@article {7652,
	title = {Sclerostin: A possible target for the management of cancer-induced bone disease},
	journal = {Expert Opinion on Therapeutic Targets},
	volume = {16},
	year = {2012},
	note = {Cited By :17Export Date: 21 February 2017},
	month = {2012},
	pages = {761 - 769},
	abstract = {Introduction: Sclerostin is a cysteine-knot-containing protein, which is produced by osteocytes and inhibits osteoblast function. The aim of this review is to summarize the data about the role of sclerostin in cancer-induced bone disease. Areas covered: We performed a thorough search for articles in the PubMed using the words "sclerostin, cancer, multiple myeloma", and for similar abstracts that were presented in the ASH and ASCO annual meetings (2005 2011). In multiple myeloma, sclerostin is produced by myeloma cells and elevated in the serum or the plasma of the patients, and correlates with extensive bone disease and adverse myeloma features. In prostate cancer, sclerostin expression is reduced and in combination with bone morhogenetic protein-6 and noggin expression may serve as prognostic predictor for metastatic progression. In breast cancer, in vitro data suggest that the malignant cell induces the expression of sclerostin to inhibit osteoblasts in the metastatic bone area. Expert opinion: Sclerostin may play a role in inhibiting bone formation in the biology of bone metastases in breast cancer and of myeloma-related bone disease. The results of phase I/II studies with anti-sclerostin drugs in subjects with low bone mass may lead to the potential clinical investigation of these agents in cancer-indauced bone disease. {\textcopyright} 2012 Informa UK, Ltd.},
	keywords = {Bone, Cancer, Metastases, myeloma, Sclerostin, Wnt signaling},
	url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84863959463\&doi=10.1517\%2f14728222.2012.697154\&partnerID=40\&md5=a0cbb8cd4a6643d4f54873b7b64d2b84},
	author = {Gkotzamanidou, M. and Dimopoulos, M.A. and Kastritis, E. and Christoulas, D. and Moulopoulos, L.A. and Terpos, E.}
}
