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1
Jiang, Chongming, Evelien Schaafsma, Yanding Zhao, Thinh Nguyen, Kenneth Zhu, and Chao Cheng. "Abstract LB528: A microglia associated gene signature predicts survival risk in glioma patients." Cancer Research 82, no. 12_Supplement (June 15, 2022): LB528. http://dx.doi.org/10.1158/1538-7445.am2022-lb528.
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Abstract Background: Gliomas are common tumors that affect the brain and spinal cord. A complex tumor microenvironment is one of the leading reasons for a poor prognosis in glioma patients. Microglia, as part of the immune microenvironment of gliomas, may facilitate glioma growth and invasion. However, the correlation between the microglia abundance and glioma prognosis has not been clarified. Method: Our goal was to examine the relationship between microglia abundance and glioma prognosis. We analyzed the single-cell RNA sequences of human and mouse glioma cells to identify microglia marker genes. Then, we built a LASSO Cox regression model of microglia abundance signatures in gliomas. The Cancer Genome Atlas (TCGA) dataset (Low-grade gliomas, LGG) was used as the training cohort. The Repository of Molecular Brain Neoplasia Data (REMBRANDT) dataset and Chinese Glioma Genome Atlas (CGGA) dataset was used to validate the model as the validation cohorts. Findings: Overall survival was significantly lower in those with a high level of microglia infiltration. Additionally, we found that microglia could interact with the tumor microenvironment and genomic features of gliomas, making microglia abundance negatively associated with the prognosis of glioma patients. Microglia abundance was positively correlated with immune genes expression and immune-related pathways. By applying our LASSO Cox regression model to gliomas, we found that patients with high-risk scores had significantly shorter overall survival (OS) than those with low-risk scores. Conclusions: Taken together, our findings suggest that microglia abundance may be negatively associated with survival in gliomas. Based on the novel microglia abundance signatures, we developed a high accuracy LASSO Cox regression model. In this study, we demonstrated that the model accurately predicted the prognosis of glioma patients and could offer new therapeutic targets for microglial-directed therapies. Keywords: Gliomas; Microglia abundance; LASSO Cox regression; TCGA; Signature.- 1 - Citation Format: Chongming Jiang, Evelien Schaafsma, Yanding Zhao, Thinh Nguyen, Kenneth Zhu, Chao Cheng. A microglia associated gene signature predicts survival risk in glioma patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr LB528.
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Zhao, Shiguang. "BIOM-63. DIAGNOSIS AND PROGNOSTIC SIGNIFICANCE OF CIRCULATING miR-2276-5p IN PLASMA OF GLIOMA PATIENTS." Neuro-Oncology 22, Supplement_2 (November 2020): ii15. http://dx.doi.org/10.1093/neuonc/noaa215.060.
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Abstract Circulating microRNAs (miRNAs) in plasma have the potential to become diagnostic and prognostic biomarkers for various cancers. This study hopes to use plasma circulating miRNAs as biomarkers for diagnosis and prognosis of glioma patients. METHOD: In this study, the plasma circulating miRNAs of 124 patients with glioma and 36 controls was collected to detect the relative expression of miR-2276-5p, and the specificity and sensitivity of the diagnosis were verified by ROC curve. The follow-up survival status was analyzed by cox regression analysis. RESULT: In the GSE 139031 database, it was found that the expression of circulating miR-2276-5p in plasma of glioma patients was significantly lower than that of patients with non-gliomas. Using our plasma samples, and it is indicated that the expression of circulating miR-2276-5p in plasma is lower than that of healthy patients, and compared with low-grade gliomas, patients with high-grade gliomas have a lower expression of circulating miR-2276-5p. ROC curve analysis found that the AUC value was 0.851. The low expression of circulating miR-2276-5p in plasma of glioma patients indicates a poor prognosis of glioma patients, After univariate and multifactorial cox regression analysis, which can be used as an independent prognostic risk factor for glioma patients (P< 0.05). CONCLUSION: The expression of circulating miR-2276-5p in plasma of glioma patients was significantly lower than that of the control group, compared with low-grade gliomas, patients with high-grade gliomas have a lower expression of circulating miR-2276-5p. The lower the relative expression of circulating miR-2276-5p indicated that glioma patients had a worse prognosis.
