Ji-Ping Wang

TL;DR: The weight of evidence supports the possibility that both ER-dependent and independent mechanisms are involved in the carcinogenic process and anti-estrogens block only receptor mediated pathways whereas the aromatase inhibitors block both.

TL;DR: These studies provide the first direct evidence that in situ synthesis of E2 in breast tumors, as opposed to peripheral aromatization and uptake from plasma, can enhance tissue E2 levels and stimulate tumor growth.

TL;DR: The results suggest that ER‐independent actions of E2 can influence breast tumor development in concert with ER dependent effects, and suggest 1 mechanism whereby AIs, which block E2 synthesis, would be more effective for breast cancer prevention than use of antiestrogens, which only block ER‐mediated effects.

TL;DR: It is demonstrated that hypersensitivity to E2 could occur under more complex in vivo conditions and that MAP kinase activation is enhanced under these circumstances.