MGMT gene silencing and benefit from temozolomide in glioblastoma
MGMT gene silencing and benefit from temozolomide in glioblastoma
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DOI：
10.1056/nejmoa043331
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发表时间：
2005-03-10
影响因子：
158.5
通讯作者：
Stupp, R
中科院分区：
文献类型：
--
作者：
Hegi, ME;Diserens, A;Stupp, R
背景：表观遗传沉默的MGMT（O（sup 6）-甲基鸟嘌呤-DNA甲基转移酶）DNA修复基因的启动子甲基化损害DNA修复，并已与较长的生存期与胶质母细胞瘤患者接受烷化剂agents.METHODS：我们测试之间的关系MGMT沉默的肿瘤和生存的患者谁参加了一项随机试验比较放疗单独与放疗结合伴随和辅助治疗替莫唑胺。甲基化特异性聚合酶链反应分析确定MGMT启动子的甲基化状态。结果：在206例可评估病例中，MGMT启动子甲基化率为45%。无论治疗与否，MGMT启动子甲基化是独立的有利预后因素（P
BACKGROUND:Epigenetic silencing of the MGMT (O(sup 6)-methylguanine-DNA methyltransferase) DNA-repair gene by promoter methylation compromises DNA repair and has been associated with longer survival in patients with glioblastoma who receive alkylating agents.METHODS:We tested the relationship between MGMT silencing in the tumor and the survival of patients who were enrolled in a randomized trial comparing radiotherapy alone with radiotherapy combined with concomitant and adjuvant treatment with temozolomide. The methylation status of the MGMT promoter was determined by methylation-specific polymerase-chain-reaction analysis.RESULTS:The MGMT promoter was methylated in 45 percent of 206 assessable cases. Irrespective of treatment, MGMT promoter methylation was an independent favorable prognostic factor (P