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Li, shaoqun, Mingyao Lai, Jiangfen Zhou, junjie Zhen, and Linbo Cai. "PATH-22. GENETIC VARIATION BETWEEN IDH MUTANT AND IDH WILD-TYPE GLIOMA." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi119. http://dx.doi.org/10.1093/neuonc/noab196.474.
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Abstract OBJECTIVE The prognosis of IDH mutant glioma was significantly different from that of IDH wild-type glioma. In order to explore the differences between them at the genetic level, we analyzed the genetic results of IDH mutant and IDH wild-type glioma. METHODS This study analyzed the clinical data and genetic results of 45 glioma patients from Jan. 2017 to Dec. 2019, exploring relevant prognostic indicators and the difference in genetic profile between IDH mutant glioma and IDH wild-type glioma. RESULTS 45 patients were included in this study, including 15 IDH mutant glioma patients and 30 IDH wild-type glioma patients. Genetic analysis showed that there was no difference in tumor mutation burden (TMB) and microsatellite instability (MSI) between IDH mutant glioma and IDH wild-type glioma. But somatic mutation between IDH mutant and IDH wild-type glioma was different. The expressions of IDH1, CIC, SYNE1 and TP53 were different in the two groups, among which IDH1 and CIC were more significantly different. Copy number variations (CNV) was also different between IDH mutant glioma and IDH wild-type glioma. STIL occured more frequently in IDH wild-type gliomas. Genetic analysis also showed the difference in variant allel frequence (VAF). IDH mutant gliomas were more likely to be combined with ATRX and TP53 mutations, while IDH wild-type gliomas, in addition to the combination of TP53 mutations, often also combined with the mutations of NF1, BRAF and PTEN. In survival analysis, glioma with IDH mutation has a good prognosis, and IDH wild-type patients have a poor prognosis. In IDH wild-type patients, patients with PTEN mutation have a worse prognosis. CONCLUSION There is an obvious genetic difference between IDH mutation and IDH wild-type glioma, and PTEN mutation is a poor prognostic factor for IDH wild-type patients.
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Priambada, Dody, Muhamad Thohar Arifin, Surya Pratama Briliantika, Dian Widyaningrum, Abdi Saputro, Azka Tajussyarof El Muzakka, Yuriz Bakhtiar, Krisna Tsaniadi Prihastomo, and Zainal Muttaqin. "Serum GFAP and EGFR as Supportive Diagnostic Biomarker of Glioma Patients: A Single-Center Study." Open Access Macedonian Journal of Medical Sciences 10, B (April 20, 2022): 1093–96. http://dx.doi.org/10.3889/oamjms.2022.9021.
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Background : High grade Gliomas (HGGs) (World Health Organization grade III and IV) are aggressive brain tumors with a poor prognosis. Serum concentrations of GFAP and EGFR are theoretically raised in glioma patients, especially primary HGGs
Aim : To look at serum levels of GFAP and EGFR in patients with Gliomas (Low Grade and High-Grade Glioma) and see if they were related to clinical outcome, MRI parameter and pathological features.
Method : Between 2020-2021, pre-operative blood samples were taken from 39 patients with radiologically diagnosed glioma who were performed for tumour excision. The time between blood collection and surgical resection was an average of 10 days. GFAP and EGFR serum were compared in glioma and non-glioma patients.
Result : Glioma patients had average of serum GFAP 747.93 + 1349.49 pg/ml and average of Serum EGFR 9.25 + 3.17 ng/ml. Non glioma average of GFAP and EGFR respectively were 292.91 + 369.30 pg/ml and 7.81 + 3.38 ng/ml.From all variable, we performed normality test using the Saphiro-wilk normality test and all variable were no normally distribution with p<0.05
Conclusion : Circulating GFAP and EGFR are promising method for “supportive” methods for differentiate between glioma and non-glioma patients, especially high grade glioma
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Kim, Junhyung, Min Woo Park, Young Joon Park, Ju Won Ahn, Jeong Min Sim, Suwan Kim, Jinhyung Heo, et al. "miR-542-3p Contributes to the HK2-Mediated High Glycolytic Phenotype in Human Glioma Cells." Genes 12, no. 5 (April 23, 2021): 633. http://dx.doi.org/10.3390/genes12050633.
