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Background: Oligodendroglioma is known for its relatively better prognosis and responsiveness to radiotherapy and chemotherapy. However, little is known about the evolution of genetic changes as oligodendroglioma progresses. Methods: In this study, we evaluated gene evolution invivo during tumor progression based on deep whole‐genome sequencing data (ctDNA). We analyzed longitudinal genomic data from six patients during tumor evolution, of which five patients developed distant recurrence. Results: Whole‐exome sequencing demonstrated that the rate of shared mutations between the primary and recurrent samples was relatively low. In two cases, even well‐known major driver mutations in CIC and FUBP1 that were detected in primary tumors were not detected in the relapse samples. Among these cases, two patients had a conversion from the IDH mutation in the originating state to the IDH1 wild state during the process of gene evolution under chemotherapy treatment, indicating that the cell phenotype and genetic characteristics of oligodendroglioma may change during tumor evolution. Two patients received long‐term temozolomide (TMZ) treatment before the operation, and we found that recurrence tumors harbored mutations in the PI3K/AKT and Sonic hedgehog (SHh) signaling pathways. Hypermutation occurred with mutations in MMR genes in one patient, contributing to the rapid progression of the tumor. Conclusion: Oligodendroglioma displayed great spatial and temporal heterogeneity during tumor evolution. The PI3K/AKT and SHh signaling pathways may play an important role in promoting treatment resistance and distant relapse during oligodendroglioma evolution. In addition, there was a tendency to increase the degree of tumor malignancy during evolution. Distant recurrence may be a later event duringoligodendroglioma progression. ClinicalTrials.gov, Identifier: NCT05512325. [ABSTRACT FROM AUTHOR]

Abstract Background Low‐grade gliomas (LGGs) are primary diffuse slow‐growing brain tumors derived from glial cells. The management of these tumors is dependent on their location, which often harbors eloquent areas. We retrospectively recorded the location of diffuse gliomas to identify whether specific differences exist between the histological types. Methods We analyzed 102 patients with previous histological diagnosis of WHO‐II astrocytomas (62) and WHO‐II oligodendrogliomas (40) according to WHO‐2016 classification. MRI sequences (T2‐FLAIR) were used for tumor volume segmentation and to create a frequency map of their locations within the Montreal Neurological Institute (MNI) space. The Brain‐Grid (BG) system (standardized radiological tool of intersected lines according to anatomical landmarks) was created and merged with a tractography atlas for infiltration analysis. Results Astrocytomas frequently infiltrated association and projection white matter pathways within fronto‐temporo‐insular regions on the left side. Oligodendrogliomas infiltrated larger white matter networks (association‐commissural‐projection) of the frontal lobe bilaterally. A critical number of infiltrated BG voxels (7 for astrocytomas, 10 for oligodendrogliomas) significantly predicted shorter overall survival (OS) in both groups. Bilateral tumor extension in astrocytomas and preoperative tumor volume in oligodendrogliomas were independent prognostic factors for shorter OS. Conclusions Astrocytomas and oligodendrogliomas differ in preferential location, and this has an impact on the type and the extent of white matter involvement. The number of BG voxels infiltrated reflected different tumor invasiveness and its impact on OS in both groups. All this new information may be valuable in neurosurgical oncology to classify and plan treatment for patients with diffuse gliomas.

