Laboratory of Brain Tumor Biology and Genetics, Neuroscience Research Center, Lausanne University Hospital, Chemin des Boveresses 155, CLE-C306, 1066 Epalinges, Lausanne, Switzerland.
Division of Neurosurgery, Lausanne University Hospital, Lausanne, Switzerland.
Acta Neuropathol. 2018 Apr;135(4):601-615. doi: 10.1007/s00401-018-1810-6. Epub 2018 Jan 24.
The optimal treatment for patients with low-grade glioma (LGG) WHO grade II remains controversial. Overall survival ranges from 2 to over 15 years depending on molecular and clinical factors. Hence, risk-adjusted treatments are required for optimizing outcome and quality of life. We aim at identifying mechanisms and associated molecular markers predictive for benefit from radiotherapy (RT) or temozolomide (TMZ) in LGG patients treated in the randomized phase III trial EORTC 22033. As candidate biomarkers for these genotoxic treatments, we considered the DNA methylome of 410 DNA damage response (DDR) genes. We first identified 62 functionally relevant CpG sites located in the promoters of 24 DDR genes, using the LGG data from The Cancer Genome Atlas. Then we tested their association with outcome [progression-free survival (PFS)] depending on treatment in 120 LGG patients of EORTC 22033, whose tumors were mutant for isocitrate dehydrogenase 1 or 2 (IDHmt), the molecular hallmark of LGG. The results suggested that seven CpGs of four DDR genes may be predictive for longer PFS in one of the treatment arms that comprised MGMT, MLH3, RAD21, and SMC4. Most interestingly, the two CpGs identified for MGMT are the same, previously selected for the MGMT-STP27 score that is used to determine the methylation status of the MGMT gene. This score was higher in the LGG with 1p/19q codeletion, in this and other independent LGG datasets. It was predictive for PFS in the TMZ, but not in the RT arm of EORTC 22033. The results support the hypothesis that a high score predicts benefit from TMZ treatment for patients with IDHmt LGG, regardless of the 1p/19q status. This MGMT methylation score may identify patients who benefit from first-line treatment with TMZ, to defer RT for long-term preservation of cognitive function and quality of life.
对于低级别胶质瘤(LGG)WHO 分级 II 患者的最佳治疗方法仍存在争议。总生存期因分子和临床因素而异,范围为 2 年至 15 年以上。因此,需要进行风险调整治疗以优化预后和生活质量。我们旨在确定机制和相关分子标志物,以预测接受随机 III 期 EORTC 22033 试验治疗的 LGG 患者从放疗(RT)或替莫唑胺(TMZ)中获益。作为这些遗传毒性治疗的候选生物标志物,我们考虑了 410 个 DNA 损伤反应(DDR)基因的 DNA 甲基组。我们首先使用癌症基因组图谱中的 LGG 数据,在 24 个 DDR 基因的启动子中鉴定出 62 个功能相关的 CpG 位点。然后,我们根据 EORTC 22033 中 120 名 LGG 患者的肿瘤是否存在异柠檬酸脱氢酶 1 或 2(IDHmt)突变,即 LGG 的分子标志,测试了它们与无进展生存期(PFS)的相关性。结果表明,四个 DDR 基因的七个 CpG 可能是治疗组中一个的 PFS 更长的预测因素,该治疗组包含 MGMT、MLH3、RAD21 和 SMC4。最有趣的是,为 MGMT 选择的两个 CpG 与之前为用于确定 MGMT 基因甲基化状态的 MGMT-STP27 评分选择的相同。在具有 1p/19q 缺失的 LGG 中,该评分在本研究和其他独立的 LGG 数据集中更高。它在 TMZ 中对 PFS 具有预测作用,但在 EORTC 22033 的 RT 臂中没有预测作用。这些结果支持以下假设,即高评分预测 IDHmt LGG 患者接受 TMZ 治疗的获益,而与 1p/19q 状态无关。该 MGMT 甲基化评分可能会识别出从 TMZ 一线治疗中获益的患者,从而推迟 RT 以长期保持认知功能和生活质量。