Paraganglioma (PGL) is a rare non-epithelial neuroendocrine neoplasm that can occur in multiple locations within the body. Most PGLs grow slowly and are benign, but some can metastasize to distant sites. Reports of brain metastatic PGL are relatively rare, particularly those with comprehensive case histories. A 52-year-old Asian female patient presented with a headache that had persisted for over a month. In 2018, the patient underwent surgical resection of a hepatic mass, with postoperative pathology confirming the diagnosis of primary hepatic PGL. In 2021, she received neurosurgical treatment, and histopathological and molecular analysis of the excised brain tissue revealed mutations in the CD274, KMT2B, and SDHB genes within the tumor cells. The final integrated pathological assessment confirmed a diagnosis of brain metastatic PGL, classified as a pseudohypoxia-driven subtype. Following temozolomide chemotherapy, no evidence of brain recurrence was observed as of June 2024. However, the patient developed multiple enlarged lymph nodes, with suspicious lesions detected in the thoracic, abdominal, pyramidal, and rib regions. Brain metastatic PGL is relatively rare and presents significant challenges in clinical practice, requiring careful consideration in diagnosis and treatment. Here, we present a case of PGL originating in the liver and metastasizing to the brain, reporting its clinical, radiological, histopathological, and molecular pathological features and the treatment process. A review of the relevant literature is also included to raise clinical awareness of this condition and provide new insights for diagnosis and treatment.

Understanding the complex cellular and spatial organization of glioblastoma (GBM) and its microenvironment is crucial for improving diagnosis and treatment. Here we integrated 121 spatial transcriptomics, single-cell RNA sequencing, single-cell assay for transposase-accessible chromatin using sequencing and patch sequencing profiles from 100 patients to characterize primary GBM tissue. We identified four malignant cellular communities that exhibited consistent patterns of cell-type compositions, gene expression and intercellular interactions across patients. We identified two subpopulations of mesenchymal-like (MES-like) tumor cells: MES-Hyp, colocalized with monocyte-derived brain macrophages in hypoxic regions; and MES-Ast, associated with endothelial cells, pericytes and vascular smooth muscle cells. We also predicted and experimentally verified cell subtypes and ligand-receptor pairs involved in intercellular communications in each cellular community. Furthermore, patch sequencing analysis revealed that synaptic connections with glioma cells were predominantly formed between neurons and oligodendrocyte-progenitor-like tumor cells. Overall, our study provides insights into the spatial organization and intercellular communication in GBM, offering potential therapeutic targets.

Cold atmospheric plasma (CAP) exhibits potent anti-tumor activity against glioblastoma in vitro, yet the in vivo therapeutic efficacy of CAP may be restricted by the limited direct penetration depth of CAP. In glioblastoma, effective drug delivery to tumor tissue is crucial to glioblastoma treatment. The complex tumor microenvironment (TME) of glioblastoma and the limited permeability of the blood-brain barrier (BBB) are major obstacles to drug delivery into tumor tissue. Through comprehensive in vitro and in vivo studies, we characterize a novel tripartite mechanism of CAP therapy that overcomes these limitations. Rather than the conventional penetration-limited mechanisms, the results reveal that CAP exerts its therapeutic effects via three distinct but synergistic pathways: BBB integrity modulation, exploitation of cerebrospinal fluid (CSF)-mediated ROS distribution to deep tumor regions, and tumor-endothelial paracrine signaling network activation. This multimodal action collectively overcomes glioblastoma TME barriers, establishing CAP as a systemic microenvironmental regulator rather than merely a local cytotoxic agent. These findings provide a transformative framework for clinical translation of CAP-based glioblastoma therapy.

