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
TypeArticle
Titlec-erbB2 oncoprotein expression, gene amplification, and chromosome 17 aneusomy in apocrine adenosis of the breast
AuthorsSelim, 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.

PublisherWiley
JournalThe Journal of Pathology
ISSN0022-3417
Electronic1096-9896
Publication dates
Print26 May 2000
Publication process dates
Deposited26 Sep 2023
Output statusPublished
Digital Object Identifier (DOI)https://doi.org/10.1002/(sici)1096-9896(200006)191:2<138::aid-path611>3.0.co;2-j
Permalink -

https://repository.mdx.ac.uk/item/8zv3v

  • 37
    total views
  • 0
    total downloads
  • 1
    views this month
  • 0
    downloads this month

Export as

Related outputs

Positive correlational shift between crevicular antimicrobial peptide LL-37, pain and periodontal status following non-surgical periodontal therapy. A pilot study
Madruga, D., Garcia, M., Martino, L., Hassan, H., Elayat, G., Ghali, L. and Ceballos, L. 2023. Positive correlational shift between crevicular antimicrobial peptide LL-37, pain and periodontal status following non-surgical periodontal therapy. A pilot study. BMC Oral Health. 23 (1), p. 335. https://doi.org/10.1186/s12903-023-03023-w
An overview of angiogenesis in bladder cancer
Elayat, G., Punev, I. and Selim, A. 2023. An overview of angiogenesis in bladder cancer. Current Oncology Reports. 25 (7), pp. 709-728. https://doi.org/10.1007/s11912-023-01421-5
Phytochemical modulation of apoptosis and autophagy: strategies to overcome chemoresistance in leukaemic stem cells in the bone marrow microenvironment
Owen, H., Appiah, S., Hasan, N., Ghali, L., Elayat, G. and Bell, C. 2017. Phytochemical modulation of apoptosis and autophagy: strategies to overcome chemoresistance in leukaemic stem cells in the bone marrow microenvironment. in: Zeng, B. and Zhao, K. (ed.) Neurobiology of Chinese Herb Medicine Elsevier.
Cyclin D-1 protein over-expression is not associated with gene amplification in benign and atypical apocrine lesions of the breast
Elayat, Ghada, Selim, Abdel-Ghani A., Gorman, Patricia, Tomlinson, Ian and Wells, Clive A. 2011. Cyclin D-1 protein over-expression is not associated with gene amplification in benign and atypical apocrine lesions of the breast. Pathology - Research and Practice. 207 (2), pp. 75-78. https://doi.org/10.1016/j.prp.2010.06.003
Cell turnover in apocrine metaplasia and apocrine adenosis of the breast
Elayat, G., Selim, A. and Wells, C. 2010. Cell turnover in apocrine metaplasia and apocrine adenosis of the breast. Annals of Diagnostic Pathology. 14 (1), pp. 1-7. https://doi.org/10.1016/j.anndiagpath.2009.05.001
Alterations of the cell cycle regulators cyclin D1, cyclin A, p27, p21, p16, and pRb in apocrine metaplasia of the breast
Elayat, G., Selim, A. and Wells, C. 2009. Alterations of the cell cycle regulators cyclin D1, cyclin A, p27, p21, p16, and pRb in apocrine metaplasia of the breast. Breast Journal. 15 (5), pp. 475-482. https://doi.org/10.1111/j.1524-4741.2009.00762.x
Cell cycle alterations and their relationship to proliferation in apocrine adenosis of the breast
Elayat, G., Selim, A. and Wells, C. 2009. Cell cycle alterations and their relationship to proliferation in apocrine adenosis of the breast. Histopathology. 54 (3), pp. 348-354. https://doi.org/10.1111/j.1365-2559.2009.03223.x
Non-operative breast pathology: Apocrine lesions
Wells, C. and Elayat, G. 2007. Non-operative breast pathology: Apocrine lesions. Journal of Clinical Pathology. 60 (12), pp. 1313-1320. https://doi.org/10.1136/jcp.2006.040626
C-myc oncoprotein expression and gene amplification in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast
Selim, A., Elayat, G., Naase, M. and Wells, C. 2002. C-myc oncoprotein expression and gene amplification in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast. The Breast. 11 (6), pp. 466-472. https://doi.org/10.1054/brst.2002.0474
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
Selim, A., Elayat, G. and Wells, C. 2002. 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. Virchows Archiv. 441, p. 449–455. https://doi.org/10.1007/s00428-002-0691-0
Loss of heterozygosity and allelic imbalance in apocrine metaplasia of the breast: Microdissection microsatellite analysis
Selim, A., Ryan, A., Elayat, G. and Wells, C. 2002. Loss of heterozygosity and allelic imbalance in apocrine metaplasia of the breast: Microdissection microsatellite analysis. The Journal of Pathology. 196 (3), pp. 287-291. https://doi.org/10.1002/path.1043