title: Vascular normalization in cerebral angiogenesis: friend or foe?
abstract: Current antiangiogenic therapies have led to the observation that such agents can lead to improved tumor vessel structure and function termed "vascular normalization" which reduces tumor burden. However, vessel normalization is a transient process, and patients often develop resistance/poor response to anti-vascular strategies that remains an important clinical challenge. Therefore, increasing effort has been made to better understand the cellular and molecular mechanisms of vascular normalization and its contribution to immunomodulation. Herein, we summarize the recent effort to better understand the cellular and molecular mechanisms of vascular normalization with a focus on preclinical genetic models. These studies remain important directions for a mechanistic understanding of the complexities of the maintenance of BBB integrity and the impact of its breakdown on tumor dissemination and pharmaco-distribution of therapeutics.
authors: Department of Surgery, University of California San Diego, La Jolla, CA, USA.
authors: Jisook
authors: J
authors: Lee
authors: Andrew
authors: A
authors: Baird
authors: Brian P
authors: BP
authors: Eliceiri
mesh_terms: D020533:Angiogenesis Inhibitors / Q000493:pharmacokinetics / Q000627:therapeutic use; D000818:Animals; D001812:Blood-Brain Barrier / Q000378:metabolism / Q000503:physiopathology; D016543:Central Nervous System Neoplasms / Q000098:blood supply* / Q000188:drug therapy / Q000276:immunology; D002536:Cerebral Arteries / Q000378:metabolism / Q000503:physiopathology; D019008:Drug Resistance, Neoplasm; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D006801:Humans; D055806:Microvessels / Q000378:metabolism / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000473:pathology / Q000503:physiopathology; D018919:Neovascularization, Physiologic; D014018:Tissue Distribution; D019139:Tumor Escape
chemical_list: D020533:Angiogenesis Inhibitors