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
Link To Document :
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