| First Author | Matin A | Year | 1998 |
| Journal | APMIS | Volume | 106 |
| Issue | 1 | Pages | 174-82 |
| PubMed ID | 9524576 | Mgi Jnum | J:46683 |
| Mgi Id | MGI:1201832 | Doi | 10.1111/j.1699-0463.1998.tb01333.x |
| Citation | Matin A, et al. (1998) Testicular teratocarcinogenesis in mice--a review. APMIS 106(1):174-82 |
| abstractText | Spontaneous testicular germ cell tumours in humans and mice are remarkable for their diverse composition. These tumours are usually composed of an extraordinary variety of cell and tissue types including muscle, skin, bone, cartilage, and neuroepithelia. Their diverse composition reflects their origin from totipotent primordial germ cells at about Day 12 of fetal development. Although much is known about the development of these tumours, remarkably little is known about the genetics of the mammalian primordial germ cell lineage or about the genes that control susceptibility to spontaneous testicular germ cell tumours in humans or mice. Conventional genetic analysis of susceptible 129/Sv mice is difficult because of the large number of susceptibility genes and their low penetrance. We are taking advantage of the Ter mutation to simplify the genetic analysis. Various evidence suggests that Tel is neither necessary nor sufficient for tumourigenesis. Instead, Tel acts as a modifier, dramatically increasing tumour incidence from similar to 1% in +/+ males, to similar to 17% in Ter/+ males and similar to 94% in Ter/Ter males. Segregation analysis suggests that Ter increases tumour incidence by requiring some, but perhaps not all, of the 129/Sv-derived susceptibility genes. With standard crosses that segregate for the Tel mutation, identification not only of Ter but also of these 129/Sv-derived susceptibility genes should be possible. In this paper, we review the genetics and development of germ cell tumours in 129/Sv mice, summarize the status of Ter mapping, and provide evidence that different genetic pathways lead to unilateral and bilateral tumours. |
