Bone marrow angiogenesis in myeloma and its precursor disease: a prospective clinical trial

In multiple myeloma (MM), increased angiogenesis of the bone marrow (BM) involves a complex interplay of proangiogenic and antiangiogenic molecules induced by plasma cells (PCs) within the BM microenvironment, with eventual balance tipped in favor of an ‘angiogenic switch,’ as the disease transitions to MM from preceding monoclonal gammopathy of undetermined significance (MGUS) and smoldering MM (SMM).1, 2 The dynamic nature of angiogenesis can be exploited by highly active anti-myeloma agents, such as thalidomide, its derivatives, the immunomodulatory drugs (IMiDs™) and proteasome inhibitors, which not only interfere with tumor vessel growth, but also cause significant regression of the tumor vasculature both in vitro and in vivo. Therefore, there is great interest in studying the role of angiogenesis in MM to define therapeutic targets, prognostic and predictive biomarkers, as well as monitor disease activity longitudinally.