The great MYC escape in tumorigenesis

被引:84
作者
Dang, CV [1 ]
O'Donnell, KA
Juopperi, T
机构
[1] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Program Pathobiol, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA
关键词
D O I
10.1016/j.ccr.2005.08.005
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Increased 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.
引用
收藏
页码:177 / 178
页数:2
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[11]   DNA AND RNA FROM UNINFECTED VERTEBRATE CELLS CONTAIN NUCLEOTIDE-SEQUENCES RELATED TO THE PUTATIVE TRANSFORMING GENE OF AVIAN MYELOCYTOMATOSIS VIRUS [J].
SHEINESS, D ;
BISHOP, JM .
JOURNAL OF VIROLOGY, 1979, 31 (02) :514-521