Glioblastoma (GBM), one of the most aggressive brain tumors, has a 5-year survival rate of less than 5%. Current standard therapies, including surgery, radiotherapy, and temozolomide (TMZ) chemotherapy, are limited by drug resistance and the blood-brain barrier. Integrating expression quantitative trait loci (eQTL) and protein quantitative trait loci (pQTL) data has shown promise in uncovering disease mechanisms and therapeutic targets. This study combined eQTL and pQTL analyses to identify potential GBM-related genes and circulating plasma proteins for therapeutic exploration. Using transcriptomic data from The Cancer Genome Atlas (TCGA), we identified 2,528 differentially expressed genes, including GPX7 and CXCL10. eQTL-MR analysis identifies GBM-associated differentially expressed genes and constructs a protein-protein interaction (PPI) network.Integrating pQTL data from the deCODE database, pQTL-MR, and colocalization analyses validated the therapeutic potential of GPX7 and CXCL10.These findings provide new perspectives on GBM biology and suggest actionable targets for therapy. Despite limitations due to sample size and population-specific data, this study highlights GPX7 and CXCL10 as promising candidates for further investigation and lays the foundation for targeted GBM treatments.

Abstract Background In assessing the clinical utility and safety of 3.0 T intraoperative magnetic resonance imaging (iMRI) combined with multimodality functional MRI (fMRI) guidance in the resection of functional area gliomas, we conducted a study. Method Among 120 patients with newly diagnosed functional area gliomas who underwent surgical treatment, 60 were included in each group: the integrated group with iMRI and fMRI and the conventional navigation group. Between-group comparisons were made for the extent of resection (EOR), preoperative and postoperative activities of daily living based on the Karnofsky performance status, surgery duration, and postoperative intracranial infection rate. Results Compared to the conventional navigation group, the integrated navigation group with iMRI and fMRI exhibited significant improvements in tumor resection (complete resection rate: 85.0% vs. 60.0%, P = 0.006) and postoperative life self-care ability scores (Karnofsky score) (median ± interquartile range: 90 ± 25 vs. 80 ± 30, P = 0.013). Additionally, although the integrated navigation group with iMRI and fMRI required significantly longer surgeries than the conventional navigation group (mean ± standard deviation: 411.42 ± 126.4 min vs. 295.97 ± 96.48 min, P<0.0001), there was no significant between-group difference in the overall incidence of postoperative intracranial infection (16.7% vs. 18.3%, P = 0.624). Conclusion The combination of 3.0 T iMRI with multimodal fMRI guidance enables effective tumor resection with minimal neurological damage.

In this work, the effects of cold atmospheric-pressure plasma (CAP) on glioblastoma are evaluated comprehensively. After CAP treatment, U251 cell viability, migration, and invasion functions were inhibited, while an appropriate dose of CAP had no inhibitory effect on human brain glial cell line cells. Western blots indicated that expression of caspase-3 was upregulated with ki-67 expression downregulated. Moreover, mitochondrial membrane potential decreased, and energy metabolisms of U251 cells were influenced afterward. TUNEL assays and comet assays suggested the DNA damage of U251 cells after CAP treatment. Furthermore, as one of the DNA damage responses associated pathways, the AKT (AKT8 virus oncogene cellular homolog) signaling pathway was also indicated in the work. The findings raise great promise for clinical applications of CAP in glioblastoma treatments. Cold atmospheric-pressure plasma-induced apoptosis of glioblastoma cells selectively by damaging its cellular DNA and inhibiting phosphorylation of the AKT-mTOR signaling pathway.image

