© The Author 2006. Published by Oxford University Press.
EDITORIAL |
Tumor Cell Populations Differ in Angiogenic Activity: A Model System for Spontaneous Angiogenic Switch Can Tell Us Why
Affiliation of authors: Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Bethesda, MD
Correspondence to: Giovanna Tosato, MD, Bldg. 10, 12C205, 10 Center Dr., Bethesda, MD 20892 (e-mail: tosatog@mail.nih.gov).
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Aggressive, life-threatening cancers grow progressively locally, produce distant metastases, and are insensitive to cytotoxic and cytostatic drugs. A hallmark of progressive cancer growth is the subversion of the vascular supply in the whole area that is involved with tumor. In 1945, Glen Algire published in this Journal studies supporting the conclusion that "the rapid growth of tumor explants is dependent on the development of a rich vascular supply" (1). We now know that many tumors are dependent on neovascularization to sustain their expansion, that tumor cells themselves can produce proangiogenic factors, and that certain drugs targeting these factors can be effective anticancer drugs.
Tumorigenesis represents a multistep process that leads to the accumulation of genetic alterations, including gain-of-function mutations in oncogenes and loss-of-function mutations in tumor suppressor genes (2). One such step is known as the "angiogenic switch," via which tumor cells acquire