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Volume 35, Issue 7, Pages 553-562 (November 2009)


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Survivin: A new target for anti-cancer therapy

Bríd M. RyanabCorresponding Author Informationemail address, Norma O’Donovancfemail address, Michael J. Duffydegemail address

Received 3 February 2009; received in revised form 13 May 2009; accepted 15 May 2009. published online 26 June 2009.

Summary 

Survivin is one of the most cancer-specific proteins identified to date, being upregulated in almost all human tumors. Biologically, survivin has been shown to inhibit apoptosis, enhance proliferation and promote angiogenesis. Because of its upregulation in malignancy and its key role in apoptosis, proliferation and angiogenesis, survivin is currently attracting considerable attention as a new target for anti-cancer therapies. In several animal model systems, downregulation of survivin or inactivation of its function has been shown to inhibit tumor growth. Strategies under investigation to target survivin include antisense oligonucleotides, siRNA, ribozymes, immunotherapy and small molecular weight molecules. The translation of these findings to the clinic is currently ongoing with a number of phase I/II clinical trials targeting survivin in progress. These include use of the antisense oligonucleotide LY2181308, the low molecular weight molecule inhibitor YM155 and survivin-directed autologous cytotoxic T lymphocytes. The optimum use of survivin antagonists in the treatment of cancer is likely to be in combination with conventional cancer therapies.

a Cancer Prevention Fellowship Program, Office of Preventive Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4258, USA

b Laboratory of Human Carcinogenesis, Centre for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4258, USA

c National Institute for Cellular Biotechnology, Dublin City University, Dublin 9, Ireland

d Department of Pathology and Laboratory Medicine, St. Vincent’s University Hospital, Dublin 4, Ireland

e UCD School of Medicine and Medical Science, Conway Institute, University College Dublin, Dublin 4, Ireland

Corresponding Author InformationCorresponding author. Tel.: +1 301 496 5886; fax: +1 301 496 1497.

f Tel.: +353 1 700 7497; fax: +353 1 700 5484.

g Tel.: +353 1 209 4378; fax: +353 1 269 6018.

PII: S0305-7372(09)00085-1

doi:10.1016/j.ctrv.2009.05.003


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