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- W2776139938 abstract "p53 protects cells from genetic assaults by triggering cell-cycle arrest and apoptosis. Inactivation of p53 pathway is found in the vast majority of human cancers often due to somatic missense mutations in TP53 or to an excessive degradation of the protein. Accordingly, reactivation of p53 appears as a quite promising pharmacological approach and, effectively, several attempts have been made in that sense. The most widely investigated compounds for this purpose are PRIMA-1 (p53 reactivation and induction of massive apoptosis )and PRIMA-1Met (APR-246), that are at an advanced stage of development, with several clinical trials in progress. Based on publications referenced in PubMed since 2002, here we review the reported effects of these compounds on cancer cells, with a specific focus on their ability of p53 reactivation, an overview of their unexpected anti-cancer effects, and a presentation of the investigated drug combinations." @default.
- W2776139938 created "2018-01-05" @default.
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- W2776139938 creator A5091892350 @default.
- W2776139938 date "2017-12-16" @default.
- W2776139938 modified "2023-10-11" @default.
- W2776139938 title "PRIMA-1 and PRIMA-1Met (APR-246): From Mutant/Wild Type p53 Reactivation to Unexpected Mechanisms Underlying Their Potent Anti-Tumor Effect in Combinatorial Therapies" @default.
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- W2776139938 doi "https://doi.org/10.3390/cancers9120172" @default.
- W2776139938 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5742820" @default.
- W2776139938 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29258181" @default.
- W2776139938 hasPublicationYear "2017" @default.
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