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(1) Background: The elevation of glucose metabolism is linked to high-grade gliomas such as glioblastoma multiforme (GBM). The high glycolytic phenotype is associated with cellular proliferation and resistance to treatment with chemotherapeutic agents in GBM. MicroRNA-542-3p (miR-542-3p) has been implicated in several tumors including gliomas. However, the role of miR-542-3p in glucose metabolism in human gliomas remains unclear; (2) Methods: We measured the levels of cellular proliferation in human glioma cells. We measured the glycolytic activity in miR-542-3p knockdown and over-expressed human glioma cells. We measured the levels of miR-542-3p and HK2 in glioma tissues from patients with low- and high-grade gliomas using imaging analysis; (3) Results: We show that knockdown of miR-542-3p significantly suppressed cellular proliferation in human glioma cells. Knockdown of miR-542-3p suppressed HK2-induced glycolytic activity in human glioma cells. Consistently, over-expression of miR-542-3p increased HK2-induced glycolytic activity in human glioma cells. The levels of miR-542-3p and HK2 were significantly elevated in glioma tissues of patients with high-grade gliomas relative to that in low-grade gliomas. The elevation of HK2 levels in patients with high-grade gliomas were positively correlated with the high levels of miR-542-3p in GBM and low-grade gliomas (LGG) based on the datasets from the Cancer Genome Atlas (TCGA) database. Moreover, the high levels of miR-542-3p were associated with poor survival rate in the TCGA database; (4) Conclusions: miR-542-3p contributes to the HK2-mediated high glycolytic phenotype in human glioma cells.
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Kim, Junhyung, Min Woo Park, Ju Won Ahn, Jeong Min Sim, Suwan Kim, Young Joon Park, Jinhyung Heo, et al. "TAMI-47. MIR-542-3P CONTRIBUTES TO THE HK2-MEDIATED HIGH GLYCOLYTIC PHENOTYPE IN HUMAN GLIOMA CELLS." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi208. http://dx.doi.org/10.1093/neuonc/noab196.830.
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Abstract BACKGROUND The elevation of glucose metabolism is linked to high-grade gliomas such as glioblastoma multiforme (GBM). The high glycolytic phenotype is associated with cellular proliferation and resistance to treatment with chemotherapeutic agents in GBM. MicroRNA-542-3p (miR-542-3p) has been implicated in several tumors including gliomas. However, the role of miR-542-3p in glucose metabolism in human gliomas remains unclear. METHODS We measured the levels of cellular proliferation in human glioma cells. We measured the glycolytic activity in miR-542-3p knockdown and over-expressed human glioma cells. We measured the levels of miR-542-3p and HK2 in glioma tissues from patients with low- and high-grade gliomas using imaging analysis. RESULTS We show that knockdown of miR-542-3p significantly suppressed cellular proliferation in human glioma cells. Knockdown of miR-542-3p suppressed HK2-induced glycolytic activity in human glioma cells. Consistently, over-expression of miR-542-3p increased HK2-induced glycolytic activity in human glioma cells. The levels of miR-542-3p and HK2 were significantly elevated in glioma tissues of patients with high-grade gliomas relative to that in low-grade gliomas. The elevation of HK2 levels in patients with high-grade gliomas were positively correlated with the high levels of miR-542-3p in GBM and low-grade gliomas (LGG) based on the datasets from the Cancer Genome Atlas (TCGA) database. Moreover, the high levels of miR-542-3p were associated with poor survival rate in the TCGA database. CONCLUSIONS miR-542-3p contributes to the HK2-mediated high glycolytic phenotype in human glioma cells.
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Tran Anh Duc, Nguyen Thanh Bac, Nguyen Van Ba, and Nguyen Duc Lien. "Study on some clinical features, histopathology and mutations in IDH, P53 genes, mgmt methylation in patients with high-grade glioma." VietNam Military Medical Unisversity 47, no. 6 (September 8, 2022): 191–99. http://dx.doi.org/10.56535/jmpm.v47i6.66.
