The osteoblastic niche in the context of multiple myeloma. (25th November 2014)

• Record Type: Journal Article
• Authors: Toscani, Denise; Bolzoni, Marina; Accardi, Fabrizio; Aversa, Franco; Giuliani, Nicola
• Other Names: Zaidi Mone guestEditor.
• Is Part Of: Annals of the New York Academy of Sciences. Volume 1335(2015)
• Page Start: 45
• Page End: 62
• Publication Date: 2014-11-25
• Subjects: myeloma -- osteoblast -- osteocyte -- bone disease -- Wnt signaling -- Toscani, D., M. Bolzoni, F. Accardi, et al. 2014. The osteoblastic niche in the context of multiple myeloma. In "MARROW, " ed. by M. Zaidi. Ann. N.Y. Acad. Sci. xxxx: 1–18.; Medical sciences -- Periodicals; Medicine -- Periodicals; Science -- Periodicals; 610
• DOI: 10.1111/nyas.12578
• Languages: English
• ISSNs: 0077-8923

Abstract

Abstract : The osteoblastic niche has a critical role in the regulation of hemopoietic stem cell (HSC) quiescence and self‐renewal and in the support of hematopoiesis. Several mechanisms are involved in the crosstalk between stem cells and osteoblasts, including soluble cytokines, adhesion molecules, and signal pathways such as the wingless‐Int (Wnt), Notch, and parathyroid hormone pathways. According to the most recent evidence, there is an overlap between osteoblastic and perivascular niches that affects HSC function involving mesenchymal stromal and endothelial cells and a gradient of oxygen regulated by hypoxia inducible factor (HIF)‐1α. Derived from plasma cells, multiple myeloma (MM) is a hematopoietic malignancy characterized by a peculiar dependency on the bone microenvironment. Quiescent MM cells may reside in the osteoblastic niche for protection from apoptotic stimuli; in turn, MM cells suppress osteoblast formation and function, leading to impairment of bone formation and the development of osteolytic lesions. Several recent studies have investigated the mechanisms involved in the relationship between osteoblasts and MM cells and identified potential therapeutic targets in the osteoblastic niche, including the HIF‐1α, Runx2, and Wnt (both canonical and noncanonical) signaling pathways.