The Journal of Experimental Medicine
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Published online 13 November 2006 doi:10.1084/jem.20312iti1
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 12, 2566-2566
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IN THIS ISSUE

Raising more than just hope for cancer treatment


Figure 1
Tumor size in mice is reduced by Viagra treatments (right).

Bedroom performance-boosting Viagra also boosts the immune system's battle against cancer, report Serafini et al on page 2691.

In cancer patients, though the body generates tumor-specific antibodies, their efficacy is neutralized by the tumor itself. Tumors recruit cells such as myeloid-derived suppressor cells (MDSCs) and regulatory T cells, which suppress the body's immune system, thus allowing the tumors to escape immune recognition. Borrello's team has been investigating ways to overcome this immunosuppression.

Suppression of T cells by MDSCs requires, among other things, nitric oxide production. The team reasoned, therefore, that reducing nitric oxide levels might boost immunity in cancer patients. They thus turned to Viagra. Besides its well-known vasodilatory effect, Viagra also reduces nitric oxide production through a separate but linked pathway.

The team gave Viagra to mice with colon carcinoma and found that the immune systems of the mice were indeed boosted. The mice had an increased number of cytotoxic T cells, and tumor outgrowth was reduced by 50–70%. Viagra also provided a boost to T cells transferred to the mice using adoptive cell therapy, with tumor growth being reduced still further.

Viagra, either alone or in conjunction with transferred T cells, did not eradicate the tumors but did significantly slow their progression. Eradication would require a full understanding of the multiple, complex pathways that lead to tumor-induced immunosuppression. In the meantime, the immediate availability of viagra means its potential clinical use can be readily tested. Formula



Ruth Williams

ruth.williams{at}rockefeller.edu


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Related Article

Phosphodiesterase-5 inhibition augments endogenous antitumor immunity by reducing myeloid-derived suppressor cell function
Paolo Serafini, Kristen Meckel, Michael Kelso, Kimberly Noonan, Joseph Califano, Wayne Koch, Luigi Dolcetti, Vincenzo Bronte, and Ivan Borrello
J. Exp. Med. 2006 203: 2691-2702. [Abstract] [Full Text] [PDF]




This Article
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