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Objectives: To describe some genes' clinical, histopathological and mutational characteristics in patients with high-grade glioma. Subjects and methods: A descriptive study was conducted on 52 high-grade glioma patients who met the research criteria at Vietnam National Cancer Hospital (Tan Trieu campus) from 1st January 2019 to 12th December 2020. Results: The mean age of the study patients was 45.2 ± 14.4; men accounted for the majority (61.5%). The main reason for the patient's admission was headache, hemiplegia, epilepsy... The average Karnofski score of the patient was 68.5 ± 14.7 points. The results of IDH gene mutation show that patients with grade III GCC have a higher positive rate than grade IV, P53 gene mutations occur mainly in grade IV GCC patients, MGMT methylation occurs on 57% of study patients. Conclusion: High-grade glioma is common in men aged over 40. Common clinical symptoms are headache, hemiplegia, and epilepsy. IDH gene mutations are seen in grade III gliomas, P53 gene mutations are common in grade IV gliomas.
* Keywords: High-grade glioma; IDH gene mutation; P53 gene mutation; MGMT methylation.
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Vattemi, Emanuela, Giovanna Cipollini, Cristina Dealis, Lorena Rossi, Susanne Baier, Elisabetta Cretella, Giovanni Di Meglio, et al. "Genetic polymorphisms of EGF 5'-UTR in patients with glioma: A possible predictive marker of outcome." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e13009-e13009. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e13009.
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e13009 Background: Epidermal growth factor (EGF) plays an important role in carcinogenesis. An adenine (A) to guanine (G) single nucleotide polymorphism at position 61 in the 5'-untranslated region (5'-UTR) of the EGF gene has been found to be associated with levels of EGF production and contribute to the risk of glioma. However, published data are contradictory. EGF +61G/A polymorphism may contribute to the risk of glioma in different ethnic group. Patients with glioma and GG genotype have been reported to have a risk of poorer otucome than patients with AA genotype. Purpose of this study is to investigate the potential role of this polymorphism in cancer progression and its role as predictive marker of outcome in glioma caucasian patients. Methods: EGF 61A/G polymorphism (rs4444903) was analyzed in glioma patients and was determined by means of Polymerase Chain Reaction and Direct Sequencing method (GenBank reference sequence-accession no. AC005509) from blood samples. Association of this genetic polymorphism with clinical and pathological data of patients was evaluated. Results: We investigated EGF +61G/A polymorphism in 24 glioma patients . EGF +61G allele has been found in 67% of glioma patients (25% G/G genotype and 42% A/G genotype). In astrocytomas, EGF +61G allele represents a 83% frequency; in glioblastomas and in oligodendrogliomas, EGF +61G allele frequency represents respectively 71% and 50%. In WHO IV gliomas, the EGF +61G allele represents a 63% frequency, (27% G/G and 36% A/G ), in WHO III gliomas a 77% frequency (33% G/G and 44% A/G ) and in WHO II gliomas a 50% frequency (100% A/G ). Median PFS of glioblastoma patients was 9 months. 83% of glioblastoma patients with a relapsing disease showed the G/G and A/G genotype. No difference was detected in the others histotypes. Conclusions: Our data conferm previous studies which reported G allele as a risk factor for glioma in Caucasian. G/A and G/G genotypes seem to be more rappresentative in high grade gliomas . Despite limited number of patients, our study supports the predictive role of EGF 61 A/G polymorphism in GBM. Additional large studies are warranted to confirm the role of EGF polymorphism as indipendent prognostic factor in glioma.
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Bracci, Paige, Terri Rice, Helen Hansen, Stephen Francis, Sean Lee, Lucie McCoy, Pavan Shrestha, et al. "EPID-08. PRE-SURGERY IMMUNE PROFILES OF ADULT GLIOMA PATIENTS." Neuro-Oncology 22, Supplement_2 (November 2020): ii79—ii80. http://dx.doi.org/10.1093/neuonc/noaa215.326.
