Targeting Therapies for the p53 Protein in Cancer Treatments

The tumour suppressor protein p53 was discovered over 40 years ago and is arguably one of the most important proteins protecting us from developing tumours. In response to stress, p53 decides whether the stress is severe enough to destroy the cell or whether a repair program is initiated. Decreased p53 function strongly increases the chances of developing cancers and in more than half of all human cancers, the p53 gene is found to be mutated. Gene mutations lead to the complete loss of protein expression or to the expression of mutant forms of p53. Hundreds of different mutant p53 proteins are found in human cancers. Some display a loss of wildtype function, and others gain novel functions in promoting metastasis and chemoresistance, but the majority will display a combination of both to varying degrees. Although advances have been made recently, no strategies targeting p53 are in routine use in clinical practice. Many proposed targeting therapies aim to restore or increase wildtype p53 function. Others aim to make use of vulnerabilities caused by a loss of p53 function or mutant p53 expression.

In this Special Issue, we will discuss the differences between these targeting strategies and explore at what stage of drug development they are.

Dr. Patricia A.J. Muller
Guest Editor

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