Multiple Myeloma (MM) is a malignancy of immunoglobulin (Ig)-synthesizing plasma cells, that home to and expand in the bone marrow. Although presenting with the same histological features, MM is characterised by a high genomic heterogeneity. There is a growing awareness that the interactions between MM plasma cells, stromal cells, hematopoietic cells, and the extracellular matrix (ECM) is as important as the genetic changes in the disease progression. Pathophysiological interactions of myeloma cells within the bone marrow microenvironment are highlighted by the progressionassociated bone disease and neovascularization, and are witnessed by autocrine/paracrine circuits that activate multiple signalling pathways and affect the most important aspects of the malignant phenotype, i.e., apoptosis/survival, proliferation, invasion, bone damage and angiogenesis.
Neovascularization, the formation of new vessels, represents one of the principal aspects of these interactions and a constant hallmark of disease progression.
This process is supported by angiogenic factors such as Vascular Endothelial Growth Factor (VEGF), Fibroblast Growth Factor-2 (FGF-2) and Hepatocyte Growth Factor (HGF) which are directly secreted by the tumour plasma cells and the stromal cells.
Roberto Ria, Multiple Myeloma: The Role of Angiogenesis in Disease Progression
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Last date updated on July, 2014