie, B=7201872727en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.issnl0143-3334-

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