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dc.contributor.authorEllis, P Aen
dc.contributor.authorSaccani-Jotti, Gen
dc.contributor.authorClarke, Robert Ben
dc.contributor.authorJohnston, S Ren
dc.contributor.authorAnderson, Elizabethen
dc.contributor.authorHowell, Anthonyen
dc.contributor.authorA'Hern, Ren
dc.contributor.authorSalter, Jen
dc.contributor.authorDetre, Sen
dc.contributor.authorNicholson, Ren
dc.contributor.authorRobertson, Jen
dc.contributor.authorSmith, I Een
dc.contributor.authorDowsett, Men
dc.date.accessioned2010-03-24T14:46:14Z
dc.date.available2010-03-24T14:46:14Z
dc.date.issued1997-08-07
dc.identifier.citationInduction of apoptosis by tamoxifen and ICI 182780 in primary breast cancer. 1997, 72 (4):608-13 Int. J. Canceren
dc.identifier.issn0020-7136
dc.identifier.pmid9259399
dc.identifier.doi10.1002/(SICI)1097-0215(19970807)72:4<608::AID-IJC10>3.0.CO;2-7
dc.identifier.urihttp://hdl.handle.net/10541/94898
dc.description.abstractHormonal breast cancer therapies have traditionally been considered cytostatic, but recent pre-clinical data suggest that anti-oestrogens can induce apoptosis. The aim of this study was to assess whether tamoxifen (TAM) and ICI 182780 (ICI) could induce apoptosis in human breast cancer, and whether this was related to oestrogen receptor status. We measured apoptosis in primary breast cancer patients before and after pre-surgical treatment with 20 mg/day TAM (study 1) or 6 or 18 mg/day ICI (study 2). In each study there was a randomised non-treatment (NT) control group. TAM significantly increased apoptotic index (AI) in ER+ but not in ER- tumours. There was a significant increase in AI following treatment with ICI. Insufficient pairs of samples were available to determine whether this change was confined to ER+ tumours, but in a cross-sectional analysis AI was significantly higher in excision biopsies for ICI-treated than NT patients for ER+ but not ER- tumours. Our results provide clinical evidence that apoptosis may be induced in ER+ primary breast cancer by both non-steroidal and steroidal anti-oestrogens.
dc.language.isoenen
dc.subjectBreast Canceren
dc.subjectOestrogen Antagonistsen
dc.subjectOestrogen Receptorsen
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshAged, 80 and over
dc.subject.meshAntineoplastic Agents
dc.subject.meshAntineoplastic Agents, Hormonal
dc.subject.meshApoptosis
dc.subject.meshBiopsy
dc.subject.meshBreast Neoplasms
dc.subject.meshCombined Modality Therapy
dc.subject.meshEstradiol
dc.subject.meshEstrogen Antagonists
dc.subject.meshFemale
dc.subject.meshHumans
dc.subject.meshLongitudinal Studies
dc.subject.meshMiddle Aged
dc.subject.meshParaffin Embedding
dc.subject.meshPlacebos
dc.subject.meshReceptors, Estrogen
dc.subject.meshTamoxifen
dc.titleInduction of apoptosis by tamoxifen and ICI 182780 in primary breast cancer.en
dc.typeArticleen
dc.contributor.departmentDepartment of Biochemical Endocrinology, Royal Marsden NHS Trust, London, UK.en
dc.identifier.journalInternational Journal of Cancer.en
html.description.abstractHormonal breast cancer therapies have traditionally been considered cytostatic, but recent pre-clinical data suggest that anti-oestrogens can induce apoptosis. The aim of this study was to assess whether tamoxifen (TAM) and ICI 182780 (ICI) could induce apoptosis in human breast cancer, and whether this was related to oestrogen receptor status. We measured apoptosis in primary breast cancer patients before and after pre-surgical treatment with 20 mg/day TAM (study 1) or 6 or 18 mg/day ICI (study 2). In each study there was a randomised non-treatment (NT) control group. TAM significantly increased apoptotic index (AI) in ER+ but not in ER- tumours. There was a significant increase in AI following treatment with ICI. Insufficient pairs of samples were available to determine whether this change was confined to ER+ tumours, but in a cross-sectional analysis AI was significantly higher in excision biopsies for ICI-treated than NT patients for ER+ but not ER- tumours. Our results provide clinical evidence that apoptosis may be induced in ER+ primary breast cancer by both non-steroidal and steroidal anti-oestrogens.


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