Abstract：
:Over the past decade, the well-documented role of vascular endothelial growth factor (VEGF) in tumor angiogenesis has led it to become one of the leading therapeutic targets for the treatment of cancer. Emerging evidence from genetically modified animal models, however, suggests that elevated levels of VEGF, or a proangiogenic phenotype, may impede, rather than promote, early tumor development and progression. For example, hypermorph VEGF transgenic mice display delayed progression of a retroviral-induced murine leukemia, and knockdown of VEGF expression within the myeloid compartment accelerates tumor progression. Several mechanisms have been proposed to explain this paradox, whereby VEGF induces changes within the hematopoietic compartment and tumor microenvironment through recruitment of tumor inhibitory monocytic cells and the negative regulation of tumor angiogenesis. Thus, it is apparent that the levels of VEGF expression in both tumor and nontumor tissues, as well as the context and timing of its modulation relative to cancer induction, play an important role in determining the effects of VEGF expression on tumorigenicity. In light of these recent findings, the various mechanisms underlying the negative role of VEGF during early tumor development, progression, and metastasis will be discussed.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Vecchiarelli-Federico LM,Cervi D,Haeri M,Li Y,Nagy A,Ben-David Ydoi
10.1158/0008-5472.CAN-09-3592subject
Has Abstractpub_date
2010-02-01 00:00:00pages
863-7issue
3eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-09-3592journal_volume
70pub_type
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