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首页> 外文期刊>The Canadian Journal of Neurological Sciences: le Journal Canadien des Sciences Neurologiques >Relationship between O6-methylguanine-DNA methyltransferase levels and clinical response induced by chloroethylnitrosourea therapy in glioma patients.
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Relationship between O6-methylguanine-DNA methyltransferase levels and clinical response induced by chloroethylnitrosourea therapy in glioma patients.

机译：胶质瘤患者O6-甲基鸟嘌呤-DNA甲基转移酶水平与氯乙基亚硝基脲治疗诱导的临床反应之间的关系。

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BACKGROUND: Adjuvant nitrosourea chemotherapy fails to prolong survival significantly as many tumors demonstrate resistance to these drugs. It has been documented in cell lines that O6-methylguanine DNA methyltransferase (MGMT) plays an important role in chloroethylnitrosourea (CENU) drug resistance. METHODS: We evaluated MGMT expression in 22 glioma specimens by using an immunofluorescence assay and compared the results with clinical responses of the patients to CENU-based chemotherapy. RESULTS: Eight tumor samples had no detectable MGMT, whereas other samples had from 9,989 to 982,401 moleculesucleus. In one group (12 patients), the tumor decreased in size or was stable (effective group), whereas in the other group (10 patients), the tumor demonstrated continuous growth during chemotherapy (progressive group). The Mer- patients (MGMT < 60,000 moleculesucleus) appeared to have more chance of stable disease or response to CENU therapy than the Mer+ patients (MGMT > 60,000 moleculesucleus) (X2 = 4.791, p = 0.0286). In patients with glioblastomas multiforme (GBMs), the median time to progression (TTP) of Mer+ patient was shorter than that of Mer- patient (t = 2.04, p = 0.049). As a corollary, the MGMT levels were significantly higher in GBM tumors from the progressive group than those from the effective group (t = 2.26, p = 0.029). However, there was no significant correlation between MGMT levels and either the survival time (r = 0.04, p = 0.8595) or TTP (r = 0.107, p = 0.6444). CONCLUSION: This study suggests that being MGMT positive is indicative of a more aggressive disease that progresses more rapidly with CENU therapy. However, MGMT negative tumors are not always sensitive to CENU agents, suggesting that other factors are also important.
机译：背景：亚硝基脲辅助化疗不能显着延长生存期，因为许多肿瘤显示出对这些药物的耐药性。在细胞系中已证明O6-甲基鸟嘌呤DNA甲基转移酶（MGMT）在氯乙基亚硝基脲（CENU）耐药性中起重要作用。方法：我们通过免疫荧光分析评估了22例神经胶质瘤标本中MGMT的表达，并将结果与​​基于CENU化疗的患者的临床反应进行了比较。结果：8个肿瘤样品没有检测到MGMT，而其他样品具有9989至982401分子/核。在一组（12例患者）中，肿瘤缩小或稳定（有效组），而在另一组（10例患者）中，肿瘤在化疗期间显示出持续增长（进展组）。与Mer +患者（MGMT> 60,000分子/核）相比，Mer患者（MGMT <60,000分子/核）似乎更有可能获得稳定的疾病或对CENU治疗的反应（X2 = 4.791，p = 0.0286）。在患有多形性胶质母细胞瘤（GBM）的患者中，Mer +患者的中位进展时间（TTP）短于Mer-患者（t = 2.04，p = 0.049）。结果，进展组的GBM肿瘤中MGMT水平显着高于有效组（t = 2.26，p = 0.029）。但是，MGMT水平与生存时间（r = 0.04，p = 0.8595）或TTP（r = 0.107，p = 0.6444）之间没有显着相关性。结论：这项研究表明，MGMT呈阳性表明CENU疗法可导致疾病进展更快。但是，MGMT阴性肿瘤并不总是对CENU药物敏感，这表明其他因素也很重要。

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