Journal
JOURNAL OF CLINICAL MEDICINE
Volume 9, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/jcm9061765
Keywords
angiogenesis; microenvironment; multiple myeloma; vascular endothelial growth factor; vascular endothelial growth factor receptor
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Funding
- Associazione Italiana per la Ricerca sul Cancro (AIRC) [20441]
- MIUR [PRIN 2009WCNS5C_004]
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The interaction between the bone marrow microenvironment and plasma cells plays an essential role in multiple myeloma progression and drug resistance. The vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) pathway in vascular endothelial cells activates and promotes angiogenesis. Moreover, VEGF activates and promotes vasculogenesis and vasculogenic mimicry when it interacts with VEGF receptors expressed in precursor cells and inflammatory cells, respectively. In myeloma bone marrow, VEGF and VEGF receptor expression are upregulated and hyperactive in the stromal and tumor cells. It has been demonstrated that several antiangiogenic agents can effectively target VEGF-related pathways in the preclinical phase. However, they are not successful in treating multiple myeloma, probably due to the vicarious action of other cytokines and signaling pathways. Thus, the simultaneous blocking of multiple cytokine pathways, including the VEGF/VEGFR pathway, may represent a valid strategy to treat multiple myeloma. This review aims to summarize recent advances in understanding the role of the VEGF/VEGFR pathway in multiple myeloma, and mainly focuses on the transcription pathway and on strategies that target this pathway.
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