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Australasian Biotechnology (backfiles)
ISSN: 1036-7128
Vol. 8, No. 2, 1998
Bioline Code: au98019
Full paper language: English
Document type: Research Article
Document available free of charge

Australasian Biotechnology (backfiles), Vol. 8, No. 2, 1998

 en Prostate Cancer Gene Therapy


Australasian Biotechnology,
Volume 8 Number 2, March/April 1998, pp. 99-106


Prostate Cancer Gene Therapy

Russell PJ, Martiniello-Wilks R, Lockett LJ, Brookes DE, Zandvliet D, Watt F, Molloy PL, Khatri A, and Both GW.

Code Number:AU98019
Sizes of Files:
Text: 29K
Graphics: Line drawings (gif) - 57K

Recent developments in molecular biology have provided the opportunity for new gene therapy-based approaches for treating prostate cancer. A range of approaches are being taken for different cancer types, with over a hundred clinical trials of gene therapy for cancer currently approved in the USA. Three types of approach with potential application for prostate cancer have been tested in animal models. Attempts have been made to "rectify" mutations contributing to cancers by re-introduction of normal tumour suppressor genes. In a number of instances, this has led to induction of apoptotic cell death with substantial tumour regression. Several laboratories have introduced genes into tumour cells, either ex vivo or in vivo, to express cytokines and/or immune costimulatory molecules, in order to stimulate the immune system and enhance specific targeting of cancer cells. This could be of considerable therapeutic benefit for prostate cancers which are generally poorly immunogenic. A further approach, and one which we have been investigating, is termed enzymedirected prodrug therapy (EPT). In EPT, a gene encoding an enzyme foreign to mammalian cells, eg. Herpesvirus thymidine kinase (HSVTK) or E. coli purine nucleoside phosphorylase (PNP), is introduced into the tumour cells where it is expressed. The appropriate prodrug substrate for the enzyme, eg. ganciclovir for HSVTK or 6-methyl purine 2deoxyriboside for PNP, is given systemically but is only metabolised to its toxic product at the tumour site. Using recombinant adenovirus we have delivered both of these EPT systems to PC3 prostate cancer cells xenografted in nude mice. Both systems exhibited strong suppression of tumour growth and enhanced mouse survival. Approaches to developing targeting specificity for these systems and their application to prostate cancer patients are discussed.

Copyright 1998 Australian Biotechnology Association Ltd.


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