© 2004 by Oxford University Press
© 2004 Oxford University Press
EDITORIAL |
Versipelostatin: Unfolding an Unsweetened Death
Correspondence to: Edward A. Sausville, MD, PhD, Greenebaum Cancer Center, University of Maryland, 22 S. Greene St., Baltimore, MD 21201 (e-mail: esausville@umm.edu)
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The classical basis for successful cancer chemotherapeutic regimens has been the induction of tumor shrinkage, or response, in animal models of cancer, usually mice bearing syngeneic or xenografted human tumors. Historically, agents that had activity in a high proportion of such models had a statistically increased likelihood of demonstrating value in Phase II clinical efficacy trials in humans (1). Based on such behavior, Phase III trials could be planned to assess utility in prolonging survival. The antiproliferative mechanisms of successful conventional cytotoxic compounds in most cases ultimately involve apoptosis, or programmed cell death, with concomitant decrease in clonogenic potential of cells from treated tumors.
During the past 15 years, a number of cellular pathways leading to tumor cell apoptosis have been defined. DNA-damaging agents appear capable of activating a range of
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