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Clive A. Wells

Researcher at Queen Mary University of London

Publications -  9
Citations -  226

Clive A. Wells is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Apocrine & Ductal carcinoma. The author has an hindex of 7, co-authored 9 publications receiving 215 citations. Previous affiliations of Clive A. Wells include St Bartholomew's Hospital.

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Consistency of staining and reporting of oestrogen receptor immunocytochemistry within the European Union—an inter-laboratory study

TL;DR: To assess the variability of oestrogen receptor (ER) testing using immunocytochemistry, centrally stained and unstained slides from breast cancers were circulated to the members of the European Working Group for Breast Screening Pathology, who were asked to report on both slides.
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Expression of c-erbB2, p53, Bcl-2, Bax, c-myc and Ki-67 in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast

TL;DR: It is indicated that a subset of breast lesions containing APM epithelium show abnormal oncoprotein and apoptosis-related protein expression and have a higher proliferation rate.
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Epithelial patchy necrosis in Crohn's disease

TL;DR: Electron and light microscopic studies of the intestinal epithelium in Crohn's disease demonstrated localized areas of damage to the superficial epithelia, occurring without accompanying acute inflammation.
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Platelet-derived growth factor expression in phyllodes tumors and fibroadenomas of the breast.

TL;DR: PDGF influences the pathogenesis of fibroepithelial breast tumors and that PDGF-dependent paracrine and autocrine mechanisms may operate, and it is possible that assessment of PDGF and PDGFRbeta expression could contribute to the management of these tumors in the future.
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C-myc oncoprotein expression and gene amplification in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast

TL;DR: The results of this study indicate that c-myc overexpression appears to occur early in breast oncogenesis, suggesting that this particular genetic alteration constitutes a late event in the pathogenesis of breast carcinomas.