• Title of article

    The great MYC escape in tumorigenesis

  • Author/Authors

    Dang، نويسنده , , Chi V. and O’Donnell، نويسنده , , Kathryn A. and Juopperi، نويسنده , , Tarja، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2005
  • Pages
    2
  • From page
    177
  • To page
    178
  • Abstract
    Summary sed wild-type MYC expression occurs frequently in human cancers, except in Burkitt’s lymphoma, where the translocated MYC allele is frequently mutated at several hotspots, including a major one at threonine-58. Acute MYC expression increases p53 or ARF levels and induces apoptosis, and previous transgenic animal studies revealed frequent inactivating mutations of p53 or p19ARF in transgenic Myc-induced lymphomas. Lowe and coworkers (Hemann et al., 2005) demonstrate that wild-type MYC can also trigger apoptosis by inducing Bim, which neutralizes Bcl-2. In contrast, the MYC point mutants failed to induce Bim, promoting murine lymphomas that escaped both wild-type p53 and p19ARF, and in doing so, evaded apoptosis.
  • Journal title
    Cancer Cell
  • Serial Year
    2005
  • Journal title
    Cancer Cell
  • Record number

    1335681