关键词: Glioma MGMT promoter methylation Molecular typing Perfusion magnetic resonance imaging Positron-emission tomography

Mesh : Brain Neoplasms / diagnostic imaging genetics DNA Modification Methylases / genetics DNA Repair Enzymes / genetics Glioma / diagnostic imaging genetics Humans Magnetic Resonance Imaging / methods Methylation Positron-Emission Tomography / methods Tumor Suppressor Proteins / genetics Tyrosine

来  源:   DOI:10.1007/s00330-022-08606-9

Abstract:
OBJECTIVE: To investigate the effects of O6-methylguanine DNA methyltransferase (MGMT) promoter methylation status of gliomas on O-(2-18F-fluoroethyl)-L-tyrosine ([18F]FET) uptake and cerebral blood flow (CBF) of arterial spin labeling (ASL), evaluated by hybrid PET/MR. Stereotactic biopsy was used to validate the findings.
METHODS: A set of whole tumor and reference volumes of interest (VOIs) based on PET/FLAIR imaging were delineated and transferred to the corresponding [18F]FET PET and CBF maps in 57 patients with newly diagnosed gliomas. The mean and max tumor-to-brain ratio (TBR) and normalized CBF (nCBF) were calculated. The predictive efficacy of [18F]FET PET and CBF in determining MGMT promoter methylation status of glioma were evaluated by whole tumor analysis and stereotactic biopsy. The correlation between PET/MR parameters and MGMT promoter methylation were analyzed using histological specimens acquired from multiple stereotactic biopsies.
RESULTS: Based on the analysis of whole tumor volume and biopsy site, TBRmean, TBRmax, nCBFmean, and nCBFmax showed no statistically significant differences between gliomas with and without MGMT promoter methylation (all p > 0.05). Furthermore, stereotactic biopsy demonstrated that TBRmean, TBRmax, nCBFmean, and nCBFmax showed no correlation with MGMT promoter methylation (r = -0.117, p = 0.579; r = -0.161, p = 0.443; r = -0.271, p = 0.191; r = -0.300, p = 0.145; respectively).
CONCLUSIONS: MGMT promoter methylation status shows no effect on [18F]FET uptake and CBF of ASL in gliomas. Stereotactic biopsy validates it and further reveals there is no correlation of [18F]FET PET uptake and CBF with the percentages of MGMT promoter methylation.
CONCLUSIONS: • Based on whole tumor VOI assessment, MGMT promoter methylation status shows no effect on [18F]FET uptake and CBF of ASL in gliomas. • For WHO grade IV glioblastomas, [18F]FET PET and ASL parameters based on hybrid PET/MR fail to predict the MGMT promoter methylation status. • Stereotactic image-based histology reveals that there is no correlation of [18F]FET PET uptake and CBF with the status and percentages of MGMT promoter methylation in gliomas.
摘要:
目的:研究脑胶质瘤O6-甲基鸟嘌呤DNA甲基转移酶(MGMT)启动子甲基化状态对O-(2-18F-氟乙基)-L-酪氨酸([18F]FET)摄取和动脉自旋标记(ASL)脑血流量(CBF)的影响。通过混合PET/MR评估。立体定向活检用于验证发现。
方法:在57例新诊断的神经胶质瘤患者中,根据PET/FLAIR成像描绘了一组完整的肿瘤和感兴趣的参考体积(VOIs),并转移到相应的[18F]FETPET和CBF图。计算平均和最大肿瘤-脑比率(TBR)和标准化CBF(nCBF)。[18F]FETPET和CBF在确定胶质瘤MGMT启动子甲基化状态中的预测功效通过全肿瘤分析和立体定向活检来评估。使用从多个立体定向活检获得的组织学标本分析PET/MR参数与MGMT启动子甲基化之间的相关性。
结果:基于对整个肿瘤体积和活检部位的分析,TBRmean,TBRmax,nCBFmean,和nCBFmax在有和没有MGMT启动子甲基化的胶质瘤之间没有统计学意义(均p>0.05)。此外,立体定向活检显示TBRmean,TBRmax,nCBFmean,nCBFmax与MGMT启动子甲基化无相关性(r=-0.117,p=0.579;r=-0.161,p=0.443;r=-0.271,p=0.191;r=-0.300,p=0.145)。
结论:MGMT启动子甲基化状态对胶质瘤中ASL的[18F]FET摄取和CBF无影响。立体定向活检证实了这一点,并进一步揭示了[18F]FETPET摄取和CBF与MGMT启动子甲基化的百分比没有相关性。
结论:•基于整个肿瘤VOI评估,MGMT启动子甲基化状态对胶质瘤中ASL的[18F]FET摄取和CBF没有影响。•对于WHOIV级胶质母细胞瘤,基于混合PET/MR的[18F]FETPET和ASL参数无法预测MGMT启动子甲基化状态。•基于立体定向图像的组织学显示[18F]FETPET摄取和CBF与胶质瘤中MGMT启动子甲基化的状态和百分比没有相关性。
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