Background: Although aberrant expression of N6‐methyladenine (m6A) methylation‐related genes contribute to tumorigenesis in many solid tumors, the prognostic value of the m6A‐related genes and their correlation with clinicopathological features in gliomas need advanced study. Methods: The clinical and sequencing data of 288 patients with glioma were extracted from Chinese Glioma Genome Atlas database. By univariate and multivariable Cox regression analysis, the m6A‐related prognostic genes were identified, and their correlation with clinicopathological features was further analysis. A nomogram was constructed by R software and the performance of it was assessed by calibration and time‐dependent receiver operating characteristic curve. Results: Nine m6A‐related genes were identified as independent prognostic factors, which were mostly enriched in RNA splicing, regulation of immune response and vesicle‐mediated transport. By expression value and regression coefficient of these genes, we constructed risk score of each patient, which was highly associated with clinicopathological features. Kaplan–Meier curve showed that the prognosis of patients with high‐risk scores was significantly worse than that with low‐risk scores (HR = 4.30, 95% CI = 3.16–5.85, p < 0.0001). A nomogram was constructed based on the nine m6A‐related genes signature and clinicopathological features with well‐fitted calibration curves (c‐index = 0.82), showing high specificity and sensitivity (area under the curve for 1‐, 3‐, and 5‐years survival probability = 0.874, 0.918, and 0.934). Conclusions: A nine m6A‐related genes signature was identified in gliomas. The m6A‐related risk score is a novel prognostic factor for patients with glioma, and is associated with clinicopathological features. Moreover, the nomogram based on the nine m6A‐related genes signature and clinicopathological features had good efficacy in predicting the survival probability. [ABSTRACT FROM AUTHOR]

Background: The prognosis of lower‐grade glioma (LGG) differs from that of other grades gliomas. Although lots of studies on the prognostic biomarkers of LGG have been reported, few have significant clinical impact. Alternative splicing (AS) events can affect cell function by splicing precursor mRNA. Therefore, a prognostic model for LGG based on AS events are important to establish. Methods: RNA sequencing, clinical, and AS event data of 510 LGG patients from the TCGA database were downloaded. Univariate Cox regression analysis was used to screen out prognostic‐related AS events and LASSO regression and multivariate Cox regression were used to establish prognostic risk scores for patients in the training set (n = 340). After validation, a nomogram model was established based on the AS signature and clinical information, which was able to predict 1‐, 3‐, and 5‐year survival rates. Finally, considering the regulatory effect of splicing factors (SFs) on AS events, an AS‐SF regulatory network was analyzed. Results: The most common AS event was exon skipping and the least was mutually exclusive exons. All the seven AS events were related to the prognosis of LGG patients, regardless of whether they were separated or considered as a whole event (integrated AS event), and the integrated AS event had the most significant correlation. After further inclusion of clinical indicators, eight factors were screened out: age, new event, KPS, WHO grade, treatment, integrated AS signature, IDH1 and TP53 mutation status, and a nomogram model was established. The study also constructed an AS‐SF regulatory network. Conclusion: The AS events and clinical factors that can predict the prognosis of LGG patients were screened, and a prognostic prediction model was established. The results of this study can play an important role in clinical work to better evaluate the prognosis of patients and impact treatment options. [ABSTRACT FROM AUTHOR]

Background: Gliomas evade current therapies through primary and acquired resistance and the effect of temozolomide is mainly restricted to methylguanin‐O6-methyltransferase promoter (MGMT) promoter hypermethylated tumors. Further resistance markers are largely unknown and would help for better stratification. Methods: Clinical data and methylation profiles from the NOA‐08 (104, elderly glioblastoma) and the EORTC 26101 (297, glioblastoma) studies and 398 patients with glioblastoma from the Heidelberg Neuro‐Oncology center have been analyzed focused on the predictive effect of DNA damage response (DDR) gene methylation. Candidate genes were validated in vitro. Results: Twenty‐eight glioblastoma 5'‐cytosine‐phosphat‐guanine‐3' (CpGs) from 17 DDR genes negatively correlated with expression and were used together with telomerase reverse transcriptase (TERT) promoter mutations in further analysis. CpG methylation of DDR genes shows highest association with the mesenchymal (MES) and receptor tyrosine kinase (RTK) II glioblastoma subgroup. MES tumors have lower tumor purity compared to RTK I and II subgroup tumors. CpG hypomethylation of DDR genes TP73 and PRPF19 correlated with worse patient survival in particular in MGMT promoter unmethylated tumors. TERT promoter mutation is most frequent in RTK I and II subtypes and associated with worse survival. Primary glioma cells show methylation patterns that resemble RTK I and II glioblastoma and long term established glioma cell lines do not match with glioblastoma subtypes. Silencing of selected resistance genes PRPF19 and TERT increase sensitivity to temozolomide in vitro. Conclusion: Hypomethylation of DDR genes and TERT promoter mutations is associated with worse tumor prognosis, dependent on the methylation cluster and MGMT promoter methylation status in IDH wild‐type glioblastoma. [ABSTRACT FROM AUTHOR]