Glioma is the most common malignant tumor of the central nervous system, with EZH2 playing a crucial regulatory role. This study further explores the abnormal expression of EZH2 and its mechanisms in regulating glioma progression. Additionally, it was found that IHMT-337 can potentially be a therapeutic agent for glioma. The prognosis, expression, and localization of EZH2 were determined using bioinformatics, IHC staining, Western blot (WB) analysis, and immunofluorescence (IF) localization. The effects of EZH2 on cell function were assessed using CCK-8 assays, Transwell assays, and wound healing assays. Public databases and RT-qPCR were utilized to identify downstream targets. The mechanisms regulating these downstream targets were elucidated using MS-PCR and WB analysis. The efficacy of IHMT-337 was demonstrated through IC50 measurements, WB analysis, and RT-qPCR. The effects of IHMT-337 on glioma cells in vitro were evaluated using Transwell assays, EdU incorporation assays, and flow cytometry. The potential of IHMT-337 as a treatment for glioma was assessed using a blood–brain barrier (BBB) model and an orthotopic glioma model. Our research confirms significantly elevated EZH2 expression in gliomas, correlating with patient prognosis. EZH2 facilitates glioma proliferation, migration, and invasion alongside promoting SLC12A5 DNA methylation. By regulating SLC12A5 expression, EZH2 activates the WNK1-OSR1-NKCC1 pathway, enhancing its interaction with ERM to promote glioma migration. IHMT-337 targets EZH2 in vitro to inhibit WNK1 activation, thereby suppressing glioma cell migration. Additionally, it inhibits cell proliferation and arrests the cell cycle. IHMT-337 has the potential to cross the BBB and has successfully inhibited glioma progression in vivo. This study expands our understanding of the EZH2-SLC12A5 axis in gliomas, laying a new foundation for the clinical translation of IHMT-337 and offering new insights for precision glioma therapy.

This study aims to explore the inhibitory effects of combined metformin and simvastatin therapy on the malignant progression of glioma. The research specifically examines how the maturation of SREBP2 as a transcription factor affects the expression of GLUT1 and GLUT6 in glioma cells. Additionally, it investigates the impact of this combination therapy on the biological functions and energy metabolism of glioma cells. To assess the functions of GLUT1/6, sh-GLUT1/6 plasmids were employed. The study determined the half-maximal inhibitory concentrations (IC50) of metformin and simvastatin using the CCK-8 assay. Subsequently, the effects of these drugs on glioma metabolism, proliferation, and apoptosis were explored in vitro and in vivo, using drug concentrations significantly lower than their respective IC50 values. The impact of drug treatment on GLUT1/6 and SREBP2 expression levels was also evaluated. The study elucidated the significant impact of GLUT1/6 on glioma cell functions, resulting in decreased glucose uptake. Moreover, it unveiled the regulatory role of SREBP2 in GLUT1 and GLUT6 transcription, alongside revealing differential expression of SREBP2 precursor and mature forms within gliomas. Following combined drug therapy, GLUT1/6 expression decreased, while the precursor form of SREBP2 increased, and mature SREBP2 reduced. This dual-drug treatment effectively modulated glioma cell energy metabolism. Subsequent in vivo experiments affirmed the augmented anti-tumor efficacy of combined drug therapy. Specifically, the synergistic action of metformin and simvastatin reshaped glioma metabolism, curbed malignant proliferation, promoted apoptosis, and demonstrated superior anti-tumor effects both in vitro and in vivo compared to individual administration of metformin or simvastatin. Importantly, the combination therapy achieved these effects at lower doses, rendering it a safer treatment option.

Glioblastoma (GBM) presents significant challenges due to its invasive nature and genetic heterogeneity. In this study, we investigated the impact of Small VCP/P97-Interacting Protein (SVIP) on GBM progression. Our results revealed elevated expression of Insulin-like Growth Factor Binding Protein 2 (IGFBP-2) and STIP1 homology and U-box containing protein 1 (STUB1), coupled with reduced SVIP levels in GBM samples. Notably, high IGFBP-2 expression correlated with poor prognosis. Mechanistically, SVIP competitively inhibited STUB1, selectively binding to VCP/p97, thereby reducing PTEN degradation. This SVIP-mediated regulation exerted influence on the PTEN/PI3K/AKT/mTOR pathway, leading to the suppression of GBM progression. Co-localization experiments demonstrated that SVIP hindered PTEN ubiquitination and degradation by outcompeting STUB1 for VCP/p97 binding. Moreover, SVIP overexpression resulted in reduced activation of AKT/mTOR signaling and facilitated autophagy. In vivo experiments using a GBM xenograft model substantiated the tumor-suppressive effects of SVIP, evident by suppressed tumor growth, decreased IGFBP-2 expression, and improved survival rates. Collectively, our findings underscore the functional significance of SVIP in GBM progression. By inhibiting STUB1 and stabilizing PTEN, SVIP modulates the expression of IGFBP-2 and attenuates the activation of the PI3K/AKT/mTOR pathway, thereby emerging as a promising therapeutic target for GBM treatment.

