Vascular Endothelial Growth Factor and Its Relationship to Inflammatory Mediators

• Published in: Clinical cancer research Vol. 13; no. 10; pp. 2825 - 2830
• Main Authors: ANGELO, Laura S, KURZROCK, Razelle
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 15.05.2007
• Subjects: Antineoplastic agents; Autocrine-paracrine signaling; Biological and medical sciences; Cell Growth/Signaling Pathways; Humans; Immune System - metabolism; Inflammation - complications; Inflammation - immunology; Inflammation Mediators - metabolism; inflammatory cytokines; Medical sciences; Mycobacterium tuberculosis; Neoplasms - blood supply; Neoplasms - immunology; Neovascularization, Pathologic - immunology; Pharmacology. Drug treatments; vascular endothelial growth factor; Vascular Endothelial Growth Factor A - metabolism; Inflammation; Vascular endothelium growth factor
• ISSN: 1078-0432; 1557-3265
• DOI: 10.1158/1078-0432.CCR-06-2416

Inflammation occurs in response to host injury or infection, as the result of an autoimmune disease, or in response to the development of a tumor. Although the immune system may be helpful in fighting the tumor, it may also fuel the tumorigenic process. In fact, recent data suggest a strong link between chronic inflammation, angiogenesis, and the development of cancer. For example, inflammation and scarring caused by recurring infections with Mycobacterium tuberculosis may be a cause for cancers of the lung. Inflammatory breast cancer exhibits increased angiogenesis and lymphangiogenesis and has a higher metastatic potential than noninflammatory breast cancer. Nonsteroidal anti-inflammatory drugs have been proposed as preventives for the development of colon carcinoma and ovarian cancer. Inhibition of nuclear factor-κB contributes to the proposed mechanism of action. Inflammatory cytokines, including interleukin-6, serve as autocrine and paracrine growth factors for several cancers, and high levels of these cytokines may correlate with a poor prognosis and increased production of angiogenic factors. The state of the art of our understanding of this critical interaction is reviewed.