Testicular teratomas: Germ cells cycling in the wrong direction.
Testicular teratomas: Germ cells cycling in the wrong direction.
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睾丸畸胎瘤：生殖细胞以错误的方向循环。
DOI：
10.1080/15384101.2016.1154369
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Salz,HelenK
中科院分区：
文献类型：
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作者：
Salz,HelenK
畸胎瘤，来自希腊语的工作tera意思是怪物，是生殖细胞肿瘤，包含来自所有3个胚层的分化良好的细胞，如头发，骨骼，牙齿和神经元。1生殖细胞如何不遵循正常的发育程序，而是开始分化成体细胞组织，这是一个尚未解决的迷人问题。配子发生开始于胚胎发生的早期，此时原始生殖细胞被指定为不同于体细胞。2原始生殖细胞分化后进行有丝分裂并迁移到性腺。一旦进入性腺，它们就开始性别特异性分化，最终导致精子或卵子的产生。在小鼠中，性别特异性差异已经在胚胎性腺中检测到。在卵巢中，生殖细胞开始减数分裂，然后进入减数分裂停滞期直到排卵。在睾丸中，生殖细胞不启动减数分裂，而是进入G1/G 0有丝分裂停滞，直到出生后。当它们停滞时，两性的生殖细胞也下调一组多能性基因，这是原始生殖细胞命运的初始特化和维持所必需的（图1）。长期以来，人们一直认为，如果男性胚胎生殖细胞不能按时停止生长，它们将在成年后引起睾丸畸胎瘤。[1]几年前进行的研究为这一观点提供了相当大的支持，将胚胎中生殖细胞的长期增殖与成人中畸胎瘤的发生率联系起来。此外，发现这些增殖的生殖细胞异位表达许多基因，包括细胞周期蛋白D1编码基因Ccnd 1。3，4虽然细胞周期蛋白D1是一种已知的人类致癌基因，5细胞周期蛋白D1在小鼠畸胎瘤发生中起类似作用的可能性至今仍未得到证实。在《细胞周期》的这卷中，Jason Heaney和他的同事，包括作为联合第一作者的Denise Lanza和艾米丽Dawson，报告说他们有明确的证据表明畸胎瘤的形成需要细胞周期蛋白D1的异常表达。[6]为了建立他们的案例，Lanza等人，首先确定细胞周期蛋白D1蛋白是生殖细胞中唯一异常表达的D型细胞周期蛋白，其不能按计划进入细胞周期停滞。这是通过比较胎儿生殖细胞中
Teratomas, from the Greek work tera meaning monster, are germ cell tumors which contain well-differentiated cells from all 3 germ layers, such as hair, bone, teeth and neurons. 1 How germ cells fail to follow their normal developmental program, and instead begin to differentiate into somatic tissues is a fascinating problem that has yet to be solved. Gametogenesis begins early in embryogenesis when the primordial germ cells are specified as distinct from somatic cells. 2 After specification, the primordial germ cells divide mitotically and migrate to the gonad. Once in the gonad, they initiate sexspecific differentiation, eventually leading to the production of either sperm or eggs. In the mouse, sex-specific differences are already detected in the embryonic gonad. In the ovary, germ cells initiate meiosis, then enter meiotic arrest until ovulation. In the testis, germ cells do not initiate meiosis and instead enter G1/G0 mitotic arrest until after birth. As they arrest, germ cells of both sexes also downregulate a set of pluripotency genes, which were necessary for the initial specification and maintenance of primordial germ cell fate (Fig. 1). It has long been thought that if male embryonic germ cells fail to arrest on schedule they will give rise to testicular teratomas in the adult. 1 Studies carried out several years ago provided considerable support for this idea by correlating prolonged germ cell proliferation in the embryo with teratoma incidence in the adult. 3, 4 Moreover, these proliferating germ cells were found to ectopically express a number of genes, including the Cyclin D1 encoding gene Ccnd1. 3, 4 Although Cyclin D1 is a known human oncogene, 5 the possibility that Cyclin D1 plays a similar role in teratoma initiation in mice has remained untested-until now.In this volume of Cell Cycle, Jason Heaney and colleagues, including Denise Lanza and Emily Dawson as joint first authors, report that they have unequivocal evidence that aberrant expression of Cyclin D1 is required for teratoma formation. 6 To build their case, Lanza et al., first establish that the Cyclin D1 protein is the only aberrantly expressed D-type Cyclin in germ cells that fail to enter cell cycle arrest on schedule. This was done by comparing expression in fetal germ cells