Immunohistochemical analysis in ethinylestradiol-treated XXXX after prior long-term estrogen-deprivation therapy.

@entity1 @entity23447 @entity1782 @entity0 @entity7273 @entity5345
BACKGROUND: @entity1782 ( @entity1782 ) positive @entity0 can often be treated by hormone therapy; however a certain population of @entity1782 -positive @entity1 become resistant to hormone therapy after long-term hormone treatment. Ethinylestradiol (EE2) is a derivative of estrogen, which has shown promising effects in these @entity1 . METHODS: We successfully obtained tissue samples from 6 @entity1 undergoing EE2 treatment and examined 13 well-known @entity0 -related factors by immunohistochemistry. Of the 6 @entity1 , 5 responded but one @entity1 did not. RESULTS: Before EE2 treatment, staining for both @entity1782 and @entity23447 ( @entity23447 ) was strong in the nucleus, and the @entity7273 ( @entity7273 ) was almost no staining. EE2 treatment significantly down-regulated @entity1782 and up-regulated @entity7273 while nuclear and cytosolic @entity23447 were oppositely down- and up-regulated, respectively. Cytosolic staining of @entity5345 was significantly up-regulated by EE2 whereas nuclear staining tended to decrease. Individual comparisons suggested less induction of @entity7273 and decreasing AKT but increasing pAKT in the non-responder following EE2 treatment. CONCLUSIONS: Our observations revealed that EE2 activated @entity1782 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.
