Imaging and molecular pathological analysis of elderly gliomas

doi:10.19854/j.cnki.1008-2425.2022.02.0002

Abstract

Abstract: Objective To investigate the clinical imaging and molecular pathological features of elderly patients with brain tumor. Methods A retrospective analysis of imaging,promoter methylation of O6-methylguanine-DNA-methyltransferase (MGMT) and IDH1R132H in 43 elderly patients with brain tumor with complete follow-up data from May 2016 to May 2020 in the First Affiliated Hospital of University of Science and Technology of China And 1p/19q co-deletion and prognosis of patients. Results Among the 43 elderly patients,32 cases were high-grade glioma and 11 cases were low-grade glioma.The MRI manifestations of high-grade gliomas were as follows:slightly long T1 mixed with T2 signals,with unclear boundaries,obvious uneven enhancement on enhanced scan,accompanied by cystic changes of different sizes,and patchy edema around the lesions.The mean survival time of elderly gliomas was 14.12± 9.09 months,the mean survival time of elderly high-grade gliomas was 9.69± 3.94 months,and the mean survival time of elderly low-grade gliomas was 27.00± 7.31 months.There was a significant difference in survival between high-grade and low-grade elderlygliomas (P<0.0001).The demethylation degree of MGMT promoter in elderly gliomas was 27.90%,and the positive rate of MGMT methylation promoter in high-grade tumors was only 15.63%.The IDH1R132H mutation rate was only 34.88%,among which,the IDH1R132H mutation rate in high-grade glioma was only 18.75%.Combined deletion of 1p/19q accounted for 20.93%,of which only 12.50% were high-grade gliomas.Moreover,these molecular pathological markers were statistically significant in different grades of geriatric gliomas. Conclusion The Results of this single-center study showedthatelderly gliomas are mainly high-grade gliomas,brain gliomas have obvious imaging specificity,MGMT promoter methylation,IDH1R132H mutation and 1p/19q combined deletion have statistical differences in different grades of elderly gliomas.

Key words: Elderly, Glioma, Magnetic resonance imaging, Molecular pathology, Clinical prognosis analysis

摘要： 目的探讨老年脑肿瘤患者的临床影像学资料和分子病理学特征。方法回顾性分析中国科学技术大学附属第一医院2016年5月到2020年5月的43例具有完整随访资料的老年脑肿瘤患者的影像学和O6-甲基鸟嘌呤-DNA-甲基转移酶(MGMT)启动子甲基化、异柠檬酸脱氢酶1R132H位点突变(IDH1R132H突变)和1p/19q联合缺失等分子病理学指标与患者预后的关系。结果 43例老年患者中,高级别胶质瘤32例,低级别胶质瘤11例;老年高级别胶质瘤磁共振表现为:斑片状稍长T1混杂T2信号,边界不清,增扫描呈现明显的不均匀强化表现,多伴有大小不等的囊性变,病灶周围可见片状水肿。老年脑胶质瘤的平均生存期为14.12± 9.09个月,其中老年高级别胶质瘤平均生存期为9.69±3.94个月,老年低级别胶质瘤平均生存期为27.00±7.31个月。高级别与低级别胶质瘤具有明显的生存差异(P＜0.0001);老年胶质瘤中MGMT启动子去甲基化程度为27.90%,其中高级别肿瘤MGMT启动子甲基化阳性率仅为15.63%;IDH1R132H突变率仅为34.88%,其中,高级别胶质瘤中IDH1R132H突变率仅为18.75%;1p/19q联合缺失占20.93%,其中高级别脑胶质瘤中仅占12.50%。而且,这些分子病理标志物在老年胶质瘤中不同级别中具有明显的统计学差异。结论本单中心研究结果表明:老年胶质瘤以高级别为主,脑胶质瘤具有明显的影像学特征,MGMT启动子甲基化、IDH1R132H突变和1p/19q联合缺失在不同级别老年胶质瘤中具有统计学差异。

关键词: 老年, 胶质瘤, 磁共振成像, 分子病理学, 临床预后分析

CLC Number:

R739.41

Ye Chengkun, Xu Ben, Niu Chaoshi. Imaging and molecular pathological analysis of elderly gliomas[J]. Chinese Journal of Stereotactic and Functional Neurosurgery, 2022, 35(2): 71-74.

