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Cancer Research 68, 4959, July 1, 2008. doi: 10.1158/0008-5472.CAN-08-0182
© 2008 American Association for Cancer Research

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iASPP Inhibition: Increased Options in Targeting the p53 Family for Cancer Therapy

Helen S. Bell1 and Kevin M. Ryan1,2

1 Tumour Cell Death Laboratory, Beatson Institute for Cancer Research, Cancer Research UK Beatson Laboratories and 2 Glasgow Centre for Cancer Research, University of Glasgow, Glasgow, United Kingdom

Requests for reprints: Kevin M. Ryan, Beatson Institute for Cancer Research, Garscube, Estate, Switchback Road, Glasgow G61 1BD, UK. Phone: 441413303655; Fax: 441419426521; E-mail: k.ryan{at}beatson.gla.ac.uk.

Key Words: p53 • p73 • iASPP • cancer • therapy

Strategies to induce p53 for cancer therapy offer appeal but many tumors harbor inactivating p53 mutations. One way to address this situation may be to activate the p53-related protein p73, which functions similarly, but unlike p53, is rarely lost or mutated in cancer. Along these lines, a recent study reports that a p53-derived peptide that targets iASPP—a common negative regulator of p53 family members—can effectively trigger tumor cell death by a p73-dependent mechanism. These findings promote further study of iASPP targeting as a therapeutic strategy to activate p73. [Cancer Res 2008;68(13):4959–62]




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P. Lunghi, A. Costanzo, L. Mazzera, V. Rizzoli, M. Levrero, and A. Bonati
The p53 Family Protein p73 Provides New Insights into Cancer Chemosensitivity and Targeting
Clin. Cancer Res., November 1, 2009; 15(21): 6495 - 6502.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2008 by the American Association for Cancer Research.