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Abstract Changes in glioma patients’ immune profiles over the course of disease may predict outcomes. DNA based immunomethylomics quantifies blood immune cells based on cell specific DNA methylation signatures. To assess changes in immune profiles, we are longitudinally collecting blood samples from glioma patients pre-surgery and at other clinically relevant time points. Here we report patients’ pre-surgery immune profiles. All patients underwent biopsy or resection of a presumed new glioma or recurrent lower grade glioma. Blood DNA methylation was assessed with Illumina EPIC methylation arrays. Relative cell fractions of CD4, CD8, B-cells, natural killer cells, monocytes, and neutrophils, were estimated via our validated deconvolution algorithm. Total nucleated cell counts from Nexcelom cytometry were used to compute absolute cell counts. Other measures include total lymphocytes, CD4/CD8 ratio, neutrophil to lymphocyte ratio (NLR), and lymphocyte to monocyte ratio (LMR)). The first 125 participants includes 56 newly diagnosed glioblastomas (GBM), 28 newly diagnosed grade II-III gliomas, and 41 recurrent grade II-III gliomas. Median patient age is 49 years. 53 (43%) had recent dexamethasone exposure. In overall non-parametric analyses, most cell subsets, especially CD4, differed across grade, diagnosis group, WHO classification and dexamethasone exposure. In post-hoc pairwise analyses, immune profiles of IDH wildtype GBM patients who had taken dexamethasone differed from patients with GBM or grade II-III glioma who had not taken dexamethasone; they had clinically relevant and statistically significantly lower absolute CD4 counts, total white cell counts, and percent of total lymphocytes, and higher absolute neutrophil counts, NLR and LMR. However, some dexamethasone naïve GBM patients also had altered immune profiles. Comparisons of relative immune cell fractions with those from 454 non-glioma controls from the UCSF Adult Glioma Study showed that across grade and WHO classification, for the most part, immune profiles of glioma patients not exposed to dexamethasone did not differ from controls.
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Li, D., Y. Chen, C. Guo, Q. Yang, S. Wu, Y. Xia, J. Zeng, et al. "P03.09 Real world management and prognosis of glioma patients:SYSUCC report from China." Neuro-Oncology 21, Supplement_3 (August 2019): iii26—iii27. http://dx.doi.org/10.1093/neuonc/noz126.090.
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Abstract Background: The conventional way of patient treatment should be following guidelines. While in clinical practice, patients received treatments very often away from suggested guideline. In this report, we reviewed glioma patients received real world treatment at Sun Yat-sen University Cancer Center (SYSUCC) and results of this patient series. Methods: Total of 1215 glioma patients received surgery at SYSUCC from 2000 to 2017 were enclosed for analysis. The pathologic diagnosis of patients has followed WHO classification (initially 2007 standard, than 2016 standard). Results: A total of 1001 newly diagnosed brain glioma patients were analyzed, including 90 cases WHO grade I, 307 grade II, 239 grade III and 365 grade IV. The median age of onset was 14 (1–75), 35 (2–69), 41 (8–82) and 50 (2–86) years old, respectively, for grade I, II, III and IV glioma patients. Tumor total resection was achieved in 567 patients (57.5%). Among all patients, 331 high-grade gliomas (54.8%) and 159 low-grade glioma (40.1%) received radiotherapy, whereas 285 high-grade gliomas (47.1%) and 80 low-grade tumors (20.2%) received chemotherapy. Among high-grade gliomas, the median OS of glioblastoma, anaplastic astrocytoma and anaplastic oligodendroglial tumors were 17.7 months (15.7–19.7 months), 33.7 months (24.0–43.4 months) and 110.6 months (43.5–177.7 months), respectively, whereas the median OS of low-grade gliomas was not reach. The 5-year survival rate of grade I, II, III and IV gliomas was 94.7%, 73.7%, 45.1% and 18.6%, respectively. Multivariate analysis identified that onset age, Karnofsky performance status, tumor location, preoperative seizure, pathological subtype, resection extent and post-surgical treatment were independent predictors of OS for patients with high-grade gliomas. Patients received post-surgical radiotherapy and (or) chemotherapy had better survival than those without adjuvant treatment (grade III: 53.3 vs. 20.6 months, p =0.012; grade IV: 22.9 vs. 12.3 months, p < 0.001). For low-grade gliomas, patients’ age, Ki-67 index, tumor subtype and resection extent were associated with clinical outcomes. Conclusions: Glioma patients received treatments do not always following guidelines in clinical practice. Although standard care for patients may beneficial for prognosis, personalized treatment may more acceptable for patients and even resulting better outcome which should keep in mind in routine clinical practice.
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Bai, Ya-hui, Yun-bo Zhan, Bin Yu, Wei-Wei Wang, Li Wang, Jin-qiao Zhou, Ruo-kun Chen, et al. "A Novel Tumor-Suppressor, CDH18, Inhibits Glioma Cell Invasiveness Via UQCRC2 and Correlates with the Prognosis of Glioma Patients." Cellular Physiology and Biochemistry 48, no. 4 (2018): 1755–70. http://dx.doi.org/10.1159/000492317.