叶成坤, 徐奔, 牛朝诗. 老年胶质瘤的影像学及分子病理学分析[J]. 立体定向和功能性神经外科杂志, 2022, 35(2): 71-74.

References

[1] Uddin MS,Mamun AA,Alghamdi BS,et al.Epigenetics of glioblastoma multiforme: From molecular mechanisms to therapeutic approaches[J].Semin Cancer Biol,(2020) 345~353.
[2] Ostrom QT,Gittleman H,Xu J,et al.CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2009-2013[J].Neuro Oncol,2016,18(suppl5):v1~v75.
[3] Pei L,Jones KA,Shboul ZA,et al.Deep Neural Network Analysis of Pathology Images With Integrated Molecular Data for Enhanced Glioma Classification and Grading[J].Front Oncol,2021,11:668694.
[4] Kros JM,Huizer K,Hernandez-Lain A,et al.Evidence-Based Diagnostic Algorithm for Glioma: Analysis of the Results of Pathology Panel Review and Molecular Parameters of EORTC 26951 and 26882 Trials[J].J Clin Oncol,2015,33(17):1943~1950
[5] Di Stefano AL,Enciso-Mora V,Marie Y,Desestret V,Labussiere M,Boisselier B,et al.Association between glioma susceptibility loci and tumour pathology defines specific molecular etiologies[J].Neuro Oncol,2013,15(5):542~547.
[6] 中国医师协会脑胶质瘤专委会老年胶质瘤学组.中国老年胶质瘤患者术前评估专家共识(2019年)[J].协和医学杂志,2019,10(4):326~335.
[7] Miller JJ,Cahill DP.MGMT promoter methylation and hypermutant recurrence in IDH mutant lower-grade glioma[J].Neuro Oncol,2020,22(11):1553~1554.
[8] Moitra P,Chatterjee A,Kota PK,et al.Temozolomide-induced myelotoxicity and single nucleotide polymorphisms in the MGMT gene in patients with adult diffuse glioma:a single-institutional pharmacogenetic study[J].J Neurooncol,2022,156(3):625~634.
[9] Picca A,Berzero G,Di Stefano AL,et al.The clinical use of IDH1 and IDH2 mutations in gliomas[J].Expert Rev Mol Diagn,2018,18(12):1041~1051.
[10] Bunse L,Schumacher T,Sahm F,et al.Proximity ligation assay evaluates IDH1R132H presentation in gliomas[J].J Clin Invest,2015,125(2):593~606.
[11] Lin W,Qiu X,Sun P,et al.Association of IDH mutation and 1p19q co-deletion with tumor immune microenvironment in lower-grade glioma[J].Mol TherOncolytics,2021;21:288~302.
[12] Laghari AA,Khalid MU,Qadeer N,et al.Prognostic value of 1p/19q chromosomal codeletion in patients with oligodendroglioma[J].J Pak Med Assoc.2019;69(1):132~134.
[13] Iwadate Y,Matsutani T,Hara A,et al.Eighty percent survival rate at 15 years for 1p/19q co-deleted oligodendroglioma treated with upfront chemotherapy irrespective of tumor grade[J].J Neurooncol.2019;141(1):205~211.
[14] Frazer B,Kearney H,Cryan J,et al.Absence of 1p/19q codeletion in oligodendroglioma-like areas of pilocytic astrocytomas[J].Clin Neuropathol.2018;37(4):182~185.
[15] Cahill DP,Louis DN,Cairncross JG.Molecular background of oligodendroglioma: 1p/19q,IDH,TERT,CIC and FUBP1[J].CNS Oncol.2015;4(5):287~294.