Journal
GENES & DEVELOPMENT
Volume 15, Issue 22, Pages 2934-2939Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.929901
Keywords
Dmp1 transcription factor; Arf; p53; Mdm2; Myc; cancer; tumor suppression
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Funding
- NCI NIH HHS [P30 CA021765, CA21765] Funding Source: Medline
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Loss of Dmp1, an Arf transcriptional activator, leads to spontaneous tumorigenesis in mice, causing death from various forms of cancer by two years of age. Retention and expression of the wild-type Dmp1 allele in tumors arising in Dmp1(+/-) mice demonstrate that Dmp1 can be haplo-insufficient for tumor suppression. The mean latency of Ep-Myc-induced B-cell lymphomas is halved on a Dmp1(-/-) or Dmp1(+/-) genetic background. Although p53 mutations or Arf deletion normally occur in similar to 50% of Ep-Myc-induced lymphomas, Dmp1 loss obviates selection for such mutations, indicating that Dmp1 is a potent genetic modifier of the Arf-p53 pathway in vivo.
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