| Objective: The most improtant progress in the recent 30 years is the establishment of the significance of angiogenesis and antiangiogenesis treatment in tumor control. Vasculogenesis and angiogenesis are two different process. This process, called vasculogenesis ,involves the de novo differentiation of endothelial cell(EC) from mesodermal precursor to form the primitive blood vessel network. It is only seen in the earlier period of embryogenesis and organ formation. The distinct process of blood vessels generation from existing vessels ,called angiogenesis can be seen in the period of embryogenesis and postnatal. The physiological angiogenesis is a strict controlled progress and takes important role in tissue repair, wound healing and female reproductive cycle. Pathologic angiogenesis is an unlimited, uncontrolled process and accelerates the progress of the disease. The growth of the tumor can be divided into two stages called avascular stage and vascular stage. In the avascular stage, the delivery of nutrients and the removal of waste products from the tumor bed are transferred by simple diffusion through the surrounding tissue. So the growth of the tumor is restricted. The diameter of the tumor is less than 1～2mm at this stage；The occurrence of novel vessel in vascular stage facilitates the growth of tumor and makes it possible to transfer to the distant place. In fact, angiogenesis is crucial for the conversion to a malignant phenotype. The ability of angiogenesis in tumor determines its potency of growth, infiltration and metastasis in tumor. Controlling the angiogenesis in tumor can inhibite the growth of the tumor. There is accumulating evidence show that angiogenesis supports the growth of the solid tumors and few data are available regarding angiogenesis in hematological malignancies. There isno related research in domestic. In recently foreign scholars find that there is increased bone marrow angiogenesis in patients with different hematological malignancies such as acute leukemia, multiple myeloma(MM), myelodysplastic syndromes(MDS) and the degree of neovascularization correlates with the stage of the diseases. But there also have adverse conclusions. Tumor cells and the peripheral stroma cells can secrect growth factor which can promote the migration and proliferation of vascular endothelial cells to accelerate neovascularization. Vascular endothelial cell growth factor (VEGF) is considered to be the most potent stimulator of angiogenesis in vivo. The biology role of VEGF involves accelerating the proliferation and differentiation of the vascular endothelial cell, improving the permeability of vessels and altering extracellular matrix to facilitate the growth of the vessel. VEGF can also promote the growth of hemopoietic progenitor. The high level of VEGF is considered to be an independent prognosis factor for poor clinical outcome and disease progression in acute myeloid leukemia. The biologic activity of VEGF is mediated by interaction with its affinity receptors expressed on most endothelial cells. Three major functional VEGF receptors (VEGFR) have been identified: VEGF receptor -1(VEGFR1/Flt-1), VEGF receptor-2(VEGFR2/KDR) and VEGF receptor-3(VEGFR3). All of them are receptor tyrosine kinase family members. VEGFR1 and VEGFR2 are distributed mainly on endothelial cells and VEGFR3 mainly relate to the formation of lymphatic vessel. The antiangiogenic therapies of tumor were proposed by Folkman and great progresses were made only in the recently years. There is increasing evidence that antiangiogenic therapies may induce tumor dormancy or stabilization. The realization of antiangiogenic can be accomplished by decreasing the production of VEGF, blocking its binding to receptors, blocking signal transduction, inhibition of matrix metalloproteinases, or blockade of endothelial cells activation. There are numerous drugs have been proved to have antiangiogenesis role. Arsenic trioxide are also showed to have antiangiogenic role in the recentlyresearch of Roboz. To study the r...
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