Background: Due to their rarity, the clinicopathological characteristics and prognostic factors of spinal cord gliomas are still unclear. Here, we aimed to clarify these issues in a cohort of 108 spinal cord astrocytomas. Methods: We characterized the clinicopathological characteristics, including 2016 World Health Organization (WHO) grade, age, sex, location, segment length, resection, pre‐ and postsurgery, Modified McCormick Scale (MMS), radio‐ and chemotherapy, and Ki‐67 and H3 K27M mutations, in 108 spinal cord astrocytomas through heatmaps. The Cox regression analysis and Kaplan‐Meier curves were used to study the prognostic value of these clinicopathological features. Results: There are a total 38 H3 K27M‐mutant tumors, including 31 cases with histological grade II/III tumors. The age of low‐grade astrocytoma patients (WHO grade I/II, n = 54) was significantly younger (27.0 vs 35.5 years, P =.001) than those with high‐grade tumors (WHO grade III/IV, n = 54). All patients underwent surgical resection with neurophysiological monitoring, and the surgery did not result in significant changes in MMS. The presurgery MMS was associated with overall survival in the high‐grade subgroup (P =.008) but not in the low‐grade subgroup (P =.312). While, the high content of resection improved the survival of only patients with low‐grade astrocytomas (P =.016) but not those with high‐grade astrocytomas (P =.475). Both the low‐grade and high‐grade astrocytomas had no obvious benefit from neither adjuvant chemotherapy nor radiotherapy (all P >.05). Conclusions: We characterized the clinicopathological characteristics and their prognostic values in 108 spinal cord astrocytomas, which could help with evidence‐based management of spinal cord astrocytomas. [ABSTRACT FROM AUTHOR]

Background: Epigenetic inactivation of O6‐methylguanine‐methyltransferase (MGMT) gene by methylation of its promoter is predictive of Temozolomid (TMZ) response in glioblastoma (GBM). MGMT is located on chromosome 10q26 and the loss of chromosome 10q is observed in 70% of GBMs. In this study, we assessed the hypothesis that the dual inactivation of MGMT, by hypermethylation of MGMT promoter and by loss the long arm of chromosome 10 (10q), may confer greater sensitivity to TMZ. Methods: A total of 149 tumor samples from patients diagnosed with GBM based on the WHO 2016 classification were included in this retrospective study between November 2016 and December 2018. Methylation status of MGMT promoter was evaluated by pyrosequencing and status of chromosome 10q was assessed by array comparative genomic hybridization. Results: Glioblastoma patients with chromosome 10q loss associated with hypermethylation of MGMT promoter had significantly longer overall survival (OS) (P =.0024) and progression‐free survival (PFS) (P =.031). Indeed, median OS of patients with dual inactivation of MGMT was 21.5 months compared to 12 months and 8.1 months for groups with single MGMT inactivation by hypermethylation and by 10q loss, respectively. The group with no MGMT inactivation had 9.5 months OS. Moreover, all long‐term survivors with persistent response to TMZ treatment (OS ≥ 30 months) displayed dual inactivation of MGMT. Conclusions: Our data suggest that the molecular subgroup characterized by the dual inactivation of MGMT receives greater benefit from TMZ treatment. The results of our study may be of immediate clinical interest since chromosome 10q status and methylation of MGMT promoter are commonly determined in routine practice. [ABSTRACT FROM AUTHOR]

