论文部分内容阅读
作者使用基础PCR技术对57例脑肿瘤和25例结直肠的p16外显子1进行了检测,发现p16外显子1的缺失具有显著的特异性:26/38例成胶质细胞瘤有一个纯合子缺失,而14例神经管胚细胞瘤、5例室管膜瘤和25例结直肠癌的p16外显子1没有任何缺失发生。没有p16缺失的另外12例成胶质细胞瘤其基因内突变的缺乏,表明可能有一种不同于p16的基因是9P21缺失的靶。为了证实这种可能性,作者检测了p16周围80kb区域内的8个序列—标记位点:p16的3个外显子,3个序列—标记位点(伴随p16的着丝粒的)标志物和3’末端约有
Using basic PCR techniques, 57 patients with brain tumors and 25 patients with colorectal p16 exon 1 were detected and found that p16 exon 1 deletion was significantly specific: 26/38 glioblastoma have a Homozygotes were missing, while no deletion of p16 exon 1 in 14 cases of neuroblastoma, 5 cases of ependymoma and 25 cases of colorectal cancer occurred. The absence of intragenic mutations in another 12 glioblastomas without p16 deletion suggests that there may be a different target for p16 than the 9P21 deletion. To confirm this possibility, the authors tested 8 sequences within the 80 kb region around p16 - marker sites: 3 exons of p16, 3 sequence-marker sites (centromeric with p16) And 3’end