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PMID: 16169462 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

The great MYC escape in tumorigenesis.

Cancer cell ·Vol. 8 ·No. 3 ·2005-09-00 ·Pages 177-8

Dang CV, O'donnell KA, Juopperi T

Abstract

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.

MeSH Terms
Animals Apoptosis Burkitt Lymphoma/genetics Gene Expression Regulation, Neoplastic Genes, myc Humans Lymphoma/genetics,pathology Models, Biological Mutation Neoplasms/genetics,pathology
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Dang Chi V
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. cvdang@jhmi.edu
O'donnell Kathryn A
Juopperi Tarja
Article Info
Journal
Cancer cell
Abbr.
Cancer Cell
ISSN
1535-6108
Published
2005-09-00
Pages
177-8
Language
English
Region
United States
NLM ID
101130617
Subset
IM
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