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Mutant p53-Driven Tumorigenesis

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p53 in the Clinics

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Abstract

Most tumors inactivate the p53 tumor suppressor pathway via single nucleotide changes of the TP53 gene itself, which produces proteins with missense mutations. p53 mutant proteins clearly lose normal p53 activities. Some are partial loss of function mutations that retain some activities and probably cooperate with other changes in the p53 pathway to initiate tumor development. Many p53 mutants also exhibit gain-of-function and dominant negative properties. Several mouse models with p53 missense mutations have been generated and these now offer opportunities to study the effects of chemotherapeutic modalities.

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Authors and Affiliations

  1. Department of Dermatology, University of Colorado Denver, Aurora, CO, USA

    Tamara Terzian

  2. Center for Regenerative Medicine and Stem Cell Biology, University of Colorado Denver, Aurora, CO, USA

    Tamara Terzian

  3. Department of Genetics, University of Texas M.D. Anderson Cancer Center, Houston, TX, 77030, USA

    Guillermina Lozano

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  1. Tamara Terzian
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  2. Guillermina Lozano
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Correspondence to Guillermina Lozano .

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Editors and Affiliations

  1. International Prevention Research Instit, 95 cours Lafayette, Lyon, 69006, France

    Pierre Hainaut

  2. International Agency for Cancer Research, 150 Cours Albert-Thomas, Lyon, 69372, France

    Magali Olivier

  3. Cancer Center Karolinska (CCK), Dept. Oncology and Pathology, Karolinska Institute, Karolinska Institutet, Stockholm, 171 76, Sweden

    Klas G. Wiman

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Terzian, T., Lozano, G. (2013). Mutant p53-Driven Tumorigenesis. In: Hainaut, P., Olivier, M., Wiman, K. (eds) p53 in the Clinics. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-3676-8_5

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