title: Tumor angiogenesis and anti-angiogenic therapy.
abstract: Anti-angiogenic therapy is an anti-cancer strategy that targets the new vessels that       grow to provide oxygen and nutrients to actively proliferating tumor cells. Most of the       current anti-cancer reagents used in the clinical setting indiscriminately target all rapidly       dividing cells, resulting in severe adverse effects such as immunosuppression, intestinal       problems and hair loss. In comparison, anti-angiogenic reagents theoretically have fewer side       effects because, except in the uterine endometrium, neoangiogenesis rarely occurs in healthy       adults. Currently, the most established approach for limiting tumor angiogenesis is blockade       of the vascular endothelial growth factor (VEGF) pathway. In line with the results of       preclinical studies, significant therapeutic effects of VEGF blockers have been reported in       various types of human cancers, even in patients with progressive/recurrent cancer who could       not otherwise be treated. However, some patients are refractory to this treatment or acquire       resistance to VEGF inhibitors. Moreover, several studies have shown that VEGF blockade damages       healthy vessels and results in adverse effects such as hemorrhagic and thrombotic events. In       recent research that indicated possible ways to overcome these problems, several       VEGF-independent and tumor-selective pro-angiogenic mechanisms were discovered that could be       targeted in combination with or without conventional VEGF blockade. These findings offer       opportunities to greatly improve current anti-angiogenic treatment for cancer.
authors: Center for Integrated Medical Research, School of Medicine, Keio University, Tokyo, Japan. ykubo33@a3.keio.jp
authors: Yoshiaki
authors: Y
authors: Kubota
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D042682:Angiopoietins / Q000037:antagonists & inhibitors / Q000378:metabolism; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology; D019008:Drug Resistance, Neoplasm / Q000187:drug effects; D005346:Fibroblast Growth Factors / Q000037:antagonists & inhibitors / Q000378:metabolism; D006801:Humans; D016173:Macrophage Colony-Stimulating Factor / Q000037:antagonists & inhibitors / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects / Q000276:immunology; D061965:Matrix Metalloproteinase Inhibitors; D020782:Matrix Metalloproteinases / Q000378:metabolism; D009369:Neoplasms / Q000098:blood supply* / Q000188:drug therapy* / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000517:prevention & control*; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors
chemical_list: D020533:Angiogenesis Inhibitors; D042682:Angiopoietins; D000970:Antineoplastic Agents; D016207:Cytokines; D061965:Matrix Metalloproteinase Inhibitors; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D042461:Vascular Endothelial Growth Factor A; D000072483:Placenta Growth Factor; D005346:Fibroblast Growth Factors; D016173:Macrophage Colony-Stimulating Factor; D020782:Matrix Metalloproteinases