de Foy K A, Gayther S A, Colledge W H, Crockett S, Scott I V, Evans M J, Ponder B A
CRC Human Cancer Genetics Research Group, Addenbrooke's Hospital, Cambridge, UK.
Br J Cancer. 1998 May;77(10):1642-4. doi: 10.1038/bjc.1998.269.
Female transgenic mice lacking a functional c-mos proto-oncogene develop ovarian teratomas, indicating that c-mos may behave as a tumour-suppressor gene for this type of tumour. We have analysed the entire coding region of the c-MOS gene in a series of human ovarian teratomas to determine whether there are any cancer-causing alterations. DNA from twenty teratomas was analysed by single-strand conformational analysis (SSCA) and heteroduplex analysis (HA) to screen for somatic and germline mutations. In nine of these tumours the entire gene was also sequenced. A previously reported polymorphism and a single new sequence variant were identified, neither of which we would predict to be disease-causing alterations. These results suggest that mutations in the coding region of the c-MOS gene do not play a significant role in the genesis of human ovarian teratomas.
缺乏功能性c-mos原癌基因的雌性转基因小鼠会发生卵巢畸胎瘤,这表明c-mos可能作为这类肿瘤的肿瘤抑制基因发挥作用。我们分析了一系列人类卵巢畸胎瘤中c-MOS基因的整个编码区,以确定是否存在任何致癌性改变。通过单链构象分析(SSCA)和异源双链分析(HA)对来自20个畸胎瘤的DNA进行分析,以筛选体细胞和种系突变。在其中9个肿瘤中,还对整个基因进行了测序。鉴定出一个先前报道的多态性和一个新的序列变异,我们预计这两者都不是致病改变。这些结果表明,c-MOS基因编码区的突变在人类卵巢畸胎瘤的发生中不发挥重要作用。