Loss of oestrogen-receptor (ER) expression and function may explain the development of tamoxifen resistance in breast cancer. In 72 paired biopsies the immunohistochemical expression of ERs was reduced from 51% before tamoxifen treatment to 29% at progression or relapse, with a reduction in mean H-score from 90 to 61 (P<0.001, paired t-test). However, there was no significant change in progesterone receptor (PgR) or pS2 expression, markers of ER function. Tumours which developed acquired resistance after primary tamoxifen treatment frequently remained ER+ve at relapse (61%) and continued to express PgR or pS2. In contrast, those which progressed with de novo resistance were all ER−ve, although 6 of these tumours expressed high levels of PgR and/or pS2. In tumours which recurred during adjuvant tamoxifen therapy, the frequency and quantitative level both of ERs and of PgR were significantly reduced. These data imply that separate mechanisms of tamoxifen resistance may exist in these clinical subgroups.
Endocrine-Related Cancer (1995) 2 105-110
Endocrine-Related Cancer is committed to supporting researchers in demonstrating the impact of their articles published in the journal.
The two types of article metrics we measure are (i) more traditional full-text views and pdf downloads, and (ii) Altmetric data, which shows the wider impact of articles in a range of non-traditional sources, such as social media.
More information is on the Reasons to publish page.
| Sept 2018 onwards | Past Year | Past 30 Days | |
|---|---|---|---|
| Full Text Views | 129 | 1 | 0 |
| PDF Downloads | 139 | 0 | 0 |
Online ISSN: 1479-6821
Print ISSN: 1351-0088
Strengthening biomedical communities
to advance science and health
CONTACT US
Bioscientifica Ltd | Starling House | 1600 Bristol Parkway North | Bristol BS34 8YU | UK
Bioscientifica Ltd | Registered in England no 3190519
