News Release

Sugar-free approach to treating Kaposi sarcoma

Peer-Reviewed Publication

Rockefeller University Press

A sugar-loving protein drives the growth of Kaposi sarcoma (KS) tumors, according to a study published on October 1st in The Journal of Experimental Medicine. Interfering with these sugary interactions inhibited growth of Kaposi sarcomas in mice, hinting at the potential for new treatment strategies in humans.

KS is a cancer that is associated with infection with a herpes virus called HHV-8 and is prevalent in HIV patients. Effective antiretroviral drugs have decreased the incidence of KS, but the cancer eventually progresses in many patients and treatment options are limited.

A carbohydrate-binding protein called galectin-1 is released by a variety of tumors and promotes their growth and metastasis. A group of researchers at the University of Buenos Aires in Argentina now finds that blocking galectin-1 in mice bearing established Kaposi sarcomas slowed tumor growth in part by suppressing the formation of blood vessels that feed the tumor.

If the same holds true in humans, drugs targeting galectin-1 could provide new treatment options for patients with KS. These drugs might also hold promise for other diseases characterized by aberrant blood vessel growth, including macular degeneration and cardiovascular diseases.

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About The Journal of Experimental Medicine (JEM)

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.

Croci, D.O., et al. 2012. J. Exp. Med. doi:10.1084/jem.20111665

Contact information:

Gabriel Rabinovich
University of Buenos Aires
Email: gabriel.r@ibyme.conicet.gov.ar


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