e14059 Background: Meningioma is the most common primary neoplasm of the central nervous system (CNS) in adults. Genetic variants ( NF2, AKT1, TRAF7 etc.) are strongly related to the subtypes of meningioma. TERT promoter mutation or homozygous CDKN2A and/or CDKN2B deletion are independent evidence for diagnosing WHO grade 3 meningioma according to 5 th CNS WHO. Our study reclassifies meningiomas using a clinical and molecular real-world dataset. Methods: This study retrospectively analyzed the genomic alteration of 347 Chinese meningioma patients during 2019-2022. Next-generation sequencing (NGS) was performed to detect gene mutations in tumor samples. Results: TERT promoter mutation or CDKN2A/B deletion were identified in 11% (n = 39) of patients ( TERT 5.2%, CDKN2A 8.1%, CDKN2B 8.6%). Of these cases, histologic grade information was available for 26 patients, 14(53.8%) of whom were reclassified as WHO grade 3 meningiomas, including four histologic grade 1 and ten histologic grade 2. There is a male preponderance in reclassified patients (56.4% vs. 40.0%, p < 0.05), meanwhile the age showed no significant difference between them (average age: 54 vs 50, p = 0.11). The most frequently co-mutated gene was NF2. The proportion of TERT promoter mutation or CDKN2A/B deletion in NF2-mutant tumors was similar to NF2-wildtype tumors (10% vs. 11%, p > 0.05). Conclusions: In our study, 11% of Chinese adult meningioma patients found TERT promoter mutation or CDKN2A/B deletion and showed a male preponderance, among 53.8% of whom were reclassified as meningiomas WHO grade 3. Overall, these data advance the understanding of the significance of molecular profiling in the classification of meningioma patients according to the 5 th WHO CNS.

目的 探究脑胶质瘤微小核糖核酸microRNA-340(miR-340)与IDH1、P53、CD34、Ki-67表达的关系以及初步探索miR-340对胶质瘤细胞功能和葡萄糖转运蛋白1/6(glucose transporter 1/6,GLUT1/6)表达的影响.方法 采用实时荧光定量PCR(qRT-PCR)法检测脑胶质瘤组织标本及胶质瘤细胞系miR-340的表达水平;细胞功能试验检测miR-340对胶质瘤的影响;qRT-PCR、蛋白质免疫印迹检测转染miR-340对GLUT1/6表达的影响.结果 miR-340在正常脑组织中高表达,胶质瘤组织中低表达(P<0.001);miR-340 mimics可以抑制U87、U251细胞增殖、增加凋亡、减弱迁移侵袭.miR-340 mimics可以显著抑制胶质瘤细胞中GLUT1/6的表达(P<0.001).结论 胶质瘤miR-340水平降低,且与Ki-67表达呈明显负相关.miR-340通过降低胶质瘤中GLUT1/6表达从而影响胶质瘤葡萄糖转运以抑制增殖,降低恶性程度.

Understanding tumor heterogeneity and immune infiltrates within the tumor-immune microenvironment (TIME) is essential for the innovation of immunotherapies. Here, combining single-cell transcriptomics and chromatin accessibility sequencing, we profile the intratumor heterogeneity of malignant cells and immune properties of the TIME in primary central nervous system diffuse large B-cell lymphoma (PCNS DLBCL) patients. We demonstrate diverse malignant programs related to tumor-promoting pathways, cell cycle and B-cell immune response. By integrating data from independent systemic DLBCL and follicular lymphoma cohorts, we reveal a prosurvival program with aberrantly elevated RNA splicing activity that is uniquely associated with PCNS DLBCL. Moreover, a plasmablast-like program that recurs across PCNS/activated B-cell DLBCL predicts a worse prognosis. In addition, clonally expanded CD8 T cells in PCNS DLBCL undergo a transition from a pre-exhaustion-like state to exhaustion, and exhibit higher exhaustion signature scores than systemic DLBCL. Thus, our study sheds light on potential reasons for the poor prognosis of PCNS DLBCL patients, which will facilitate the development of targeted therapy.

