什么导致无路可走？
What leads from dead-end?
作者信息
Matin A
机构信息
Department of Cancer Genetics, University of Texas, MD Anderson Cancer Center, Houston, TX 77030, USA.
出版信息
Cell Mol Life Sci. 2007 Jun;64(11):1317-22. doi: 10.1007/s00018-007-6433-3.
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.
129小鼠品系发生先天性睾丸生殖细胞肿瘤（TGCT）的频率较低。小鼠中的TGCT类似于人类婴儿中发生的睾丸肿瘤（畸胎瘤）。导致129小鼠发生这些肿瘤的基因尚未确定。Ter位点的缺陷会增加TGCT的发病率，使得94%的129-Ter/Ter雄性小鼠发生TGCT。Ter突变的主要影响是胚胎发育过程中原始生殖细胞（PGC）的逐渐丧失。这导致所有小鼠品系背景下的成年Ter/Ter小鼠不育。然而，在129背景下，Ter除了导致不育外还会引发肿瘤形成。因此，Ter作为129衍生的TGCT易感基因的修饰因子。Ter被鉴定为一种使Dead-end1（Dnd1）基因失活的突变。从这个角度出发，我讨论了未来为阐明因Dnd1失活导致TGCT发生机制而可能进行研究的领域。
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