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作 者:翟广[1] 王树凯[1] 宋来君[1] 冯祖荫[1]
机构地区:[1]河南医科大学第一附属医院神经外科,郑州450052
出 处:《河南医科大学学报》2001年第3期286-288,共3页Journal of Henan Medical University
基 金:!博士研究生课题
摘 要:目的 :探讨p16基因异常与脑星形细胞瘤发生、发展的关系。方法 :利用PCR及PCR based甲基化技术检测了 5 6例不同级别的脑星形细胞瘤组织p16基因缺失及 5’CpG岛甲基化状况。结果 :18例高病理级别的脑星形细胞瘤发生了p16基因缺失 ,而低病理级别的脑星形细胞瘤无一例发生缺失 (P <0 .0 5 ) ;6例脑星形细胞瘤发生了p16基因 5’CpG岛甲基化。结论 :p16基因失活可能参与脑星形细胞瘤的病理发生、恶性进展。p16基因纯合缺失是p16基因失活的主要机制。Aim:To investigate if the abnormality of p16 gene is involved in the occurrence or malignant progression of brain glioma.Methods: Deletion and 5'CpG island methylation of p16 gene were detected in 56 cases with brain gliomas by the methods of PCR and PCR based methylation.Results: Homozygous deletions of p16 gene were found in 18 cases of malignant brain glioma, while deletion of p16 gene was not found in any low grade gliomas. Six cases of brain glioma were found to be methylated in 5'CpG island of p16 gene.Conclusion: Inactivation of p16 gene may be involved in occurrence or malignant progression of brain glioma. Homozygous deletion p16 of gene is the major mechanism for inactivation of p16 gene.
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