Amplification of the androgen receptor may not explain the development of androgen-independent prostate cancer

Edwards, J. , Krishna, N.S., Mukherjee, R., Watters, A.D., Underwood, M.A. and Bartlett, J.M.S. (2001) Amplification of the androgen receptor may not explain the development of androgen-independent prostate cancer. BJU International, 88(6), pp. 633-637. (doi: 10.1046/j.1464-410X.2001.02350.x)

[img]
Preview
Text
bartlett_bju88.pdf

79kB

Publisher's URL: http://dx.doi.org/10.1046/j.1464-410X.2001.02350.x

Abstract

Objective To examine the role of androgen receptor (AR) gene amplification and aneusomy of the X chromosome in the development of antiandrogen-resistant prostate cancer. Patients and methods Twenty patients with prostate cancer resistant to androgen-deprivation therapy were selected for study. The records of patients with tumours before and after antiandrogen therapy, and with a full clinical follow-up, were retrieved. AR gene amplification and X chromosome copy number were assessed by fluorescence in situ hybridization using a labelled probe at locus Xq11-13 for the AR gene and a labelled a-satellite probe for the X chromosome. At least 20 nuclei were scored over three tumour areas by two independent observers. Results Aneusomy of the X chromosome was reported respectively in seven (35%) and 11 (55%) tumours before and after hormone relapse, the AR gene copy number was increased in seven (35%) and 13 (65%), respectively, and AR gene amplification was detected in one (5%) and three (15%), respectively. Neither increased AR copy number nor AR amplification in primary tumours precluded a biological response to androgen-deprivation therapy. Conclusion The rate of AR gene amplification is too low to be solely responsible for the development of antiandrogen-resistant prostate cancer. Also, the presence of amplified AR and cells aneusomic for the X chromosome in primary tumours that respond to androgen-deprivation therapy suggests that an increase in AR gene copy number does not prevent a tumour from responding to this therapy. Therefore other mechanisms which could cause hormone-refractory prostate cancer must be investigated before it is understood why so many patients relapse with this disease.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Edwards, Professor Joanne and Underwood, Mr Mark
Authors: Edwards, J., Krishna, N.S., Mukherjee, R., Watters, A.D., Underwood, M.A., and Bartlett, J.M.S.
Subjects:R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
R Medicine > RB Pathology
College/School:College of Medical Veterinary and Life Sciences > Institute of Cancer Sciences
Journal Name:BJU International
Publisher:Blackwell Publishing
ISSN:1464-4096
Copyright Holders:© Copyright 2001 BJU International
First Published:First published in BJU International 88(6):633-637
Publisher Policy:Reproduced in accordance with the copyright policy of the publisher.

University Staff: Request a correction | Enlighten Editors: Update this record