Article

Shaping Genetic Alterations in Human Cancer: The p53 Mutation Paradigm

Université P.M. Curie, 4 place Jussieu, 75005 Paris, France.
Cancer Cell (Impact Factor: 23.89). 11/2007; 12(4):303-12. DOI: 10.1016/j.ccr.2007.10.001
Source: PubMed

ABSTRACT p53 mutations are found in 50% of human cancers. Molecular epidemiology has shown strong correlations between the spectrum of p53 mutations and exposure to exogenous carcinogens. This spectrum is influenced quantitatively and qualitatively by various upstream genetic filters that modulate carcinogen activation, detoxification, and/or DNA repair. In this review, we will discuss how other factors such as tissue specificity, SNP of genes associated with the p53 pathway, other genetic alterations, or p53 mutant heterogeneity can act as a second set of downstream filters that also have a profound impact on the spectrum of p53 mutations.

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Available from: Klas G Wiman, Aug 01, 2015
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    • "On the other hand, p53 has been reported to be a potential candidate for cardiac dysfunction. Also, p53 null mice showed successful regression of cardiac hypertrophy [16] but led to ectodermal tumorigenesis in such animals [17]. The bioactive macromolecular drug and p53 siRNA were selected as test molecules in our study encapsulated by the nano-construct for cardiac selective delivery and efficient regression of pathological hypertrophy without bystander effect. "
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    • "The TP53 gene is frequently mutated in many types of cancer, and most of these mutations occurred within the DBD [52]. Because we identified that VRK1 binds to p53 through this region we analysed whether some of these common p53 mutations [53] affected its binding to VRK1. "
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    FEBS letters 01/2014; 588(5). DOI:10.1016/j.febslet.2014.01.040 · 3.34 Impact Factor
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    • "In response to ionizing radiation, MDM2 undergoes rapid ATM-dependent phosphorylation prior to p53 accumulation. The increase in MDM2 basal levels induces degradation and blockade of transcriptional activity of p53 protein [14] [15]. The functional p53 polymorphism, characterized by C>G change at the second position of codon 72 (rs1042522), results in Arg>Pro amino acid substitution. "
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