P16 deletion and mutation analysis in human brain tumors
P16 deletion and mutation analysis in human brain tumors
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DOI：
10.1023/a:1005768910871
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发表时间：
1997-01-01
影响因子：
3.9
通讯作者：
Israel, MA
中科院分区：
文献类型：
--
作者：
Barker, FG;Chen, PC;Israel, MA
我们筛选了人类原发性和复发性恶性胶质瘤、幼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。单链构象多态性（SSCP）分析被用来筛选点突变，和定量聚合酶链反应为基础的测定被用来筛选纯合基因缺失。在恶性胶质瘤标本中，高级别胶质瘤中p16基因纯合缺失明显多于低级别胶质瘤。未检测到引起预测蛋白质结构改变的点突变。髓母细胞瘤表现出罕见的纯合性缺失，没有点突变。在脑膜瘤中未检测到突变。
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.