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Breast. 2002 Dec;11(6):466-72.

C-myc oncoprotein expression and gene amplification in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast.

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Department of Histopathology, St. Bartholomew's Hospital, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, University of London, West Smithfield, London EC1A 7BE, UK.


Overexpression and/or amplification of c-myc oncogene are known to occur in human breast carcinomas, particularly those of high grade. Apocrine metaplasia (APM) is a common finding within fibrocystic change, and in some cases appears to be associated with an elevated risk of subsequent breast cancer. It has been suggested that apocrine metaplasia within sclerosing adenosis of the breast, also called apocrine adenosis (AA), has a premalignant potential. Little, however, is known about cellular level genetic alterations in either APM or AA of the breast. Because of this, c-myc expression and amplification in APM and AA were studied. Fluorescence in situ hybridisation (FISH) is a methodological approach to detecting these genetic alterations. In this study, APM and AA were studied immunohistochemically to detect c-myc oncoprotein expression, and FISH was employed using a DNA probe for the c-myc gene in archival tissue sections of cases of APM and AA of the breast. Nuclear immunostaining for c-myc was seen in all APM and AA cases studied, but amplification of the c-myc gene was not seen in any cases with APM or AA. The results of this study indicate that c-myc overexpression appears to occur early in breast oncogenesis. Amplification of the c-myc gene does not occur in APM or AA of the breast, however, suggesting that this particular genetic alteration constitutes a late event in the pathogenesis of breast carcinomas.


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