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Tumor Angiogenesis: Cause or Consequence of Cancer?

Cancer Research Institute and Department of Cellular and Molecular Pharmacology, UCSF Comprehensive Cancer Center, San Francisco, California

Requests for reprints: Gerard Evan, Cancer Research Institute and Department of Cellular and Molecular Pharmacology, UCSF Comprehensive Cancer Center, 2340 Sutter Street, San Francisco, CA 94143-0875. Phone: 415-514-0438; Fax: 415-514-0878; E-mail: gevan{at}cc.ucsf.edu.

Both tumors and normal tissues need a blood supply for oxygen, nutrients, and waste removal. However, whereas normal vasculature is hierarchically assembled into efficient networks of arteries, capillaries, and veins, the blood vessels of tumors are a mess—chaotic, leaky, inefficient, and barely making do. Why the difference? Do tumor vessels lack the signals to mature or, instead, is their maturation actively suppressed? What triggers and maintains tumor vasculature? In a recent study using a switchable Myc-driven mouse tumor model, we addressed these fundamental questions. We identified the inflammatory cytokine interleukin-1ß as an essential initiating trigger of vascular endothelial growth factor–dependent angiogenesis. Here, we consider how kinetic studies using regulatable forms of Myc or other oncogenes can shed new light on the way tumors initiate and maintain their aberrant blood supplies. [Cancer Res 2007;67(15):7059–61]

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