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A common polymorphism acts as an intragenic modifier of mutant p53 behaviour

  1. Author:
    Marin, M. C.
    Jost, C. A.
    Brooks, L. A.
    Irwin, M. S.
    O'Nions, J.
    Tidy, J. A.
    James, N.
    McGregor, J. M.
    Harwood, C. A.
    Yulug, I. G.
    Vousden, K. H.
    Allday, M. J.
    Gusterson, B.
    Ikawa, S.
    Hinds, P. W.
    Crook, T.
    Kaelin, W. G.

  2. Author Address

    Kaelin WG Dana Farber Canc Inst Boston, MA 02115 USA Dana Farber Canc Inst Boston, MA 02115 USA Harvard Univ, Sch Med Boston, MA USA London Sch Hyg & Trop Med London WC1 England Inst Canc Res, Sect Cell Biol & Expt Pathol London SW3 6JB England Univ Sheffield, No Gen Hosp, Dept Gynecol Oncol Sheffield S5 7AU S Yorkshire England Univ Birmingham, CRC, Inst Canc Studies Birmingham W Midlands England Ctr Cutaneous Res London England NCI, ABL Basic Res Program, Frederick Canc Res & Dev Ctr Frederick, MD 21701 USA St Marys Hosp, Imperial Coll Sci Technol & Med, Ludwig Inst Canc Res London England Tohoku Univ, Inst Dev Aging & Canc, Dept Cell Biol Sendai Miyagi 980 Japan Harvard Univ, Sch Med, Dept Pathol Boston, MA USA Howard Hughes Med Inst Coconut Grove, FL 33133 USA
    1. Year: 2000
  2. Journal: Nature Genetics
    1. 25
    2. 1
    3. Pages: 47-54
  4. Type of Article: Article
  1. Abstract:

    The p73 protein, a homologue of the tumour-suppressor protein p53, can activate p53-responsive promoters and induce apoptosis in p53-deficient cells. Here we report that some tumour-derived p53 mutants can bind to and inactivate p73. The binding of such mutants is influenced by whether TP53 (encoding p53) codon 72, by virtue of a common polymorphism in the human population, encodes Arg or Pro. The ability of mutant p53 to bind p73, neutralize p73-induced apoptosis and transform cells in cooperation with EJ-Ras was enhanced when codon 72 encoded Arg. We found that the Arg-containing allele was preferentially mutated and retained in squamous cell tumours arising in Arg/Pro germline heterozygotes. Thus, inactivation of p53 family members may contribute to the biological properties of a subset of p53 mutants, and a polymorphic residue within p53 affects mutant behaviour. [References: 49]

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