| First Author | Matin A | Year | 2007 |
| Journal | Cell Mol Life Sci | Volume | 64 |
| Issue | 11 | Pages | 1317-22 |
| PubMed ID | 17464447 | Mgi Jnum | J:122476 |
| Mgi Id | MGI:3714451 | Doi | 10.1007/s00018-007-6433-3 |
| Citation | Matin A (2007) What leads from dead-end?. Cell Mol Life Sci 64(11):1317-22 |
| abstractText | The 129 mouse strain develops congenital testicular germ cell tumors (TGCTs) at a low frequency. TGCTs in mice resemble the testicular tumors (teratomas) that occur in human infants. The genes that cause these tumors in 129 have not been identified. The defect at the Ter locus increases TGCT incidence such that 94% of 129-Ter/Ter males develop TGCTs. The primary effect of the Ter mutation is progressive loss of primordial germ cells (PGCs) during embryonic development. This results in sterility in adult Ter/Ter mice on all mouse strain backgrounds. However, on the 129 background, Ter causes tumor development in addition to sterility. Therefore, Ter acts as a modifier of 129-derived TGCT susceptibility genes. Ter was identified to be a mutation that inactivates the Dead-end1 (Dnd1) gene. In this perspective, I discuss the possible areas of future investigations to elucidate the mechanism of TGCT development due to Dnd1 inactivation. |
