title: In pursuit of new anti-angiogenic therapies for cancer treatment.
abstract: Despite advances in surgery, radiation therapy, and chemotherapy, patients with cancer have a poor prognosis. Sustained aberrant tumor angiogenesis and metastasis is a major obstacle for effective cancer treatment. Just a few years ago, few would argue that one of the key success stories of the modern cancer medicine were the anti-angiogenic drugs targeting the vascular endothelial growth factor (VEGF) signaling pathway approved by FDA. This initial success inspired many researchers to search for new anti-angiogenic targets and drugs with the hope that one day, anti-angiogenic therapy might really become the panacea for cancer patients. Unfortunately, the limited clinical benefits achieved with anti-angiogenic drugs conflicts with the widely accepted notion that angiogenesis is a key event in tumor progression. Emerging data indicate that unique characteristics of the tumor vasculature within the tumor microenvironment may hold the key for success of anti-angiogenic therapy. In particular, the molecular and cellular alterations that sustain aberrant tumor angiogenesis in the face of angiogenic inhibitors represents novel targets for rationally designing and improving current anti-angiogenic strategies.
authors.affiliation: Department of Anatomy and Cell Biology, University of Florida, Gainesville, FL 32610, USA.
authors.forename: Jun
authors.initials: J
authors.lastname: Cai
authors.forename: Song
authors.initials: S
authors.lastname: Han
authors.forename: Ruan
authors.initials: R
authors.lastname: Qing
authors.forename: Daiqing
authors.initials: D
authors.lastname: Liao
authors.forename: Brian
authors.initials: B
authors.lastname: Law
authors.forename: Michael E
authors.initials: ME
authors.lastname: Boulton
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001557:Benzenesulfonates / Q000627:therapeutic use; D000068258:Bevacizumab; D019008:Drug Resistance, Neoplasm; D006801:Humans; D007191:Indazoles; D007211:Indoles / Q000627:therapeutic use; D009369:Neoplasms / Q000098:blood supply / Q000188:drug therapy*; D009389:Neovascularization, Pathologic / Q000188:drug therapy*; D009536:Niacinamide / Q000031:analogs & derivatives / Q000627:therapeutic use; D009841:Oligonucleotides; D010671:Phenylurea Compounds; D011725:Pyridines / Q000627:therapeutic use; D011743:Pyrimidines / Q000627:therapeutic use; D011758:Pyrroles / Q000627:therapeutic use; D011799:Quinazolines / Q000627:therapeutic use; D040262:Receptors, Vascular Endothelial Growth Factor; D011993:Recombinant Fusion Proteins / Q000627:therapeutic use; D000077157:Sorafenib; D013449:Sulfonamides / Q000627:therapeutic use; D000077210:Sunitinib; D059016:Tumor Microenvironment
chemical_list: D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D001557:Benzenesulfonates; D007191:Indazoles; D007211:Indoles; D009841:Oligonucleotides; D010671:Phenylurea Compounds; D011725:Pyridines; D011743:Pyrimidines; D011758:Pyrroles; D011799:Quinazolines; D011993:Recombinant Fusion Proteins; D013449:Sulfonamides; C533178:aflibercept; D009536:Niacinamide; D000068258:Bevacizumab; C516667:pazopanib; D000077157:Sorafenib; D040262:Receptors, Vascular Endothelial Growth Factor; C519562:imetelstat; C500926:cediranib; D000077210:Sunitinib