Translational regulation of p53 as a potential tumor therapy target
Authors: Schumacher, Björn; Gartner, Anton
Source: Future Oncology, Volume 2, Number 1, February 2006 , pp. 145-153(9)
Publisher: Future Medicine
Abstract:
The tumor suppressor p53 is a central player in apoptosis induction in response to oncogenic stimuli and DNA damage. As activation of p53 has been suggested as a prime strategy for future tumor therapy, inhibition of negative regulators of p53 activity would be a similarly desirable strategy. The small worm Caenorhabditis elegans is a model organism in which many conserved biological pathways, including the core apoptotic machinery, were elucidated. The discovery of a worm p53 homolog cep-1/p53 (which stands for C. elegans p53) that specifically induces apoptosis upon DNA damage through a pathway that is conserved from worm to man opened the way for the use of C. elegans genetics to uncover regulatory mechanisms – and hence novel therapeutic targets – of p53-mediated apoptosis. The authors have recently reported a novel mechanism of C. elegans cep-1/p53 regulation through germ line defective-1-mediated translational repression. This review discusses the potential of the worm system to screen for apoptosis-inducing cancer drugs and to identify novel p53 regulators whose human counterparts might become potential tumor therapy targets.Keywords: apoptosis; Caenorhabditis elegans; DNA damage; GLD-1; p53; translational regulation
Document Type: Research article
DOI: http://dx.doi.org/10.2217/14796694.2.1.145
Publication date: 2006-02-01
- Future Oncology provides a forum for a new era of cancer care as research efforts burgeon in this challenging area. The burden of disease is set to increase in our increasingly aged populations, but the available armamentarium is also set to grow rapidly and to offer the potential to focus on individual needs. The journal focuses on the most important advances and highlights their relevance in the clinical setting.
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