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Authors’ contributions Conception and design: FP wrote the paper. MPT and VDS have been involved in Staurosporine chemical structure drafting the manuscript and revising it critically. DG has made statistical analysis. Provision of study materials or patients: FP,MPT,VB,VDS,GLV,FG,AL,TZ, AM,LA,MCP. All authors have read and approved the final BIBW2992 clinical trial manuscript.”
“Background Tumors can grow to a maximum diameter of between 1 and 2 mm before their metabolic demands are restricted due to the diffusion limit of oxygen and lack of essential nutrients. To exceed this size or spread to Phosphatidylinositol diacylglycerol-lyase other organs, tumors require an independent blood supply. In the 1970s, Folkman et al was the first to propose the concept of antiangiogenesis as a therapeutic approach to treat solid tumors [1]. Targeting the blood supply by inhibiting the formation of blood vessel will lead to tumor

growth arrest. Numerous angiogenesis inhibitors have been therapeutically used in both preclinical and clinical settings [2]. Vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors and a VEGF-neutralizing antibody have been clinically validated to target VEGF or its receptors as an anticancer treatment. However, a number of limitations are observed in current antiangiogenic therapies. Many clinical benefits are short-lived, and enduring clinical responses are rare. While numerous trials have shown an increase in survival after patients are treated with antiangiogenic therapy, the increase for many was only a matter of months [3]. Moreover, single-agent use of antiangiogenesis appears to be insufficient to improve patient survival [4].