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dc.contributor.authorHarding, C
dc.contributor.authorOsundeko, O
dc.contributor.authorTetlow, L C
dc.contributor.authorFaragher, E B
dc.contributor.authorHowell, Anthony
dc.contributor.authorBundred, Nigel J
dc.date.accessioned2009-11-18T11:37:27Z
dc.date.available2009-11-18T11:37:27Z
dc.date.issued2000-01
dc.identifier.citationHormonally-regulated proteins in breast secretions are markers of target organ sensitivity. 2000, 82 (2):354-60 Br. J. Canceren
dc.identifier.issn0007-0920
dc.identifier.pmid10646888
dc.identifier.doi10.1054/bjoc.1999.0926
dc.identifier.urihttp://hdl.handle.net/10541/86370
dc.description.abstractAnti-oestrogen therapy is being used in an attempt to prevent breast cancer but no intermediate end points of the effect of tamoxifen on the normal breast are available. Therefore, the purpose of this study was to develop a physiological measure of oestrogen action on the breast. We measured oestrogen-stimulated and -inhibited proteins in breast secretions from women on and off anti-oestrogen therapy. Two oestrogen-stimulated proteins (pS2 and cathepsin D) and oestrogen-inhibited proteins (CP15, gross cystic disease fluid protein 15; Apo,: apolipoprotein D) were measured. Premenopausal women had significantly higher pS2 and cathepsin D in association with lower Apo D and CP15 secretion levels compared to post-menopausal women. Sequential nipple aspirates from women treated with the luteinizing hormone releasing hormone agonist goserelin (n = 9), tamoxifen (n = 9) and hormone replacement therapy (HRT) (n = 26) were measured. Following treatment with goserelin, median nipple secretion levels of pS2 fell (P < 0.02) and Apo D and CP15 rose significantly (P < 0.03 and P < 0.05 respectively). Similar changes were seen on tamoxifen therapy but not in untreated control women. Treatment with HRT resulted in a rise of pS2 (P < 0.001) and a fall in Apo D (P < 0.05). Measurement of pS2 and Apo D in nipple aspirates may prove useful intermediate end point of breast responsiveness to anti-oestrogens.
dc.language.isoenen
dc.subjectBreast Canceren
dc.subjectOestrogensen
dc.subjectOestrogen Receptorsen
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshAntineoplastic Agents, Hormonal
dc.subject.meshApolipoproteins
dc.subject.meshApolipoproteins D
dc.subject.meshBiopsy, Needle
dc.subject.meshBreast Neoplasms
dc.subject.meshCathepsin D
dc.subject.meshEstrogens
dc.subject.meshFemale
dc.subject.meshGoserelin
dc.subject.meshHormone Replacement Therapy
dc.subject.meshHumans
dc.subject.meshMiddle Aged
dc.subject.meshNipples
dc.subject.meshPostmenopause
dc.subject.meshPremenopause
dc.subject.meshProteins
dc.subject.meshReceptors, Estrogen
dc.subject.meshReference Values
dc.subject.meshTamoxifen
dc.subject.meshTumor Suppressor Proteins
dc.titleHormonally-regulated proteins in breast secretions are markers of target organ sensitivity.en
dc.typeArticleen
dc.contributor.departmentDepartment of Surgery, University Hospital of South Manchester, West Didsbury, UK.en
dc.identifier.journalBritish Journal of Canceren
html.description.abstractAnti-oestrogen therapy is being used in an attempt to prevent breast cancer but no intermediate end points of the effect of tamoxifen on the normal breast are available. Therefore, the purpose of this study was to develop a physiological measure of oestrogen action on the breast. We measured oestrogen-stimulated and -inhibited proteins in breast secretions from women on and off anti-oestrogen therapy. Two oestrogen-stimulated proteins (pS2 and cathepsin D) and oestrogen-inhibited proteins (CP15, gross cystic disease fluid protein 15; Apo,: apolipoprotein D) were measured. Premenopausal women had significantly higher pS2 and cathepsin D in association with lower Apo D and CP15 secretion levels compared to post-menopausal women. Sequential nipple aspirates from women treated with the luteinizing hormone releasing hormone agonist goserelin (n = 9), tamoxifen (n = 9) and hormone replacement therapy (HRT) (n = 26) were measured. Following treatment with goserelin, median nipple secretion levels of pS2 fell (P < 0.02) and Apo D and CP15 rose significantly (P < 0.03 and P < 0.05 respectively). Similar changes were seen on tamoxifen therapy but not in untreated control women. Treatment with HRT resulted in a rise of pS2 (P < 0.001) and a fall in Apo D (P < 0.05). Measurement of pS2 and Apo D in nipple aspirates may prove useful intermediate end point of breast responsiveness to anti-oestrogens.


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