c-erbB2 oncoprotein expression, gene amplification, and chromosome 17 aneusomy in apocrine adenosis of the breast
Article
Selim, A., Elayat, G. and Wells, C. 2000. c-erbB2 oncoprotein expression, gene amplification, and chromosome 17 aneusomy in apocrine adenosis of the breast. The Journal of Pathology. 191 (2), pp. 138-142. https://doi.org/10.1002/(sici)1096-9896(200006)191:2<138::aid-path611>3.0.co;2-j
Type | Article |
---|---|
Title | c-erbB2 oncoprotein expression, gene amplification, and chromosome 17 aneusomy in apocrine adenosis of the breast |
Authors | Selim, A., Elayat, G. and Wells, C. |
Abstract | Amplification of the c-erbB2 oncogene and numerical aberrations of chromosome 17 occur in human breast carcinomas. Apocrine adenosis (AA) of the breast has been shown occasionally to have c-erbB2 overexpression and a possible premalignant potential, but little is known about cellular level genetic alterations in AA of the breast. Fluorescence in situ hybridization (FISH) is a new approach to detect these. In this study, a series of AA was studied by immunohistochemistry for c-erbB2 protein expression and by FISH using dual colour DNA probes for the c-erbB2 gene and the centromeric region of chromosome 17. Cell membrane immunostaining was seen in 10/18 (55.6%) AA cases, but unequivocal c-erbB2 gene amplification or chromosome 17 aneusomy was not seen. The results of this study suggest that c-erbB2 overexpression without amplification may occur early in breast oncogenesis. Amplification and numerical chromosome aberrations may occur later in the pathogenesis of apocrine-derived breast carcinomas. Copyright © 2000 John Wiley & Sons, Ltd. |
Publisher | Wiley |
Journal | The Journal of Pathology |
ISSN | 0022-3417 |
Electronic | 1096-9896 |
Publication dates | |
26 May 2000 | |
Publication process dates | |
Deposited | 26 Sep 2023 |
Output status | Published |
Digital Object Identifier (DOI) | https://doi.org/10.1002/(sici)1096-9896(200006)191:2<138::aid-path611>3.0.co;2-j |
https://repository.mdx.ac.uk/item/8zv3v
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