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Background/Aims: CDH18 (cadherin 18) is specifically expressed in the central nervous system and associated with various neuropsychiatric disorders. In this study, the role of CDH18 in glioma carcinogenesis and progression was investigated. Methods: The expression of CDH18 and its prognostic value in patients with gliomas were analyzed in public database and validated by real-time PCR/immunohistochemical staining (IHC) in our cohort. CCK-8 assay, transwell migration assay, wound healing assay, clonogenic assay and tumorigenicity assay were used to compare the proliferation, invasion and migration ability of glioma cells with different expressions of CDH18. iTRAQ-based quantitative proteomic analysis were used to reveal the downstream target of CDH18. Rescue experiments were conducted to further validate the relationship between UQCRC2 and CDH18. Results: The expression of CDH18 was depressed in a ladder-like pattern from normal tissues to WHO IV gliomas, and was an independent prognostic factor in TCGA (The Cancer Genome Atlas), CGGA (the Chinese glioma genome-atlas) and our glioma cohorts (n=453). Functional experiments in vitro and in vivo demonstrated that CDH18 inhibited invasion/migration, enhanced chemoresistance and suppressed tumorigenicity of glioma cells. UQCRC2 was identified as the downstream target of CDH18 by proteomic analysis. The expression of UQCRC2 was gradually absent as the WHO grades of gliomas escalated and was positively correlated with the expression of CDH18. Furthermore, in vitro assays demonstrated that down-regulation of UQCRC2 partly reversed the inhibition of invasion/migration ability and chemoresistance in CDH18 overexpressed glioma cell lines. Survival analysis demonstrated that combined CDH18/UQCRC2 biomarkers significantly influenced the prognosis of glioma patients. Conclusions: The present research demonstrated that CDH18 exerted its tumor-suppressor role via UQCRC2 in glioma cells and CDH18 might serve as a therapeutic target for treating gliomas.
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Jadus, Martin, Neil Hoa, Lisheng Ge, Yurii Kuznetsov, Alex McPherson, Andrew Cornforth, Nabil Ahmed, and Lawrence Lamb. "Gliomas display complex cell surface topographies that resist cytolytic lymphocytes but are reversed by using fascin siRNA (48.2)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 48.2. http://dx.doi.org/10.4049/jimmunol.186.supp.48.2.
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Abstract Gliomas are invasive cancers that resist all forms of attempted therapy, but immunotherapy has improved survival for some patients. We present evidence that another level of complexity may also contribute to lack of responses by the lymphocytes towards gliomas. Atomic force microscopy of four different glioma types: human U251 and rat T9 and F98 glioma cells, including freshly isolated human GBM neurosphere cultures (containing “stem cell-like cells’), revealed a complex surface topography with numerous microvilli and filopodia. These structures were not found on other cell types. Electron microscopy and immunofluorescence microscopy of glioma cells confirmed that microvilli are present. U251 cells with microvilli resisted the cytolytic actions of different human effector cells, (lymphokine-activated killer cells, γδ T cells, conventional cytolytic T lymphocytes, [CTL], and chimeric antigen receptor redirected T cells) better than their non-microvilli expressing counterparts. Killer cells released perforin which was detected within the glioma’s microvilli/ filopodia, indicating these structures can receive the cytolytic effector molecules, but cytotoxicity is suboptimal. Transfection of fascin siRNA into U251 cells prevented the microvilli from forming and allowed cytolytic cells to kill these adherent cells just as well as the non-attached glioma cells. These microvilli play multiple roles in glioma biology, such as invasion and resistance to lymphocyte-mediated killing.
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Ren, Jinhong, Peilan Jia, Hongxia Feng, Xiuhua Li, Jinghui Zhao, and Yunxia Sun. "Involvement of poly(ADP-ribose) polymerase-1 in Chinese patients with glioma: a potential target for effective patient care." International Journal of Biological Markers 33, no. 1 (July 27, 2017): 68–72. http://dx.doi.org/10.5301/ijbm.5000267.