Background: Low‐grade gliomas (LGGs) are primary diffuse slow‐growing brain tumors derived from glial cells. The management of these tumors is dependent on their location, which often harbors eloquent areas. We retrospectively recorded the location of diffuse gliomas to identify whether specific differences exist between the histological types. Methods: We analyzed 102 patients with previous histological diagnosis of WHO‐II astrocytomas (62) and WHO‐II oligodendrogliomas (40) according to WHO‐2016 classification. MRI sequences (T2‐FLAIR) were used for tumor volume segmentation and to create a frequency map of their locations within the Montreal Neurological Institute (MNI) space. The Brain‐Grid (BG) system (standardized radiological tool of intersected lines according to anatomical landmarks) was created and merged with a tractography atlas for infiltration analysis. Results: Astrocytomas frequently infiltrated association and projection white matter pathways within fronto‐temporo‐insular regions on the left side. Oligodendrogliomas infiltrated larger white matter networks (association‐commissural‐projection) of the frontal lobe bilaterally. A critical number of infiltrated BG voxels (7 for astrocytomas, 10 for oligodendrogliomas) significantly predicted shorter overall survival (OS) in both groups. Bilateral tumor extension in astrocytomas and preoperative tumor volume in oligodendrogliomas were independent prognostic factors for shorter OS. Conclusions: Astrocytomas and oligodendrogliomas differ in preferential location, and this has an impact on the type and the extent of white matter involvement. The number of BG voxels infiltrated reflected different tumor invasiveness and its impact on OS in both groups. All this new information may be valuable in neurosurgical oncology to classify and plan treatment for patients with diffuse gliomas. [ABSTRACT FROM AUTHOR]

Introduction: Bevacizumab has demonstrated activity in glioblastoma (GBM), but the true benefits and optimal dose‐schedule are debated. A lower dose‐schedule than standard‐dose bevacizumab (10 mg/kg 2‐weekly) might offer similar benefits with lower costs. At our Institution, patients are randomly assigned at time of primary diagnosis to Neuro‐Oncologists, who have varying practices in terms of bevacizumab dose‐schedule upon progression. Methods: In a retrospective analysis we examined overall survival (OS), measured from first administered bevacizumab dose until death, according to dose‐schedule. Patients with de novo WHO Grade IV GBM who received standard‐ or reduced‐dose (5 mg/kg 2‐weekly) bevacizumab were included. MGMT methylation status and time from diagnosis to bevacizumab start were examined as prognostic variables. Clinical benefit and a comparative cost analysis were assessed. Results: In total, 1127 bevacizumab doses were administered to 118 patients [Median: 7, Range: 1‐44]. Median OS (mOS) was 5.8 months. 69 (59%) patients received standard‐dose bevacizumab (mOS: 5.97 months) and 49 patients received reduced‐dose (mOS: 5.7 months). No statistically significant difference in OS between dosing schedule was seen (HR: 1.11, P‐value:.584). Patients with MGMT methylated tumors (43%) had improved OS compared to those with unmethylated tumors; 7.03 vs 4.97 months (HR: 0.61, P‐value:.027). If all patients were treated with reduced‐dose bevacizumab, an estimated €2.4M cost reduction would be observed. Conclusions: In this retrospective study, reduced‐dose bevacizumab schedule resulted in similar OS to standard‐dose bevacizumab monotherapy with substantial cost savings. MGMT methylation appears to convey a survival benefit in the setting of bevacizumab treatment for progressive GBM. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) requires radiotherapy (RT) as its definitive management. However, GBM still has a high local recurrence rate even after RT. Cancer stem‐like cells (CSCs) might enable GBM to evade irradiation damage and cause therapeutic failure. The optimal RT plan should achieve a planning target volume (PTV) coverage of more than 95% but cannot always meet the requirements. Here, we demonstrate that irradiation with different tumor coverage rates to different brain areas has similar effects on GBM. To retrospectively analyze the relationship between PTV coverage and the survival rate in 26 malignant glioblastoma patients, we established primary cell lines from patient‐derived malignant glioblastoma cells with the PTV95 (PTV coverage of more than 95%) program (GBM‐MG1 cells) and the Non‐PTV95 (poor PTV coverage of less than 95%) program (GBM‐MG2 cells). The clinical results of PTV95 and Non‐PTV95 showed no difference in the overall survival (OS) rate (P =.390) between the two different levels of PTV coverage. GBM‐MG1 (PTV95 program) cells exhibited higher radioresistance than GBM‐MG2 (Non‐PTV95 program) cells. CD44 promotes radioresistance, CSC properties, angiogenesis and cell proliferation in GBM‐MG1 (PTV95 program) cells. GBM patients receiving RT with the PTV95 program exhibited higher radioresistance, CSC properties, angiogenesis and cell proliferation than GBM patients receiving RT with the Non‐PTV95 program. Moreover, CD44 plays a crucial role in these properties of GBM patients with the PTV95 program. [ABSTRACT FROM AUTHOR]