Objective To assess the accuracy of wearable electrocardiogram(ECG)monitoring device for detecting arrhythmias(sinus rhythm,premature ventricular contraction,premature atrial contraction,and atrial fibrillation),and heart rate in a clinical setting.Methods A total of 321 volunteers(875 ECG records)participated in this study,including 146 males(531 ECG records)and 175 females(344 ECG records).A wearable ECG monitoring device was employed to record ECGs for detecting arrhythmias and heart rate.The detection results were compared with physicians'clinical diagnostic results based on 12-lead ECG machine(regraded as the gold standard for diagnosing arrhythmias and detecting heart rate).Accuracy and consistency evaluation of the two detection methods was conducted in all the subjects,including accuracy,sensitivity,specificity,F1 score,area under curve(AUC)of the receiver operating characteristic curve,Bland-Altman consistency analysis,mean absolute error,and correlogram.Results Regarding arrhythmia identification,wearable ECG monitoring device exhibits impressive performance metrics,with an AUC of 0.98,accuracy of 0.98,sensitivity of 0.96,specificity of 0.99,and an F1 score of 0.96.In terms of heart rate monitoring,a robust correlation between the wearable ECG monitoring equipment and the ECG machine is evident,with a substantial total correlation coefficient of 0.84(P＜0.01).Bland-Altman consistency analysis reveals that the two methods display a mean difference of-0.97 times per minute,a mean standard deviation of 8.02 times per minute,and a 95%confidence interval ranging from-16.69 to 14.75 within an acceptable level.Conclusion Wearable ECG monitoring device can accurately detect arrhythmias and heart rate.

Glioblastoma is the most common malignant tumor in the central nervous system. The general transcription factor IIE subunit beta (GTF2E2) is crucial for physiological and pathological functions, but its roles in the malignant biological function of glioma remain ambiguous. CCK-8, colony formation assays, TUNEL assays, cell migration assays, wound-healing assays, and xenograft model were established to investigate the biological functions of GTF2E2 both in vitro and in vivo. GTF2E2 was overexpressed in glioma and was associated with poor prognosis of glioma patients. Biological functions of GTF2E2 were investigated both in vitro and in vi0vo by multiple experiments. Moreover, we explored the possible mechanisms of GTF2E2. In our results, we demonstrated that GTF2E2 could be regulated by miR-340-5p directly or indirectly. CCND1 was transcriptionally affected by GTF2E2 and glioma progression was then regulated. Our data presented the overexpression of GTF2E2 in glioma and indicated the association between GTF2E2 and glioma prognosis. GTF2E2 was found to be regulated by miR-340-5p and thus affect downstream gene expressions and glioma progression. Our results indicate that GTF2E2 might be a potential target in the diagnosis and treatments of glioblastoma.

BACKGROUND:Calcifying pseudoneoplasm of the neuraxis (CAPNON) is indeed a rare central nervous system lesion that can occur in central nervous system (CNS). Due to its infrequency and limited literature reports, it is challenging to diagnose and manage CAPNON.CASE PRESENTATION:In this intriguing study, we embarked on a quest to uncover the story of a 16-year-old girl who experienced bothersome headaches. Through advanced imaging techniques like computed tomography (CT) and magnetic resonance imaging (MRI), we glimpsed a delicate calcified growth within the lateral ventricles' posterior horn. Motivated by our unwavering commitment to solving mysteries, we embarked on a surgical journey that not only freed the young patient from her ailment but also shed light on the true nature of her puzzling adversary-a remarkable CAPNON.CONCLUSIONS:For patients with CAPNON who have multiple or non-respectable lesions, the primary goal is to alleviate symptoms. After alleviating the symptoms with partial resection, close monitoring of any residual lesions is essential. If there is no evidence for disease progression, a strategy of continued close observation is appropriate.

