A novel facet of tumor suppression by p53: Induction of tumor immunogenicity

Department of Microbiology
OncoImmunology (Impact Factor: 6.27). 07/2012; 1(4):541-543. DOI: 10.4161/onci.19409
Source: PubMed


Pharmacological reactivation of the p53 tumor suppressor is a promising strategy for anti-cancer therapy due to its high potential to elicit apoptosis or growth arrest in cancer cells. Recently we uncovered the mechanism of activation of the innate immune response by p53 upon its activation by small molecules.

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Available from: Galina Selivanova,
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    • "This latter outcome is mediated by the upregulation of several proteins involved in the execution of cell death [77] [78], including the pro-apoptotic BCL-2 family members BAX and BBC3, the cytoplasmic adaptor APAF1 and the death receptor CD95 [79], as well as by transcription-independent mechanisms [80] [81] [82]. More recently, an intense wave of investigation has been centered on physiological aspects of the p53 biology, unveiling a key role for baseline p53 levels in the maintenance of energetic, redox, genomic and immune homeostasis [38] [83] [84]. Thus, p53 mediates oncosuppressive functions both as it contributes to the maintenance of intracellular homeostasis (de facto preventing malignant transformation), and as it directs the elimination of irremediably damaged (hence potentially tumorigenic) cells. "
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