Multiple myeloma (MM) is a plasma cell malignancy characterized by an increase of the bone marrow angiogenesis. Angiopoietin-1 (Ang-1) is a critical factor in the regulation of physiological and pathological vessel formation that acts by binding to a specific receptor Tie2 expressed on endothelial cells. Recent evidences indicate that human MM cells produce Ang-1 and up-regulate its receptor Tie2 in bone marrow endothelial cells. An overexpression of Ang-1 has been also found in MM cells as compared to normal plasma cells. The correlation between Ang-1 expression and BM angiogenesis, demonstrated in MM patients, and the inhibitory effect of Tie2 blocking on MM-induced vessel formation suggest that Ang-1 production by MM cells is critically involved in the angiogenic process in MM. In this review we focalize our attention on Ang-1/Tie2 system and its role in MM-induced angiogenesis.
Angiopoietin-1 and myeloma-induced angiogenesis / Giuliani, Nicola; Colla, S; Morandi, F; Rizzoli, Vittorio. - In: LEUKEMIA & LYMPHOMA. - ISSN 1042-8194. - 46:(2005), pp. 29-33.
Angiopoietin-1 and myeloma-induced angiogenesis
GIULIANI, Nicola;RIZZOLI, Vittorio
2005-01-01
Abstract
Multiple myeloma (MM) is a plasma cell malignancy characterized by an increase of the bone marrow angiogenesis. Angiopoietin-1 (Ang-1) is a critical factor in the regulation of physiological and pathological vessel formation that acts by binding to a specific receptor Tie2 expressed on endothelial cells. Recent evidences indicate that human MM cells produce Ang-1 and up-regulate its receptor Tie2 in bone marrow endothelial cells. An overexpression of Ang-1 has been also found in MM cells as compared to normal plasma cells. The correlation between Ang-1 expression and BM angiogenesis, demonstrated in MM patients, and the inhibitory effect of Tie2 blocking on MM-induced vessel formation suggest that Ang-1 production by MM cells is critically involved in the angiogenic process in MM. In this review we focalize our attention on Ang-1/Tie2 system and its role in MM-induced angiogenesis.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.