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Objective: We aimed to evaluate the genetic variation of poly(ADP-ribose) polymerase-1 (PARP-1) in the development of gliomas among Chinese individuals. Materials and methods: Patients with a confirmed diagnosis of glioma and healthy individuals with no clinical symptoms of glioma were enrolled at Liaocheng People’s Hospital, China. Genetic polymorphisms were studied in plasma samples by polymerase chain reaction-restriction fragment length polymorphism assay. Cytokine levels were measured routinely in serum samples by sandwich ELISA technique. Results: A total of 120 Chinese patients with gliomas and 120 healthy Chinese individuals were included. We found that patients with the GG genotype (odds ratio [OR] 2.53, 95% confidence interval [CI] 1.46-4.38, p<0.001) and carriers of the G allele (OR 11.5, 95% CI 6.31-21.3, p<0.0001) were at high risk of developing glioma. A del/ins polymorphism of the NF-κB1 gene (OR 4.27, 95% CI 2.43-7.50, p<0.001) was also found to be associated with glioma. In addition, significantly increased cytokine levels were observed in patients with glioma (p<0.05). Conclusions: Our findings showed that PARP-1 polymorphisms are involved in the development of glioma in Chinese individuals. Also serum cytokine levels can be considered among the potential risk factors for developing glioma.
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Aabedi, alexander, Benjamin Lipkin, Jasleen Kaur, Sofia Kakaizada, Jacob Young, Anthony Lee, Saritha Krishna, Edward Chang, David Brang, and Shawn Hervey-Jumper. "TAMI-66. FUNCTIONAL ALTERATIONS IN CORTICAL PROCESSING OF SPEECH IN GLIOMA-INFILTRATED CORTEX." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi212. http://dx.doi.org/10.1093/neuonc/noab196.848.
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Abstract INTRODUCTION Recent developments in the biology of malignant gliomas have demonstrated that glioma cells interact with neurons through both paracrine signaling and electrochemical synapses. Glioma-neuron interactions consequently modulate the excitability of local neuronal circuits, and it is unclear the extent to which glioma-infiltrated cortex can meaningfully participate in neural computations. For example, gliomas may result in a local disorganization of activity that impedes the transient synchronization of neural oscillations. Alternatively, glioma-infiltrated cortex may retain the ability to engage in synchronized activity, in a manner similar to normal-appearing cortex, but exhibit other altered spatiotemporal patterns of activity with subsequent impact on cognitive processing. METHODS Here, we acquired invasive electrophysiologic recordings to sample both normal-appearing and glioma-infiltrated cortex during speech initiation in order to measure language task-related circuit dynamics of IDH-wild-type glioblastoma patients. We then applied an information theoretical framework to directly compare the encoding capacity and decodability of signals arising from these regions. RESULTS We find that glioma-infiltrated cortex engages in synchronous activity during task performance in a manner similar to normal-appearing cortex, but recruits a diffuse spatial network. On a temporal scale, we show that glioma-infiltrated cortex has lower capacity for information encoding when performing nuanced tasks such as speech production of monosyllabic versus polysyllabic words. As a result, temporal decoding strategies for distinguishing monosyllabic from polysyllabic words were feasible for signals arising from normal-appearing cortex, but not from glioma-infiltrated cortex. CONCLUSION These findings inform our understanding of cognitive processing in patients with malignant gliomas and have implications for patient survival, neuromodulation, and prosthetics in patients with malignant gliomas.
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Hu, Guangdong, Fengyuan Qian, Longgui Sha, and Zilong Wei. "Application of Deep Learning Technology in Glioma." Journal of Healthcare Engineering 2022 (February 18, 2022): 1–9. http://dx.doi.org/10.1155/2022/8507773.
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A common and most basic brain tumor is glioma that is exceptionally dangerous to health of various patients. A glioma segmentation, which is primarily magnetic resonance imaging (MRI) oriented, is considered as one of common tools developed for doctors. These doctors use this system to examine, analyse, and diagnose appearance of the glioma’s outward for both patients, i.e., indoor and outdoor. In the literature, a widely utilized approach for the segmentation of glioma is the deep learning-oriented method. To cope with this issue, a segmentation of glioma approach, i.e., primarily on the convolution neural networks, is developed in this manuscript. A DM-DA-enabled cascading approach for the segmentation of glioma, which is 2DResUnet-enabled model, is reported to resolve the problem of spatial data acquisition of insufficient 3D specifically in the 2D full CNN along with the core issue of memory consumption of 3D full CNN. For gliomas segmentation at various stages, we have utilized multiscale fusion approach, attention, segmentation, and DenseBlock. Moreover, for reducing three dimensionalities of the Unet model, a sampling of fixed region is used along with multisequence data of the glioma image. Finally, the CNN model has the ability of producing a better segmentation of tumor preferably with minimum possible memory. The proposed model has used BraTS18 and BraTS17 benchmark data sets for fivefold cross-validation (local) and online evaluation preferably official, respectively. Evaluation results have verified that edema’s Dice Score preferable average, enhancement, and core areas of the segmentation of the glioma with DM-DA-Unet perform exceptionally well on the validation set of BraTS17. Finally, average sensitivity was observed to be high as well, which is approximately closer to the best segmentation model and its effect on the validation set of BraTS1 and has segmented gliomas accurately.
