Well, talking about hormone in breast cancer there's not only ER but PR, Her-2/NEU etc. I'm neither a medical student nor a doctor and coicidentally my research is about breast cancer.
My question is, if hormone alone feeds the tumor say it by 1st diagnosis it's ER= 290 then after primary treatment 290 will be change to be less or still the same? or?
sorry if my question is incorrect and answer will be highly appreciated
Victoria, there is no simple answer to your question. Treatment of ER-positive breast cancer cells with tamoxifen decreases ER-mediated signaling but not necessarily the level of ER expression. Tamoxifen (specifically its active metabolite) is a selective estrogen receptor modulator (SERM) that binds to ER and modulates its activity rather than its expression on mRNA or protein level. On the other hand, fulvestrant, which is a selective estrogen receptor down-regulator (SERD), decreases the expression of ER on protein level (through enhanced ER degradation). As a result, the change of ER expression in breast cancer cells in response to hormone therapy is drug dependent. Situation is further complicated by the fact that the expression of ER (and also PR and HER2/neu) is not always stable and can change in the course of disease from primary to recurrent or metastatic lesions, so it is often not clear whether the observed change in ER expression is attributable to the effect of drug or drug-independent change in tumor biology, or sometimes just to tumor heterogeneity or problematic interpretation of test results for ER expression. In conclusion, there no simple answer.
Rohan: I agree that some reports showed lower levels of ER in groups of patients treated with tamoxifen compared to placebo. However, the available evidence does not support the conclusion that tamoxifen induces changes in ER-positive breast cancer cells that result in the down-regulation of ER. To name just a few reasons: (i) lack of paired data (on the same patients before and after the treatment), (ii) ER expression not consistently stable in the course of disease, (iii) lack of plausible mechanism, and (v) methodological issues. The study that you referred to reports 82.6% ER+ patients in placebo group and 69.2% ER+ patients in tamoxifen-treated group, but if we calculate 95% confidence intervals for these proportions, we will get 71.2-90.3% ER+ in placebo and 52.3-82.5% ER+ in tamoxifen groups, and these numbers are less convincing (p-val=0.148 by Fisher's test).
In addition, in vitro expression data available in Array Express (E-MTAB-2729) do not support significantly different expression of ER between tamoxifen and control treated MCF-7 cells, which are ER-positive (FC=-1.23, padj>0.1).
The point is not that tamoxifen never reduces the expression of ER in ER-positive tumor specimens. Instead, my conclusion is that this does not happen necessarily (in contrast to fulvestrant) and even in cases where it happens (on a tumor specimen level), it does not necessarily indicate causality on molecular level. To illustrate, the resistance to tamoxifen had been attributed (among other things) to the decreased expression of ER following the treatment with tamoxifen, but it does not mean that tamoxifen necessarily decreased the ER level in treated BC cells. It may just indicate that the treatment by tamoxifen favors survival of BC cells that do not express ER in mixed populations of cells (and we know that these cells are not rarely present since the expression of ER in clinical specimens can be quite heterogeneous).
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