Relevance of p53 Mutations

The high proportion of tumors with defective p53 and the increasingly detailed information on the molecular biology of p53 make this molecule a particularly attractive focus in the development of new treatments. Reintroduction of wild-type p53 activity may help to eliminate p53-deficient tumor cells by eliciting apoptosis, offering a diversity of p53-targeted strategies as illustrated by these examples  

p53 function has been restored to tumors by viral delivery of wild-type p53 (Roth, 1998 Roth et al., 1996). 

Selective destruction of p53-deficient cells can be accomplished by genetically engineered adenovirus strains unable to replicate in cells with normal p53 (Bischoff et al., 1996). 

Overexpression of the newly discovered homologs p73 and p51/p40/ ket can induce apoptosis in tumor cells lacking p53 (Jost et al., 1997 Osada et al., 1998). 

The authors thank Dr. R. Montesano, Dr. J. Hall, Dr. D. Meek, and Prof. B. Strauss for critically reading the manuscript Mrs. C. Meplan for discussions, suggestions, and help with literature searches Mr. G. Mollon for illustration work and Mrs. E. El Akroud for secretarial assistance. The authors are aware that although extensive this review is by no means exhaustive and they apologize to the authors of many important publications that are not cited due to space limitations. 

---