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Targeting the p53 tumor suppressor gene function in glioblastomas using small chemical molecules

Glioblastoma multiforme (GBM) is recognized as the most frequent and malignant glioma of which two genetically different subtypes can be distinguished. Primary, de novo glioblastomas show a p53 wild type (wt) status and in 10% of the cases hdm2 overexpression/amplifications occur. In these tumors, the inactivation of the tumor suppressor p53 is elicited by enhanced hdm2‐mediated degradation of p53. Secondary glioblastomas, on the other hand, show inactivating p53 mutations (mut) in 40% of the cases. Based on these observations, reactivating the function of p53 might hold promise for treatment of GBM. In wt p53 tumors showing increased hdm2 levels, the therapeutic strategy might be to inhibit the activity of hdm2 by treatment with small molecules like nutlin‐3. For mut p53 glioblastomas, p53 function might be restored using small chemical entities such as PRIMA‐1. Drug Dev. Res. 67:790–800, 2006. © 2007 Wiley‐Liss, Inc.