Cancer drug's survivin suppression called into question

Access through your institution Buy or subscribe There are no prizes for guessing the cellular function of the protein survivin. It was named for its ability to promote cell survival in

cancer by blocking programmed cell death—and it's a protein that has become steadily more familiar in the cancer field in recent years. Since its discovery in 1997, survivin has emerged

as one the most commonly found proteins in tumor cells. Take into account its rarity in healthy tissue, and you can understand why several companies have invested heavily in putative

antisurvivin agents, with a handful already in clinical testing. The lead compound—YM155 from Japan's Astellas Pharma—has already completed phase 2 trials for various forms of cancers.

However, new data are emerging from preclinical tests to suggest that the drug might not be working exactly as first anticipated. The first hint of trouble came in April, when researchers

from the Biological Testing Branch of the US National Cancer Institute's Developmental Therapeutics Program in Bethesda, Maryland performed a barrage of _in vitro_ tests on YM155, known

chemically as sepantronium bromide, and on a similar in-house compound called NSC80467. They found that both agents kill cells primarily by inducing DNA damage, not by suppressing survivin

directly—a finding that suggests that any effect on survivin is probably a secondary event caused by general deactivation of gene expression (_Cancer Chemother. Pharmacol._

doi:10.1007/s00280-012-1868-0, 2012). This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive

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David Holmes View author publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE

Holmes, D. Cancer drug's survivin suppression called into question. _Nat Med_ 18, 842–843 (2012). https://doi.org/10.1038/nm0612-842b Download citation * Published: 06 June 2012 * Issue

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