MRC Centre for Reproductive Health, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK.
J Pathol. 2013 Mar;229(4):497-501. doi: 10.1002/path.4167.
How invasive testicular germ cell tumours (TGCTs) develop from precursor carcinoma in situ/intratubular germ cell neoplasia unclassified (CIS/IGCNU) cells, and only after puberty, is unknown. In the current issue of The Journal of Pathology, Jørgensen and colleagues have compared the protein expression profile of CIS before and after puberty and in pre-invasive versus invasive TGCT and show that the mitosis-meiosis controller DMRT1 switches off in CIS cells postpubertally and is associated with invasiveness. They also show that CIS cells express a 'confusing' mix of pro- and anti-meiotic proteins; this may predispose CIS cells to accumulate extra chromosomal material which ultimately leads to tumourigenesis.
从癌前原位癌/小管内生殖细胞肿瘤未分类（CIS/IGCNU）细胞发展为侵袭性睾丸生殖细胞肿瘤（TGCT）的机制，以及仅在青春期后才会发生的机制尚不清楚。在本期《病理学杂志》中，Jørgensen 及其同事比较了青春期前后 CIS 以及侵袭性和非侵袭性 TGCT 中 CIS 细胞的蛋白表达谱，结果表明有丝分裂减数分裂控制器 DMRT1 在青春期后会在 CIS 细胞中失活，并且与侵袭性有关。他们还表明，CIS 细胞表达了一种“令人困惑”的促减数分裂和抗减数分裂蛋白混合物；这可能使 CIS 细胞更容易积累额外的染色体物质，最终导致肿瘤发生。
