| First Author | Mallakin A | Year | 2007 |
| Journal | Cancer Cell | Volume | 12 |
| Issue | 4 | Pages | 381-94 |
| PubMed ID | 17936562 | Mgi Jnum | J:126002 |
| Mgi Id | MGI:3760345 | Doi | 10.1016/j.ccr.2007.08.034 |
| Citation | Mallakin A, et al. (2007) Mutually exclusive inactivation of DMP1 and ARF/p53 in lung cancer. Cancer Cell 12(4):381-94 |
| abstractText | Dmp1 (Dmtf1) is activated by oncogenic Ras-Raf signaling and induces cell-cycle arrest in an Arf, p53-dependent fashion. The survival of K-ras(LA) mice was shortened by approximately 15 weeks in both Dmp1(+/-) and Dmp1(-/-) backgrounds, the lung tumors of which showed significantly decreased frequency of p53 mutations compared to Dmp1(+/+). Approximately 40% of K-ras(LA) lung tumors from Dmp1(+/+) mice lost one allele of the Dmp1 gene, suggesting the primary involvement of Dmp1 in K-ras-induced tumorigenesis. Loss of heterozygosity (LOH) of the hDMP1 gene was detectable in approximately 35% of human lung carcinomas, which was found in mutually exclusive fashion with LOH of INK4a/ARF or that of P53. Thus, DMP1 is a pivotal tumor suppressor for both human and murine lung cancers. |
