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Article: The role of androgens in mammary carcinogenesis.

TitleThe role of androgens in mammary carcinogenesis.
Authors
Issue Date2001
Citation
Italian Journal Of Anatomy And Embryology = Archivio Italiano Di Anatomia Ed Embriologia, 2001, v. 106 n. 2 Suppl 1, p. 111-125 How to Cite?
AbstractDespite extensive research, the precise mechanism of mammary carcinogenesis is unknown. We have developed an animal model in which a high incidence of mammary cancer can be induced within a period of several months using a combination of testosterone (T) and 17beta-estradiol (E2) without the addition of carcinogens. The induced mammary tumours mimic closely the human breast cancer in terms of histopathology. Our results showed that the two sex hormones work synergistically to induce a higher incidence of mammary cancer than either hormone treatment alone. The dosage of T affects only the latency period of mammary cancer but not the final incidence. The results further showed that treatment of T, either alone or in combination with E2, there was overexpression of the androgen receptor (AR) in alveolar or ductal epithelial cells but not in stromal cells. Together with overexpression of AR in epithelial cells, there was an increase in perialveolar and interlobular connective tissue as well as a decrease in surrounding adipose tissue, despite the absence of AR in stromal cells. There was also an increase in proliferation rate of fibroblast-like cells in stroma. These changes were blocked by implantation of flutamide, an antiandrogen, indicating that androgens play a crucial role in the process. These findings highlight that the effect of androgens on the stroma, may be through a paracrine action of epithelial cells. The changes in the stroma may, in turn, promote mammary carcinogeneis in a reciprocal manner.
Persistent Identifierhttp://hdl.handle.net/10722/149601
ISSN
2015 SCImago Journal Rankings: 0.316

 

DC FieldValueLanguage
dc.contributor.authorWong, YCen_US
dc.contributor.authorXie, Ben_US
dc.date.accessioned2012-06-26T05:55:47Z-
dc.date.available2012-06-26T05:55:47Z-
dc.date.issued2001en_US
dc.identifier.citationItalian Journal Of Anatomy And Embryology = Archivio Italiano Di Anatomia Ed Embriologia, 2001, v. 106 n. 2 Suppl 1, p. 111-125en_US
dc.identifier.issn1122-6714en_US
dc.identifier.urihttp://hdl.handle.net/10722/149601-
dc.description.abstractDespite extensive research, the precise mechanism of mammary carcinogenesis is unknown. We have developed an animal model in which a high incidence of mammary cancer can be induced within a period of several months using a combination of testosterone (T) and 17beta-estradiol (E2) without the addition of carcinogens. The induced mammary tumours mimic closely the human breast cancer in terms of histopathology. Our results showed that the two sex hormones work synergistically to induce a higher incidence of mammary cancer than either hormone treatment alone. The dosage of T affects only the latency period of mammary cancer but not the final incidence. The results further showed that treatment of T, either alone or in combination with E2, there was overexpression of the androgen receptor (AR) in alveolar or ductal epithelial cells but not in stromal cells. Together with overexpression of AR in epithelial cells, there was an increase in perialveolar and interlobular connective tissue as well as a decrease in surrounding adipose tissue, despite the absence of AR in stromal cells. There was also an increase in proliferation rate of fibroblast-like cells in stroma. These changes were blocked by implantation of flutamide, an antiandrogen, indicating that androgens play a crucial role in the process. These findings highlight that the effect of androgens on the stroma, may be through a paracrine action of epithelial cells. The changes in the stroma may, in turn, promote mammary carcinogeneis in a reciprocal manner.en_US
dc.languageengen_US
dc.relation.ispartofItalian journal of anatomy and embryology = Archivio italiano di anatomia ed embriologiaen_US
dc.subject.meshAndrogen Receptor Antagonistsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBreast Neoplasms - Etiology - Metabolism - Pathologyen_US
dc.subject.meshCarcinoma - Chemically Induced - Metabolism - Pathologyen_US
dc.subject.meshCell Division - Drug Effects - Physiologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshEpithelial Cells - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshEstradiol - Blood - Metabolism - Pharmacokineticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIncidenceen_US
dc.subject.meshKi-67 Antigen - Drug Effects - Metabolismen_US
dc.subject.meshMammary Neoplasms, Experimental - Chemically Induced - Metabolism - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshReaction Time - Drug Effects - Physiologyen_US
dc.subject.meshReceptors, Androgen - Metabolismen_US
dc.subject.meshReceptors, Estrogen - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshStromal Cells - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshTestosterone - Blood - Metabolism - Pharmacokineticsen_US
dc.titleThe role of androgens in mammary carcinogenesis.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.pmid11729946-
dc.identifier.scopuseid_2-s2.0-0035237423en_US
dc.identifier.hkuros65149-
dc.identifier.volume106en_US
dc.identifier.issue2 Suppl 1en_US
dc.identifier.spage111en_US
dc.identifier.epage125en_US
dc.publisher.placeItalyen_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridXie, B=7201872727en_US

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