Cholesterol serves a vital role in the occurrence and development of glioblastoma multiforme (GBM). Furthermore, cholesterol synthesis is regulated by sterol regulatory element-binding protein 2 (SREBP2), and certain glucose transporters (GLUTs) and Ras-related protein Rab11 (Rab11) small GTPase family members (Rab11s) may contribute to the process. The Cancer Genome Atlas was used to analyze the relationship between prognosis and GLUT gene expressions. To investigate the regulatory effect of Rab11s and SREBP2 on GLUTs during tumor progression, single cell RNA sequencing (scRNA-seq), western blotting and reverse transcription-quantitative PCR were performed on glioma tissues and the T98G GBM cell line. Cell viability and migration were assessed by performing MTT and wound healing assays, respectively. Moreover, the dual-luciferase reporter gene assay was conducted to predict the sterol regulatory elements in the promoter regions of the target genes. The results demonstrated that high SREBP2, GLUT1 and GLUT6 expression was associated with poor survival of patients with GBM. ScRNA-seq distinguished glioblastoma cells by EGFR and indicated the related lipid metabolism signaling pathways. Moreover, the results indicated that GLUT1 and GLUT6 were regulated by SREBP2 and Rab11s. Rab11s and SREBP2 also contributed to T98G cell viability and migration. Additionally, the results indicated that Rab11s, GLUT1 and GLUT6 were transcriptionally regulated by SREBP2. Therefore, the present study suggested that the SREBP2/Rab11/GLUT network promoted T98G cell growth, thus, identifying potential therapeutic targets for GBM.

目的 探讨磁共振波谱分析(magnetic resonance spectroscopy,MRS)代谢产物在胶质瘤分级诊断中的价值及其与Ki-67蛋白的相关关系.方法 回顾性分析2018年1月至2020年1月在我院经手术及病理证实的脑神经胶质瘤患者50例,其中低级别(WHOⅠ～Ⅱ级)胶质瘤25例、高级别(WHOⅢ～Ⅳ级)胶质瘤25例;低级别组男14例、女11例,平均年龄(48.64+11.76)岁;高级别组男19例、女6例,平均年龄(56.12+8.7)岁.所有患者术前均行3.0T磁共振1H-MRS检查,术后病理切片均行Ki-67蛋白染色观察.结果 高级别胶质瘤组肿瘤实质中心区Cho/NAA、Cr/NAA值均高于低级别胶质瘤组,差异均有统计学意义(P<0.05),两组胶质瘤患者Ki-67蛋白染色均表达呈阳性,且Ki-67表达程度与Cho/NAA比值呈正相关.结论 1H-MRS成像及术后Ki-67蛋白染色观察在脑胶质瘤术前分级诊断和术后治疗方案制定中有重要临床参考价值.