Purpose: The majority of patients with high‐risk lower grade gliomas (LGG) are treated with single‐agent temozolomide (TMZ) and radiotherapy despite three randomized trials showing a striking overall survival benefit with adjuvant procarbazine, lomustine, and vincristine (PCV) chemotherapy and radiotherapy. This article aims to evaluate the evidence and rationale for the widespread use of TMZ instead of PCV for high‐risk LGG. Methods and Materials: We conducted a literature search utilizing PubMed for articles investigating the combination of radiotherapy and chemotherapy for high‐risk LGG and analyzed the results of these studies. Results: For patients with IDH mutant 1p/19q codeleted LGG tumors, there is limited evidence to support the use of TMZ. In medically fit patients with codeleted disease, existing data demonstrate a large survival benefit for PCV as compared to adjuvant radiation therapy alone. For patients with non‐1p/19q codeleted LGG, early data from the CATNON study supports inclusion of adjuvant TMZ for 12 months. Subset analyses of the RTOG 9402 and EORTC 26951 do not demonstrate a survival benefit for adjuvant PCV for non‐1p/19q codeleted gliomas, however secondary analyses of RTOG 9802 and RTOG 9402 demonstrated survival benefit in any IDH mutant lower grade gliomas, regardless of 1p/19q codeletion status. Conclusions: At present, we conclude that current evidence does not support the widespread use of TMZ over PCV for all patients with high‐risk LGG, and we instead recommend tailoring chemotherapy recommendation based on IDH status, favoring adjuvant PCV for patients with any IDH mutant tumors, both those that harbor 1p/19q codeletion and those non‐1p/19q codeleted. Given the critical role radiation plays in the treatment of LGG, radiation oncologists should be actively involved in discussions regarding chemotherapy choice in order to optimize treatment for their patients. [ABSTRACT FROM AUTHOR]

With short survival time, glioblastoma (GBM) is the most malignant tumor in the central nervous system. Recently, epigenetic enzymes play essential roles in the regulation of tumorigenesis and cancer development of GBM. However, little is known about MYST1/KAT8/MOF, a histone acetylation enzyme, in GBM. The present study shows that MYST1 promotes GBM progression through activating epidermal growth factor receptor (EGFR) signaling. MYST1 expression was increased in GBM and was negatively correlated with prognosis in patients with glioma and GBM. Knockdown of MYST1 reduced cell proliferation and BrdU incorporation in LN229, U87, and A172 GBM cells. Besides, MYST1 downregulation also induced cell cycle arrest at G2M phase, as well as the reduced expression of CDK1, Cyclin A, Cyclin B1, and increased expression of p21CIP1/Waf1. Meanwhile, Self‐renewal capability in vitro and tumorigenecity in vivo were also impaired after MYST1 knockdown. Importantly, MYST1 expression was lowly expressed in mesenchymal subtype of GBM and was positively correlated with EGFR expression in a cohort from The Cancer Genome Atlas. Western blot subsequently confirmed that phosphorylation and activation of p‐Try1068 of EGFR, p‐Ser473 of AKT and p‐Thr202/Tyr204 of Erk1/2 were also decreased by MYST1 knockdown. Consistent with the results above, overexpression of MYST1 promoted GBM growth and activated EGFR signaling in vitro and in vivo. In addition, erlotinib, a US Food and Drug Administration approved cancer drug which targets EGFR, was able to rescue MYST1‐promoted cell proliferation and EGFR signaling pathway. Furthermore, the transcription of EGF, an EFGR ligand, was shown to be positively regulated by MYST1 possibly via H4K16 acetylation. Our findings elucidate MYST1 as a tumor promoter in GBM and an EGFR activator, and may be a potential drug target for GBM treatment. [ABSTRACT FROM AUTHOR]

