Public Release:  Targeting cancerous vessels

Rockefeller University Press

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IMAGE: Vascular endothelial cells (green) express {delta}-catenin (red). view more

Credit: DeBusk, L.M., et al. 2010. J. Exp. Med. doi:10.1084/jem.20091097

By lowering the level of a neuronal protein, researchers halted the growth of blood vessels that tumors rely on for survival. The findings are reported online in the Journal of Experimental Medicine (www.jem.org) on Jan. 4.

Formerly known for its effects on neuronal growth, the team found that the protein {delta}-catenin is also produced by cells in human blood vessels. By diminishing {delta}-catenin expression, the team disrupted vessel development, or angiogenesis, associated with inflammation in tumors and wounds. As expected, samples of human lung tumors expressed more {delta}-catenin than the surrounding tissues. And normal angiogenesis remained the same regardless of {delta}-catenin.

Because blocking {delta}-catenin stunts only inflammation-induced angiogenesis, the protein may be a promising anti-cancer target, says Charles Lin, an author on the study at Vanderbilt University Medical Center in Tennessee.

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About The Journal of Experimental Medicine

The Journal of Experimental Medicine (JEM) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JEM content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit www.jem.org.

DeBusk, L.M., et al. 2010. J. Exp. Med. doi:10.1084/jem.20091097

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