Angiogenesis signaling pathways as targets in cancer therapy

Chery A. Whipple, Murray Korc

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Cancer associated angiogenesis is often driven by an abnormal pro-angiogenic profile, a phenomenon that may also be observed in certain inflammatory states, whereas inadequate angiogenesis may be associated with inefficient tissue repair and defective collateral blood vessel formation. The angiogenic process in tumors can be compartmentalized into three main phases: inflammatory, proliferative, and remodeling. The proliferation stage is crucial for successful tumor angiogenesis. The interactions between tumor cells and host stromal cells have a profound influence on tumor cell proliferation, invasion, angiogenesis, and metastasis. The abnormal microcirculation within tumors results in areas of hypoxia, which serves to alter the metabolic profile of cancer cells and to further enhance angiogenesis. Anti-angiogenic therapy that restores the angiogenic balance and normalizes the blood vessels may prove to be a highly advantageous approach to inhibit tumor growth and metastasis. While anti-angiogenic therapies can normalize tumor vasculature and the tumor microenvironment, the effect is often transient and is dictated by the type of tumor and its location, underscoring the importance of timing and duration of therapy. However, there is a high risk that such a multitargeted approach will greatly increase health care costs and may increase to unacceptable levels the side effect profile of anti-angiogenic therapy.

Original languageEnglish (US)
Title of host publicationHandbook of Cell Signaling, 2/e
PublisherElsevier Inc.
Pages2895-2905
Number of pages11
Volume3
ISBN (Print)9780123741455
DOIs
StatePublished - Dec 1 2010

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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  • Cite this

    Whipple, C. A., & Korc, M. (2010). Angiogenesis signaling pathways as targets in cancer therapy. In Handbook of Cell Signaling, 2/e (Vol. 3, pp. 2895-2905). Elsevier Inc.. https://doi.org/10.1016/B978-0-12-374145-5.00333-8