NOTE: Although the IMF did not receive permission to post slides and audio from this presentation, we are bringing you a summary by our medical writer, Lynne Lederman, PhD.
AUTHORS: A. Vacca1, R. Ria1, A.M.L. Coluccia1, T. Cirulli1, C. Scavelli1, D. Ribatti2, F. Dammacco1
1Department of Internal Medicine and Clinical Oncology, and 2Department of Human Anatomy, Histology and Embryology, University of Bari Medical School, Bari, Italy
Angiogenesis in myeloma appears to be the result of new vessel formation by new mesenchymal cells recruited by the tumor cells. Hematopoietic stem cells from patients with myeloma before therapy as well as macrophages could differentiate into an endothelial cell type when cultured with the appropriate growth factors on a suitable support system. Factors released by myeloma and inflammatory cells appear to contribute to this process. The involvement of the vascular endothelial growth factor (VEGF) and platelet derived growth factor (PDGF) pathways in this process suggest that therapies targeting these two signaling pathways may provide a new, effective way to block the growth of myeloma cells and their associated angiogenesis. One such potential therapy, TKI-204, targets several angiogenic growth factor receptor tyrosine kinases in myeloma.