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  Vol. 297 No. 13, April 4, 2007 TABLE OF CONTENTS
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Bortezomib’s Action

Tracy Hampton, PhD

JAMA. 2007;297:1423.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The mechanism by which a drug kills cancer cells may be crucial to its effectiveness, according to new research from Rockefeller University, in New York City (Spisek R et al. Blood. doi:10.1182/blood-2006-10-054221 [published online February 13, 2007]). While most anticancer chemotherapies are immunosuppressive, bortezomib—a proteasome inhibitor— promotes an immune response.

Proteasomes regulate protein expression and function, and inhibiting them causes cell growth abnormalities and programmed cell death, particularly in cancer cells. As a cancer cell dies, heat shock proteins appear on its surface. This encourages the uptake of malignant cells by dendritic cells. The dendritic cells then alert memory and killer T cells to recognize the cancer cells as foreign, a process that could potentially lead to enhanced antitumor immunity.

The researchers also tested radiation therapy and the corticosteroid dexamethasone. These treatments failed to increase levels of heat shock proteins on the surfaces of dying cells, . . . [Full Text of this Article]







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