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    Abnormal regulation of the oestrogen receptor in benign breast lesions.

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    Authors
    Shoker, B S
    Jarvis, C
    Clarke, Robert B
    Anderson, Elizabeth
    Munro, C
    Davies, M P
    Sibson, D R
    Sloane, J P
    Affiliation
    Department of Pathology, University of Liverpool, UK. b.s.shoker@Liverpool.ac.uk
    Issue Date
    2000-10
    
    Metadata
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    Abstract
    BACKGROUND: In normal breast tissue the oestrogen receptor (ER) and the proliferation associated antigen Ki67 are negatively associated, indicating that ER+ cells are non-dividing, or that the receptor is downregulated as cells enter cycle. This relation is completely or partially lost in many ER+ breast cancers and in in situ proliferations associated with an increased cancer risk, where coexpression of the two markers is often found. AIMS: To determine whether similar changes can be identified in other risk associated breast lesions. PATIENTS/METHODS: Paraffin wax blocks from 12 cases of lactational change, 21 apocrine metaplasias, 22 duct ectasias, 20 sclerosing adenosis, 20 fibroadenomas, 19 phyllodes tumours, 20 radial scars, 21 papillomas (15 solitary and six multiple), 15 gynaecomastias, and nine postmortem male breast tissues were retrieved. Immunohistochemistry was used to determine the expression of ER and dual labelling immunofluorescence was used to detect cells expressing both ER and Ki67. RESULTS: Increased numbers of ER+ cells were seen in sclerosing adenosis, radial scars, papillomas, fibroadenomas, and phyllodes tumours but not in apocrine cysts (where no ER+ cells were detected) or duct ectasia (where normal numbers were found). As in the normal breast, the proportion of ER+ cells increased with age in all lesions with the exception of fibroadenomas. Coexpression of ER and Ki67 was found in an increased proportion of cells of all risk associated lesions studied. ER+ cells were less likely to be dividing than ER- cells in all cases, although this was significant only for sclerosing adenosis. The data on sclerosing adenosis, radial scars, papillomas, and fibroadenomas are comparable with those reported previously in hyperplasia of usual type, whereas those in duct ectasia are similar to those of the normal breast. The findings in all lesions, however, differed from those in ductal carcinoma in situ, where proportions of ER+ and ER+/Ki67+ cells are higher and the relation between ER+ cell numbers and age is lost. Thus, the nature and degree of dysregulation of ER in benign breast lesions is broadly in accordance with the degree of risk of developing breast cancer with which they are associated. In gynaecomastia, the proportions of ER+ and ER+/Ki67+ cells were comparable with those seen in benign female breast lesions, but changes with age were not observed. However, the changes in gynaecomastia were similar to those seen in normal male breast. CONCLUSION: These findings are in keeping with the contention that the dissociation of ER and Ki67 expression is a very early change in the pathway to many breast cancers. However, this change might only have preneoplastic importance in the hormonal milieu of the female breast.
    Citation
    Abnormal regulation of the oestrogen receptor in benign breast lesions. 2000, 53 (10):778-83 J. Clin. Pathol.
    Journal
    Journal of Clinical Pathology
    URI
    http://hdl.handle.net/10541/86123
    DOI
    10.1136/jcp.53.10.778
    PubMed ID
    11064673
    Type
    Article
    Language
    en
    ISSN
    0021-9746
    ae974a485f413a2113503eed53cd6c53
    10.1136/jcp.53.10.778
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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