DNA polymerase kappa (POLK), one of the specialized Y family DNA polymerases, functions in translesion synthesis and is suggested to be related with cancers. Single nucleotide polymorphisms (SNPs) in specialized DNA polymerases have been demonstrated to be associated with cancer risk. To evaluate the association of two common POLK variants (rs3213801 C>T and rs5744533 C>T) with glioma, we conducted a case‐control study and genotyped these two POLK variants in 605 patients and 1300 healthy controls. The association analysis revealed no significant correlations were observed between these two POLK SNPs and glioma risk. However, the POLK rs3213801 CT genotype was found to be higher in older glioma patients (≥40) than in younger patients (P = .026). Compared with patients harboring the CC genotype, the frequencies of POLK rs5744533 CT and CT+TT genotypes were increased in patients with lower World Health Organization (WHO) grade glioma (P = .028, 0.044, respectively). According to Kaplan‐Meier analysis and log‐rank tests, POLK SNPs were not correlated with either the overall survival or progression‐free survival. Nevertheless, multivariate analysis revealed that the age (≥40) could increase the risk of death in glioma patients (P < .05), while gross‐total resection and temozolomide treatment were found to play protective roles in glioma prognosis (P < .001, respectively). Overall, our results indicated that POLK variants rs3213801 and rs5744533 are not associated with glioma risk and prognosis. However, these polymorphisms are likely to be associated with certain glioma characteristics, such as age and WHO grade. The age, surgery types, and chemotherapy could be independent prognostic factors in glioma. More studies are required to confirm our findings. [ABSTRACT FROM AUTHOR]

CD204 is a specific marker of tumor‐associated macrophages (TAMs) in glioma. However, the expression levels of CD204 and its involvement in glioma are not fully understood. In this large‐scale study, we assessed the expression and function of CD204 in whole‐grade glioma molecularly and clinically. In total, 1323 glioma samples, including 301 microarray data and 325 RNA‐seq data from the Chinese Glioma Genome Atlas (CGGA) dataset and 697 RNA‐seq data from The Cancer Genome Atlas (TCGA) dataset, were utilized. The statistical analysis and graphical work were mainly performed using the R software. Univariate and multivariate Cox analysis demonstrated that CD204 was an independent prognosticator in glioma patients. CD204 expression was positively correlated with the grade of malignancy. CD204 was consistently upregulated in wild‐type isocitrate dehydrogenase glioma and highly expressed in mesenchymal glioblastoma. Gene ontology of CD204‐related genes showed that CD204 was most enriched in inflammatory response and immune response. It was associated with the stromal and immune populations, especially the monocytic lineage, fibroblasts, and T cells. Circos plots revealed that CD204 was closely associated with many immune checkpoint regulators, especially TIM‐3. CD204 expression is consistent with the malignant phenotype of glioma and independently predicts poor outcomes in glioma patients. Additionally, CD204+ TAMs, collaborating with other checkpoint members, may contribute to the dysfunction of T cells. These findings suggest that CD204 may be a promising target for glioma immunotherapy. [ABSTRACT FROM AUTHOR]

