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Patterns of TP53 Mutations in Human Cancer: Interplay Between Mutagenesis, DNA Repair and Selection

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25 Years of p53 Research

Somatic mutations are the cornerstone of cancer (Hanahan et al. 2000). The development of cancer involves the contributions of many heritable genetic events as well as of a large number of epigenetic changes, but what makes the turning point between untransformed and transformed cell irreversible is the acquisition of targeted, somatic mutations, conferring to cells a selective advantage for clonal proliferation. These mutations can occur in many different genes, but only a handful of them are frequently mutated in a wide variety of human cancers. They include genes of the RAS family (mainly KRAS), BRAF1, APC,α–Catenin, p16/INK4a, PTEN and TP53. After over 20 years of research on mutation detection in cancers, TP53 remains the world champion of somatic mutations, with over 70 % of all the mutations described so far in human cancers (Hainaut et al. 2000).

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  1. International Agency for Research on Cancer, World Health Organization, Lyon, France

    Hong Shi, Florence Le Calvez, Magali Olivier & Pierre Hainaut

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  1. Hong Shi
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  2. Florence Le Calvez
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  1. International Agency for Research on Cancer, World Health Organization, Lyon, France

    Pierre Hainaut

  2. Cancer Center Karolinska, Karolinska Institute, Stockholm, Sweden

    Klas G. Wiman

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Shi, H., Le Calvez, F., Olivier, M., Hainaut, P. (2007). Patterns of TP53 Mutations in Human Cancer: Interplay Between Mutagenesis, DNA Repair and Selection. In: Hainaut, P., Wiman, K.G. (eds) 25 Years of p53 Research. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-2922-6_13

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