title: [Bone metastases of breast cancer].
abstract: Bone is one of the most preferential metastatic target sites for cancers. The biological crosstalk between metastatic cancer cells and bone microenvironment is critical to the pathophysiology of bone metastases. For example, It is well established that PTH-rP production in cancer cells stimulated by bone-derived TGF-β facilitates bone metastasis through promoting bone resorption by osteoclasts, thereby establishing "vicious cycle" between metastatic cancer cells and bone. In addition, recent studies identified several new players including platelets and MDSCs which contribute to the development of bone metastasis. In this review, we will overview the current topics on the mechanism by which bone metastasis is modulated at cellular and molecular levels.
authors: Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Japan.
authors: Kenji
authors: K
authors: Hata
authors: Toshiyuki
authors: T
authors: Yoneda
mesh_terms: D001859:Bone Neoplasms / Q000556:secondary*; D001862:Bone Resorption / Q000378:metabolism / Q000473:pathology; D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D010010:Osteoclasts / Q000378:metabolism*; D044162:Parathyroid Hormone-Related Protein / Q000378:metabolism; D059016:Tumor Microenvironment
chemical_list: D044162:Parathyroid Hormone-Related Protein