Please use this identifier to cite or link to this item:
|Title:||Is tamoxifen a genotoxic carcinogen in women?|
|Publisher:||Oxford University Press (OUP)|
|Citation:||Mutagenesis, 2009, 24 (5), pp. 391-404.|
|Abstract:||The anti-oestrogen tamoxifen, which is widely used in the treatment of breast cancer and is also approved for the prevention of this disease, causes an increased incidence of endometrial cancer in women. The ability of tamoxifen to induce endometrial tumours and the underlying carcinogenic mechanisms have been a subject of intense interest over the last ∼20 years. They are central to the assessment of risks versus benefits for the drug, especially in a chemopreventive context. This review outlines the clinical justification for using tamoxifen as a chemopreventive agent and describes the genotoxic mechanisms considered responsible for tamoxifen-induced tumours in rat liver and how these might relate to women. In rat hepatic tissue, tamoxifen is metabolically activated via α-hydroxylation and sulphate conjugation to give a reactive species that binds to DNA predominantly at the N2-position of guanine, producing pro-mutagenic lesions. Whether tamoxifen–DNA adducts contribute similarly to the development of cancers in women depends on whether they can be formed in human tissues and the type of specific molecular and cellular responses they induce, if present. This review discusses the current data relating to these issues and highlights areas where further research is needed.|
|Description:||This paper was published as Mutagenesis, 2009, 24 (5), pp. 391-404. It is available from http://www.ncbi.nlm.nih.gov/pubmed/19505894 or from the journal website at http://mutage.oxfordjournals.org/content/24/5/391.abstract. DOI: 10.1093/mutage/gep022|
Metadata only entry
|Appears in Collections:||Published Articles, Dept. of Cancer Studies and Molecular Medicine|
Files in This Item:
There are no files associated with this item.
Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.