e14031 Background: KIAA1549-BRAF fusion is the most common genetic event in pilocytic astrocytoma (PA), and leads to activation of the mitogen activated protein kinase (MAPK) signaling pathway. KIAA1549-BRAF fusion has been considered to be a key variant of PA in WHO CNS5, however, fusions of BRAF with other partner genes leading to MAPK pathway activation, have been described rarely. Herein, we explore BRAF fusions profiles in Chinese glioma patients. Methods: Next generation sequencing of 131-gene profiling was performed to analyze BRAF fusions from 1955 Chinese brain tumor patients in 2019-2021. BRAF fusions were detected by following the standard operating procedure (SOP). We screened out the BRAF fusions, and calculated the mutation frequency and other rare BRAF gene fusions. Results: A total of 49 cases were detected with BRAF fusions, 36 cases were children (< 18 years old), and 13 cases were adults, with a mean age of 13 years (0-57 years). Interestingly, 39(80%) of them were KIAA1549-BRAF fusions, the most common fusion is between KIAA1549 exon 16 and BRAF exon 9 (exon 16–exon 9) followed by (exon 15–exon 9) and (exon 16–exon 11). And the other ten were rare fusions, including DENND2A-BRAF, MRPS33(Intergenic)- BRAF, BCAS1- BRAF, TMEM176B-BRAF, RNF130-BRAF, RIN2-BRAF, GNAI1-BRAF, EXOC4-BRAF, TNK2-BRAF. Most retained BRAF exons 9–18 (7/10, 70%). There was a significant statistical difference in age that the non- KIAA1549-BRAF fusions group was higher than the KIAA1549-BRAF fusions group (25 vs. 10, p < 0.005). Importantly, we identified new BRAF fusion variants resulting in RIN2-BRAF, EXOC4-BRAF, TNK2-BRAF and TMEM176B-BRAF rearrangements, which has not previously been reported in gliomas. Conclusions: We find new BRAF fusions in our 20% glioma patients. In addition, analysis of rare BRAF fusion may help guide diagnosis and develop potential targeted therapies of older PA.

Gliosarcoma (GSM), a histologic variant of glioblastoma (GBM), carries a poor prognosis with less than one year of median survival. Though GSM is similar with GBM in most clinical and pathological symptoms, GBM has unique molecular and histological features. However, as the rarity of GSM samples, the genetic information of this tumor is still lacking. Here, we take a comprehensive analysis of DNA copy number variations (CNV) in GBM and GSM. Whole genome sequencing was performed on 21 cases of GBM and 15 cases of GSM. CNVKIT is used for CNV calling. Our data showed that chromosomes 7, 8, 9, and 10 were the regions where CNV frequently happened in both GBM and GSM. There was a distinct CNV signal in chromosome 2 especially in GSM. The pathway enrichment of genes with CNV was suggested that the GBM and GSM shared the similar mechanism of tumor development. However, the CNV of some screened genes displayed a disparate form between GBM and GSM, such as AMP, BEND2, HDAC6, FOXP3, ZBTB33, TFE3, and VEGFD. It meant that GSM was a distinct subgroup possessing typical biomarkers. The pathways and copy number alterations detected in this study may represent key drivers in gliosarcoma oncogenesis and may provide a starting point toward targeted oncologic analysis with therapeutic potential.

目的 探讨影响经改良Poppen入路显微切除成人松果体区肿瘤患者预后的影响因素,以期发现导致患者预后不良的相关因素,改善患者临床预后.方法 收集中国科学技术大学附属第一医院神经外科自2015年6月-2020年7月收治并行经改良Poppen入路显微切除成人松果体区肿瘤患者临床资料,回顾性分析上述资料.结果 共纳入患者48例,患者于术后1个月行卡诺夫斯凯计分(KPS)评分,根据KPS评分结果将患者分为2组(以KPS评分70及以上为预后较好,KPS评分70分以下为预后较差,因KPS评分70分以下患者有效的抗肿瘤方案无法实施).其中预后较好患者29例,预后较差患者19例.在2组患者的单因素分析比较中,预后较差组出血量[(466.84±182.18)mL]多于预后较好组[(364.14±123.42)mL]、预后较差组术后枕叶损伤发生率(57.89％,11/19)高于预后较好组(24.14％,7/29);多因素logistic回归分析结果提示患者术后KPS评分仅与患者术后出现枕叶损伤(OR=4.887)、病变与顶盖关系相关(OR=5.870),与术前患者KPS评分及术中出血量无关.结论 研究显示改良Poppen入路进行脑肿瘤的显微外科切除能够改善患者预后,部分患者预后较差与患者肿瘤位置、术后枕叶是否损伤以及出血量多少有关.手术中应避免过度牵拉,降低枕叶损伤可能;对于肿瘤位于顶盖前方患者考虑更换手术方式;术中降低总出血量可能改善患者预后.