Abstract 17β-Estradiol (E2) promotes metastasis of triple negative breast cancer cells to
bone. Recent studies show many triple negative breast cancer cell lines lacking the 66 kDa …

The effect of 17-β-estradiol (E 2) on the induction of osteolytic lesions by estrogen receptor
(ER)-negative breast cancer cells was investigated in 4-week-old female nude mice …

Triple–negative breast cancer (TNBC) is thought to be an estradiol–independent, hormone
therapy–resistant cancer because of lack of estrogen receptor alpha 66 (ERα66). We …

Abstract Estrogen (E 2)-dependent ER+ breast cancer, the most common breast cancer
subtype, is also the most likely to metastasize to bone and form osteolytic lesions. However …

Methoxyestradiol (2ME2), a physiologic metabolite of 17β-estradiol (estrogen), has emerged
as a promising cancer therapy because of its potent growth-inhibitory and proapoptotic …

Metastasis to bone is a frequent problem of advanced breast cancer. Particularly breast
cancers, which do not express estrogen receptor α (ERα) and progesterone receptor (PR) …

Aim: Estrogen receptor α-positive (ER+) subtypes of breast cancer have the greatest
predilection for forming osteolytic bone metastases (BMETs). Because tumor-derived factors …

Abstract Although 17β‐estradiol (E2) replacement therapy has been shown to be effective in
treating postmenopausal osteoporosis, the underlying mechanism remains unclear. The …

Recently, a membrane‐based estrogen receptor (ER), ER‐α36, was identified and cloned
that transduces membrane‐initiated estrogen signaling such as activation of the mitogen …

Methoxyestradiol (2‐ME), a naturally occurring metabolite of 17β‐estradiol, is highly
cytotoxic to a wide range of tumor cells but is harmless to most normal cells. However, 2‐ME …