| It has been suggested that angiogenesis/lymphoangiogenesis is closely associated with growth, survival, tissue infiltration, distant metastasis of solid tumor ells. The pathological angiogenesis also exist in hematological diseases. But not same as in solid tumor, angiogenesis plays a special role in hematological malignancies, for that hematopoietic pregenitor cells and endothelial cells derived from hemangioblast have homologous character in spite of atavism and heterogeneity of tumor cells.Vascular Endothelial Growth Factor (VEGF)-C, a member of VEGFs family (VEGF-A, -B, -C, -D, -E, and PIGF), is regulated by inflammary cytokines and bind to both of VEGFR-2(KDR or Flk-1) and VEGFR-3(Flt-4). VEGFR-3 are expressed on lymphatic vessel and fenestrated capillaries of tumor tissue and wound in adult. VEGFR-3 can bind VEGF-C of all the proteolytic process, while fully processed VEGF-C alone activates VEGFR-2 and induce vasculogenesis during early development and angiogenesis. VEGF-C also stimulates recruitment of macrophages in pathological condition of tumor and infection. Tumor-associated macrophages means the"double-edged sword"in neoplastic progression to a certain extent. Upon activation, the tumor-associated macrophages can release a vast diversity of proangiogenic cytokines, and play a leading role in activated T- or B-cells-mediated immunological response.VEGF receptors activated by VEGFs promote the proliferation of vascular endothelial cells and spread of vascular vessel in bone marrow. Functional tyrosine kinase receptor of endothelium and/or their ligands also are expressed on some kinds of hematological malignant cells. In many subsets of acute and chronic leukemias, malignant cells express VEGFR-2,3 receptor, but also release VEGF-C. The data of follow-up showed that the expression of these protein correlates with clinical stage, value of treatment, prognosis of diseases. It was confirmed that VEGF-C derived from...
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