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 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 …

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

Breast cancer bone metastases (BMET) are incurable, primarily osteolytic, and occur most
commonly in estrogen receptor-α positive (ER+) breast cancer. ER+ human breast cancer …

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 …

Disruption of bone homeostasis caused by metastatic osteolytic breast cancer cells
increases inflammatory osteolysis and decreases bone formation, thereby predisposing …

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 …

While tumoral Smad-mediated transforming growth factor β (TGFβ) signaling drives
osteolytic estrogen receptor α-negative (ER-) breast cancer bone metastases (BMETs) in …

The bones are the most common sites of breast cancer metastasis. Upon arrival within the
bone microenvironment, breast cancer cells coordinate the activities of stromal cells …

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 …