Barker F G, Chen P, Furman F, Aldape K D, Edwards M S, Israel M A
Department of Neurological Surgery, University of California, San Francisco, USA.
J Neurooncol. 1997 Jan;31(1-2):17-23. doi: 10.1023/a:1005768910871.
We screened human primary and recurrent malignant glioma, juvenile pilocytic astrocytoma, medulloblastoma, and meningioma tissue specimens for alterations in p16 gene structure. Single strand conformation polymorphism (SSCP) analysis was used to screen for point mutations, and a quantitative polymerase chain reaction-based assay was used to screen for homozygous gene deletions. In malignant glioma specimens, homozygous p16 gene deletions were significantly more common in high-grade tumors than in low-grade gliomas. Point mutations causing alteration in predicted protein structure were not detected. Medulloblastomas showed rare homozygous deletions and no point mutations. No mutations were detected in meningiomas.
我们筛查了人类原发性和复发性恶性胶质瘤、青少年毛细胞型星形细胞瘤、髓母细胞瘤和脑膜瘤组织标本中p16基因结构的改变。采用单链构象多态性（SSCP）分析筛查点突变，并采用基于定量聚合酶链反应的检测方法筛查纯合基因缺失。在恶性胶质瘤标本中，高级别肿瘤中p16基因纯合缺失比低级别胶质瘤更为常见。未检测到导致预测蛋白质结构改变的点突变。髓母细胞瘤显示罕见的纯合缺失且无点突变。脑膜瘤中未检测到突变。
