The additional finding of enhanced, E2 dose-dependent, ERα-regulated secretion of PTHrP, an osteolytic factor expressed in most clinical BMETs[62,63], from BMET-derived ER+ breast cancer cells further supports this postulate and provides possible mechanistic insights for specific pathways downstream of tumoral ERα activation that may contribute to ER+ BMET-associated osteolysis. Here, PTHLH is linked to breast cancer.