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Authors’ contributions JY and HS designed the study. HS performed Nest RT-PCR. BX participated in the sample collection and performed the statistical analysis. HS drafted the manuscript. HS and JY revised the manuscript. All authors read and approved the final manuscript.”
“Background Tumor angiogenesis is critical for tumors to grow and spread. Four decades ago, Folkman proposed targeting the tumor vasculature as a strategy to treat cancer [1]. Since then advances in biology have provided new tools and knowledge in the area of angiogenesis. A key discovery was the identification of vascular endothelial growth factor (VEGF), a key angiogenic protein critical for the growth of endothelial cells and development of tumor blood vessels [2–4]. VEGF herein emerged as an attractive target for anticancer therapy. It has been demonstrated in animal models that neutralization VEGF could inhibit the growth of primary tumor and metastases. In small 1–2 mm foci of tumor cells, blocking the VEGF pathway inhibited the “angiogenic CBL0137 switch”, i.e. preventing tumor transformation from an avascular to vascular phase, thus maintaining a quiescent state [5].

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