Loss of mammary epithelial prolactin receptor delays tumor formation by reducing cell proliferation in low-grade preinvasive lesions

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dc.contributor.author Oakes, S. en_US
dc.contributor.author Robertson, F. en_US
dc.contributor.author Kench, J. en_US
dc.contributor.author Gardiner-Garden, M. en_US
dc.contributor.author Freen, J. en_US
dc.contributor.author Ormandy, C. en_US
dc.contributor.author Wand, Matt en_US
dc.contributor.editor en_US
dc.date.accessioned 2012-02-02T11:00:20Z
dc.date.available 2012-02-02T11:00:20Z
dc.date.issued 2007 en_US
dc.identifier 2010005194 en_US
dc.identifier.citation Oakes S. et al. 2007, 'Loss of mammary epithelial prolactin receptor delays tumor formation by reducing cell proliferation in low-grade preinvasive lesions', Nature, vol. 26, no. 4, pp. 543-553. en_US
dc.identifier.issn 0950-9232 en_US
dc.identifier.other C1UNSUBMIT en_US
dc.identifier.uri http://hdl.handle.net/10453/15577
dc.description.abstract Top quartile serum prolactin levels confer a twofold increase in the relative risk of developing breast cancer. Prolactin exerts this effect at an ill defined point in the carcinogenic process, via mechanisms involving direct action via prolactin receptors within mammary epithelium and/or indirect action through regulation of other hormones such as estrogen and progesterone. We have addressed these questions by examining mammary carcinogenesis in transplants of mouse mammary epithelium expressing the SV40T oncogene, with or without the prolactin receptor, using host animals with a normal endocrine system. In prolactin receptor knockout transplants the area of neoplasia was significantly smaller (7 versus 17%; P<0.001 at 22 weeks and 7 versus 14%; P=0.009 at 32 weeks). Low-grade neoplastic lesions displayed reduced BrdU incorporation rate (11.3 versus 17% P=0.003) but no change in apoptosis rate. Tumor latency increased (289 days versus 236 days, P<0.001). Tumor frequency, growth rate, morphology, cell proliferation and apoptosis were not altered. Thus, prolactin acts directly on the mammary epithelial cells to increase cell proliferation in preinvasive lesions, resulting in more neoplasia and acceleration of the transition to invasive carcinoma. Targeting of mammary prolactin signaling thus provides a strategy to prevent the early progression of neoplasia to invasive carcinoma. en_US
dc.language en_US
dc.publisher Nature en_US
dc.relation.isbasedon http://dx.doi.org/10.1038/sj.onc.1209838 en_US
dc.title Loss of mammary epithelial prolactin receptor delays tumor formation by reducing cell proliferation in low-grade preinvasive lesions en_US
dc.parent Oncogene en_US
dc.journal.volume 26 en_US
dc.journal.number 4 en_US
dc.publocation United States en_US
dc.identifier.startpage 543 en_US
dc.identifier.endpage 553 en_US
dc.cauo.name SCI.Mathematical Sciences en_US
dc.conference Verified OK en_US
dc.for 110300 en_US
dc.personcode 0000070449 en_US
dc.personcode 0000070450 en_US
dc.personcode 0000070451 en_US
dc.personcode 0000070452 en_US
dc.personcode 110509 en_US
dc.personcode 0000070453 en_US
dc.personcode 0000070454 en_US
dc.percentage 100 en_US
dc.classification.name Clinical Sciences en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US
dc.date.activity en_US
dc.location.activity en_US
dc.description.keywords prolactin receptor, mouse, mammary, carcinogenesis, C3(1)/SV40T en_US


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