The mechanism of tamoxifen action on glioma cell lines
type: CreativeWork
description: Tamoxifen, a member of the selective estrogen receptor modulator (SERM) family, is widely used in the treatment of estrogen-receptor (ER) positive breast cancer. It has been shown in previous studies that Tamoxifen exerts an antiproliferative effect in patients harbouring glioma. Glioma brain tumours differ from most other cancers by their diffusive invasion of the surrounding normal tissue and frequent recurrence following all forms of therapy. It is this invasive nature that ultimately contributes to their poor 6-12 month prognosis. Because of their profound devastating effect much research is currently being carried out to investigate gliomas and it seems that the chemosensitivity of gliomas, i.e. the analysis of glioma response to a specific drug, is a focal point of developing treatment, and more recently an idea of prevention. Tamoxifen is considered to exert its anitproliferative effect in ER-positive neoplasms through blocking the estrogen receptor, thus, inhibiting gene transcription and cellular proliferation. In vitro studies have shown that Tamoxifen can inhibit the growth of a brain tumour cell lines, but whether the mechanism involves oestrogen blockade remains a matter of some debate. As well as its effect in blocking estrogen receptors, Tamoxifen is also known to exert antiproliferative effects via non-receptor mediated mechanisms including the blockage of Protein Kinase C and inhibition of the MAPK family among a vast array of cellular signalling pathways. This study employed three different glioma cell lines to investigate the antiproliferative effect of Tamoxifen. The results of this study have demonstrated that Tamoxifen induces cell death in a dose-dependent manner in all three cell lines. Moreover, cells pre-treated with 50 nM of 17-estradiol for 1 week prior to treatment with Tamoxifen demonstrated no significant increase in cell death. Previous work in the University laboratory (unpublished) has indicated that Tamoxifen can affect MAPK activi…
abstract: Tamoxifen, a member of the selective estrogen receptor modulator (SERM) family, is widely used in the treatment of estrogen-receptor (ER) positive breast cancer. It has been shown in previous studies that Tamoxifen exerts an antiproliferative effect in patients harbouring glioma. Glioma brain tumours differ from most other cancers by their diffusive invasion of the surrounding normal tissue and frequent recurrence following all forms of therapy. It is this invasive nature that ultimately contributes to their poor 6-12 month prognosis. Because of their profound devastating effect much research is currently being carried out to investigate gliomas and it seems that the chemosensitivity of gliomas, i.e. the analysis of glioma response to a specific drug, is a focal point of developing treatment, and more recently an idea of prevention. Tamoxifen is considered to exert its anitproliferative effect in ER-positive neoplasms through blocking the estrogen receptor, thus, inhibiting gene transcription and cellular proliferation. In vitro studies have shown that Tamoxifen can inhibit the growth of a brain tumour cell lines, but whether the mechanism involves oestrogen blockade remains a matter of some debate. As well as its effect in blocking estrogen receptors, Tamoxifen is also known to exert antiproliferative effects via non-receptor mediated mechanisms including the blockage of Protein Kinase C and inhibition of the MAPK family among a vast array of cellular signalling pathways. This study employed three different glioma cell lines to investigate the antiproliferative effect of Tamoxifen. The results of this study have demonstrated that Tamoxifen induces cell death in a dose-dependent manner in all three cell lines. Moreover, cells pre-treated with 50 nM of 17-estradiol for 1 week prior to treatment with Tamoxifen demonstrated no significant increase in cell death. Previous work in the University laboratory (unpublished) has indicated that Tamoxifen can affect MAPK activi…
author: Cantrill, Carina
language: en
keywords: C100 - Biology
date published: 2007-04
date modified: 2026-07-24T01:36:00Z
provider: University of Central Lancashire
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Central Lancashire