May 18, 2015 05:50AM - edited May 18, 2015 06:00AM by Alpineartist
Well, I've finally been able to update on the question of whether estrogen receptor knockout affects er status of new lesions. This study on Tamoxifen suggests that long-term use of the drug in a small cohort showed a higher number of er-negative lesions in opposite breast. This article on the study quotes:
"The conclusion that there is an increase in ER-negative contralateral breast cancer was based on the results obtained on only 20 patients, 17 users of tamoxifen and three nonusers. The hazard ratio based on these numbers was 4.9 (95% CI = 1.4 to 17.4). The small number of events with a corresponding wide CI in a retrospective study does not provide clear evidence that the increased risk of ER-negative contralateral breast cancer is associated with tamoxifen use."
"No biologic data support the hypothesis that tamoxifen promotes ER-negative breast cancer. In fact, a comprehensive review of ER expression in breast cancer (12) concludes that ER expression is a stable phenotype. That is, there is no phenotypic drift, even in metastatic disease, after treatment with tamoxifen. However, there may be a decreased expression of the ER. It is known that breast cancer is heterogeneous and contains both ER-negative and ER-positive cells, which most likely have different origins, as has been recently suggested by gene-profiling studies of breast tumors (13). A more plausible scenario is that, when breast cancer is treated with tamoxifen, the ER-positive cells respond by decreasing proliferation and the ER-negative cells may continue to grow by selective pressure."
Footnote 12 above quotes:
"The concept that in breast cancers ER positivity drifts to ER negativity as a natural process of selection and increasing malignancy can no longer be supported. An alternative hypothesis is that ER is a stable phenotype in human breast cancer and ER positive-cells do not lose anti-oestrogen sensitivity by becoming ER negative."
Will provide more as it comes. Great week, all.