Cancer Chemoprevention By The Antioxidant Tempol Acts Partially Via The P53 Tumor Suppressor

Published in: Human Molecular Genetics 2005 14(12):1699-1708.

Authors: Laura Erker, Ralf Schubert, Hiroyuki Yakushiji, Carrolee Barlow, Denise Larson, James B. Mitchell5 and Anthony Wynshaw-Boris.

Affiliations:
Department of Pediatrics, Department of Medicine and Comprehensive Cancer Center, UCSD School of Medicine, La Jolla 92093, USA.

Genetic Disease Research Branch, NHGRI, NIH, Bethesda, MD 20892, USA.

Radiation Biology Branch, NCI, Bethesda, MD 20892, USA

This paper reports that the tempol treatment of cancer-prone p53-deficient mice resulted in a small but significant (25%) increase in lifespan by prolonging latency to tumorigenesis, demonstrating that existing oxidative stress and damage are not necessary for the chemopreventative effects of tempol. However, according to the authors, the relatively small effect on latency in p53-deficient mice and the finding that tempol-mediated resistance to oxidative insult was p53-dependent suggested a more direct role of p53 in the chemopreventative effects of tempol.

The authors conclude that the chemopreventative effect of tempol is not solely due to the reduction of oxidative stress and damage but may also be related to redox-mediated signaling functions that include p53 pathway activation.

Correspondence should be addressed to:

Anthony Wynshaw-Boris
San Diego School of Medicine, University of California, 9500 Gilman Drive, Mailstop 0627, La Jolla, CA 92093-0627, USA.
Email: awynshawboris@ucsd.edu

{Ralf Schubert} Present address: Department of Pediatrics, J. W. Goethe-University, Frankfurt, Germany.

{Hiroyuki Yakushiji} Present address: Department of Surgery, Taku Hospital, Saga, Japan.

{Carrolee Barlow} Present address: BrainCells Inc., San Diego, CA, USA.

Also published online

(C) Human Molecular Genetics.

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