Giuseppe Trigiante

TL;DR: The expression of ASPP is frequently downregulated in human breast carcinomas expressing wild-type p53 but not mutant p53, therefore, ASPP regulate the tumor suppression function of p53 in vivo.

TL;DR: Polymorphism in p53 may influence individual responsiveness to cancer therapy, and clinical response following cisplatin-based chemo-radiotherapy for advanced head and neck cancer is influenced by this polymorphism, cancers expressing 72R mutants having lower response rates than those expressing 72P mutants.

TL;DR: iASPP is an evolutionarily conserved inhibitor of p53; inhibition of iASPP by RNA-mediated interference or antisense RNA in C. elegans or human cells, respectively, induces p53-dependent apoptosis and could provide an important new strategy for treating tumors expressing wild-type p53.

TL;DR: It is demonstrated that the in vitro response of cells exposed to anticancer agents is strongly influenced by this SNP in wild-type p53, and that the outcome of chemo-radiotherapy of squamous carcinomas is more favourable in cancers retaining a wild- type 72R allele.

TL;DR: The identification of a new family of proteins, known as ASPPs, has led to the discovery of a novel mechanism that selectively regulates the apoptotic function, but not the cell-cycle-arrest function, of p53 and gives an insight into how p53 responds to different stress signals.