Abstract
BackgroundEstrogen receptor (ER) positive breast cancer can often be treated by hormone therapy; however a certain population of ER-positive patients become resistant to hormone therapy after long-term hormone treatment. Ethinylestradiol (EE2) is a derivative of estrogen, which has shown promising effects in these patients.MethodsWe successfully obtained tissue samples from 6 patients undergoing EE2 treatment and examined 13 well-known breast cancer-related factors by immunohistochemistry. Of the 6 patients, 5 responded but one patient did not.ResultsBefore EE2 treatment, staining for both ER and androgen receptor (AR) was strong in the nucleus, and the progesterone receptor (PgR) was almost no staining. EE2 treatment significantly down-regulated ER and up-regulated PgR while nuclear and cytosolic AR were oppositely down- and up-regulated, respectively. Cytosolic staining of BRCA1 was significantly up-regulated by EE2 whereas nuclear staining tended to decrease. Individual comparisons suggested less induction of PgR and decreasing AKT but increasing pAKT in the non-responder following EE2 treatment.ConclusionsOur observations revealed that EE2 activated ER downstream genes; however it did not stimulate cell growth. This suggests that hormone resistant cells might receive growth signals from a non-genomic pathway and this may be reflected in their sensitivity to EE2 treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s40064-015-0851-8) contains supplementary material, which is available to authorized users.
Highlights
Estrogen receptor (ER) positive breast cancer can often be treated by hormone therapy; a certain population of ER-positive patients become resistant to hormone therapy after long-term hormone treatment.Ethinylestradiol (EE2) is a derivative of estrogen, which has shown promising effects in these patients
First of all, we focused on 13 genes and factors, which are related to cancer progression and performed immunostaining to see how these genes were regulated during EE2 treatment in this study
Our results showed that when EE2 treatment ends i.e. in the post-EE2 group, tumors became resistant to EE2 and started to grow again as shown by the Ki67 index which tended to increase after treatment
Summary
Estrogen receptor (ER) positive breast cancer can often be treated by hormone therapy; a certain population of ER-positive patients become resistant to hormone therapy after long-term hormone treatment.Ethinylestradiol (EE2) is a derivative of estrogen, which has shown promising effects in these patients. Estrogen receptor (ER) positive breast cancer can often be treated by hormone therapy; a certain population of ER-positive patients become resistant to hormone therapy after long-term hormone treatment. There are several different types of anti-estrogenic agents; Tamoxifen is an antagonist of ER, and has been widely used to treat cancer in both pre- and postmenopausal women. Aromatase inhibitors (AIs) are the representative anti-estrogenic agents in post-menopausal women, and are the first choice for patients after. Fulvestrant is an estrogen receptor antagonist with no agonist effects, which works by down-regulating the estrogen receptor (Kansra et al.2005). These agents generally inhibit ER function by either decreasing production of estrogen or by blocking the ER itself
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