Purpose: Isocitrate dehydrogenase 1 (IDH1) has been proven as a prognostic and predictive marker in glioblastoma (GBM) patients. The purpose was to preoperatively predict IDH mutation status in GBM using multiregional radiomics features from multiparametric magnetic resonance imaging (MRI). Methods: In this retrospective multicenter study, 225 patients were included. A total of 1614 multiregional features were extracted from enhancement area, non‐enhancement area, necrosis, edema, tumor core, and whole tumor in multiparametric MRI. Three multiregional radiomics models were built from tumor core, whole tumor, and all regions using an all‐relevant feature selection and a random forest classification for predicting IDH1. Four single‐region models and a model combining all‐region features with clinical factors (age, sex, and Karnofsky performance status) were also built. All models were built from a training cohort (118 patients) and tested on an independent validation cohort (107 patients). Results: Among the four single‐region radiomics models, the edema model achieved the best accuracy of 96% and the best F1‐score of 0.75 while the non‐enhancement model achieved the best area under the receiver operating characteristic curve (AUC) of 0.88 in the validation cohort. The overall performance of the tumor‐core model (accuracy 0.96, AUC 0.86 and F1‐score 0.75) and the whole‐tumor model (accuracy 0.96, AUC 0.88 and F1‐score 0.75) was slightly better than the single‐regional models. The 8‐feature all‐region radiomics model achieved an improved overall performance of an accuracy 96%, an AUC 0.90, and an F1‐score 0.78. Among all models, the model combining all‐region imaging features with age achieved the best performance of an accuracy 97%, an AUC 0.96, and an F1‐score 0.84. Conclusions: The radiomics model built with multiregional features from multiparametric MRI has the potential to preoperatively detect the IDH1 mutation status in GBM patients. The multiregional model built with all‐region features performed better than the single‐region models, while combining age with all‐region features achieved the best performance. The radiomics model built with multiregional features from multiparametric magnetic resonance imaging (MRI) has the potential to preoperatively detect the isocitrate dehydrogenase 1 (IDH1) mutation status in glioblastoma (GBM) patients. The multiregional models built from all tumor subregions performed better than the single‐region models, while combining age with multiregional features achieved the best performance. [ABSTRACT FROM AUTHOR]

Background: The update of 2018 NCCN guidelines (central nervous system cancers) recommended the risk classification of postoperative patients diagnosed as adult low‐grade (WHO grade II) infiltrative supratentorial astrocytoma/oligodendroglioma (ALISA/O) should take tumor size into consideration. Moreover, the guidelines removed postoperative radiotherapy (PORT) for low risk patients. Our study aimed to explore the specific tumor size to divide postoperative patients into relatively low‐ or high risk subgroups and the effect of PORT for ALISA/O patients. Methods: We conducted a retrospective study choosing 1277 postoperative ALISA/O patients from the Surveillance, Epidemiology, and End Results database. The X‐tile analysis provided the optimal cutoff point based on tumor size. The differences between surgery alone and surgery +RT groups were balanced by propensity score‐matched analysis. The multivariable analysis and the nomogram evaluated multiple prognostic factors based on cancer‐specific survival (CSS) and overall survival (OS). Results: X‐tile plots defined 59 mm (P < 0.001) as the optimal cutoff tumor size value in terms of CSS, which was verified in multivariate analysis (P < 0.001). The Kaplan‐Meier analysis showed that the surgery alone had higher CSS and OS than surgery +RT, while the low risk group had no statistical significance after propensity score match. Multivariable analysis showed that surgery +RT was independently associated with diminished OS and CSS for high risk group, which had no statistical significance for low‐risk group. Conclusions: Our study suggested that tumor size of 59 mm was an optimal cutoff point to divide postoperative patients into relatively low‐ or high risk subgroups. PORT may not benefit patients, while the effects of PORT for low risk patients need further research. We evaluated two changes of 2018 NCCN guideline (CNS cancer), comparing with its in 2017, for patients with adult low‐grade (WHO grade II) infiltrative supratentorial astrocytoma/oligodendroglioma (ALISA/O). We concluded that tumor size of 59mm was an optimal cutoff point to divide postoperative patients into relatively low‐ or high risk subgroups and that postoperative radiotherapy (PORT) may not benefit patients. [ABSTRACT FROM AUTHOR]