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JNCI Journal of the National Cancer Institute 2001 93(13):965-967; doi:10.1093/jnci/93.13.965
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 13, 965-967, July 4, 2001
© 2001 Oxford University Press

EDITORIAL

Gene Therapy for Antiangiogenesis

Hynda K. Kleinman, Gene Liau

Affiliations of authors: H. K. Kleinman, National Institute of Dental and Craniofacial Research, Bethesda, MD; G. Liau, Genetic Therapy Inc., a Novartis Company, Gaithersburg, MD.

Correspondence to: Hynda K. Kleinman, Ph.D., National Institutes of Health, Bldg. 30, Rm. 407, Bethesda, MD 20902 (hkleinman@dir.nidcr.nih.gov).

Angiogenesis inhibitors have evolved as a new diverse class of compounds that can be used to block tumor growth (1,2). The inhibitors, which may be natural or synthetic, include protease inhibitors (i.e., tissue inhibitors of matrix metalloproteinases), tyrosine kinase inhibitors, chemokines, interleukins, and proteolytic fragments of diverse molecules (i.e., endostatin, vasostatin, canstatin, arrestin, etc.). These antiangiogenic molecules function in multiple ways, including the inhibition of endothelial cell proliferation, migration, protease activity, and tubule formation, as well as the induction of apoptosis. The antiangiogenic function of many of these molecules is well documented in vitro and in vivo, and some are currently being tested in clinical trials (http://cancertrials.nci.nih.gov). Less is known about the exact mechanism(s) of angiogenic regulation of some of the inhibitors. More than 40 endogenous inhibitors have been identified, and others may . . . [Full Text of this Article]

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