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1. Levine A, Feng WZ. The P53 pathway: what questions remain to be explored? Cell Death and Differentiation. 2006 13:1027-36. 2. DP L, LV C. T antigen is bound to a host protein in SV40-transformed cells. Nature 1979;278:261-3. 3. Joerger AC, Fersht AR. The Tumor Suppressor p53: From Structures to Drug Discovery Cold Spring Harb Perspect Biol. 2010;2:1-20. 4. Olivier M, Petitjean A, Marcel V, APe ́tre, Mounawar M. Recent advances in p53 research: an interdisciplinary perspective. Cancer Gene Therapy. 2009;16:1-12. Millions of people are living with cancer having specific mutation in p53 gene while every single person is truly unique in genetic basis or clinical manifestation. The gene encodes transcription factor p53, which plays a central role in regulating cell cycle progression, senescence, differentiation, DNA repair and apoptosis in response to DNA damage or other stress signals. P53 activity is up regulated to initiate a cascade of biological events that ultimately results in prevention of tumor development. Mutations in p53 abrogate normal tumor suppressor functions, contributing to the survival and proliferation of abnormal cells. Cancer cells containing mutant p53 are associated with more aggressive disease, increased resistance to chemotherapy and radiation therapy, and poor prognosis. However the majority of p53 mutations are missense and great number of these mutants represent GOF (Gain of Function) effect resulting increased invasion and metastasis in tumors. These mutations confer a dominant-negative activity over the remaining wild-type allele by functionally inactive hetero-oligomers interactions of the mutants with the wild-type protein. Increasing evidence indicates that many p53 mutants also gain new oncogenic properties that are independent from wild-type p53. Several factors including type of p53 mutations in cancers may limit the efficacy and application of p53 gene therapy. As a result, there is a great interest in therapeutic strategies aimed at restoring the function of p53 for the treatment of cancer. Increasing evidence demonstrate that silencing GOF mutations (targeted antisense therapy) reduce the transactivation activity of mutant p53 and induce apoptosis in cells bearing these mutations then provide a potential strategy to inhibit the oncogenic functions of mutant p53 and improve mutant p53-targeted cancer therapies.

Cancer Gene Therapy to Restore P53 Function: A New Way for an Old Aim