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- W2045242518 abstract "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." @default.
- W2045242518 created "2016-06-24" @default.
- W2045242518 creator A5017478342 @default.
- W2045242518 creator A5017717228 @default.
- W2045242518 creator A5056961768 @default.
- W2045242518 creator A5084788721 @default.
- W2045242518 date "2006-10-01" @default.
- W2045242518 modified "2023-09-24" @default.
- W2045242518 title "Targeting the p53 tumor suppressor gene function in glioblastomas using small chemical molecules" @default.
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- W2045242518 doi "https://doi.org/10.1002/ddr.20151" @default.
- W2045242518 hasPublicationYear "2006" @default.