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Updated: Aug 13, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
Vascular endothelial growth factor and its receptors in multiple myeloma
R Ria1, A M Roccaro, F Merchionne
1Department of Biomedical Sciences and Human Oncology, Bari, Italy.
Abstract:
Multiple myeloma (MM) progresses from an avascular to a vascular phase (active MM) accompanied by a significant increase in microvessel density in the bone marrow. This article summarizes the literature concerning the specific role played by vascular endothelial growth factor (VEGF) in this process. Recent applications of antiangiogenic agents that interfere with VEGF signaling and block MM progression are also described.
Insights
Multiple myeloma (MM) advances from an avascular to an active, vascular phase. Vascular endothelial growth factor (VEGF) drives this progression, and antiangiogenic therapies targeting VEGF show promise in blocking MM advancement.
Area of Science:
- Oncology
- Hematology
- Angiogenesis Research
Background:
- Multiple myeloma (MM) transitions from an avascular to a vascularized state.
- This progression, termed active MM, involves increased bone marrow microvessel density.
- Tumor angiogenesis is a critical factor in cancer growth and metastasis.
Purpose of the Study:
- To review the literature on the role of vascular endothelial growth factor (VEGF) in MM progression.
- To discuss the implications of VEGF signaling in the transition to active MM.
- To summarize the therapeutic potential of antiangiogenic agents targeting VEGF in MM.
Main Methods:
- Literature review and synthesis of existing research.
- Analysis of studies investigating VEGF's role in MM angiogenesis.
- Examination of clinical data on anti-VEGF therapies for MM.
Main Results:
- VEGF is a key mediator in the development of the vascular phase of MM.
- Increased microvessel density in the bone marrow is associated with active MM.
- Antiangiogenic agents targeting VEGF signaling have demonstrated efficacy in preclinical and clinical studies.
Conclusions:
- VEGF plays a critical role in promoting the angiogenesis required for active MM.
- Targeting VEGF signaling represents a viable therapeutic strategy to inhibit MM progression.
- Further research into anti-VEGF therapies holds promise for improving MM patient outcomes.
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