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Cheng, Ling-Gang, Wen He, Hong-Xia Zhang, Qian Song, Bin Ning, Hui-Zhan Li, Yan He, and Song Lin. "Intraoperative Contrast Enhanced Ultrasound Evaluates the Grade of Glioma." BioMed Research International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2643862.
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Objective. The aim of our study was to investigate the value of intraoperative contrast enhanced ultrasound (CEUS) for evaluating the grade of glioma and the correlation between microvessel density (MVD) and vascular endothelial growth factor (VEGF).Methods. We performed intraoperative conventional ultrasound (CUS) and CEUS on 88 patients with gliomas. All of the patients have undergone surgery and obtained the results of pathology. All patients have undergone intraoperative CUS and CEUS to compare the characteristics of different grade gliomas and the results of CUS and CEUS were compared with pathological results.Results. The time to start (TTS) and time to peak (TTP) of low grade glioma (LGG) were similar to those of edema and normal brain surrounding glioma. The enhanced extent of LGG was higher than that of the normal brain and edema. The TTS and TTP of high grade glioma were earlier than those of the edema and normal brain surrounding glioma. The enhancement of HGG was higher than that of LGG. The absolute peak intensity (API) was correlated with MVD and VEGF.Conclusion. Intraoperative CEUS could help in determining boundary of peritumoral brain edema of glioma. Intraoperative CEUS parameters in cerebral gliomas could indirectly reflect the information of MVD and VEGF.
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Sun, Jin-Zhang, Jin-Hao Zhang, Jia-Bo Li, Feng Yuan, Lu-Qing Tong, Xu-Ya Wang, Lu-Lu Chen, et al. "MXRA5 Is a Novel Immune-Related Biomarker That Predicts Poor Prognosis in Glioma." Disease Markers 2021 (June 9, 2021): 1–13. http://dx.doi.org/10.1155/2021/6680883.
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Background. Glioma is the most common primary intracranial tumor and is associated with poor prognosis. Identifying effective biomarkers for glioma is particularly important. MXRA5, a secreted glycoprotein, is involved in cell adhesion and extracellular matrix remodeling and has been reported to be expressed in many cancers. However, the role and mechanism of action of MXRA5 in gliomas remain unclear. This study was aimed at investigating the role of MXRA5 at the transcriptome level and its clinical prognostic value. Methods. In this study, RNA microarray data of 301 glioma patients from the Chinese Glioma Genome Atlas (CGGA) were collected as a training cohort and RNA-seq data of 702 glioma samples from The Cancer Genome Atlas (TCGA) were used for validation. We analyzed the clinical and molecular characteristics as well as the prognostic value of MXRA5 in glioma. In addition, the expression level of MXRA was evaluated in 28 glioma tissue samples. Results. We found that MXRA5 expression was significantly upregulated in high-grade gliomas and IDH wild-type gliomas compared to controls. Receiver operating characteristic (ROC) analysis showed that MXRA5 is a potential marker of the mesenchymal subtype of glioblastoma multiforme (GBM). We found that MXRA5 expression is highly correlated with immune checkpoint molecule expression levels and tumor-associated macrophage infiltration. High MXRA5 expression could be used as an independent indicator of poor prognosis in glioma patients. Conclusion. Our study suggests that MXRA5 expression is associated with the clinicopathologic features and poor prognosis of gliomas. MXRA5 may play an important role in the immunosuppressive microenvironment of glioma. As a secreted glycoprotein, MXRA5 is a potential circulating biomarker for glioma, deserving further investigation.
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Sriwidyani, Ni Putu, Ida Ayu Ika Wahyuniari, Herman Saputra, and I. Gusti Kamasan Nyoman Arijana. "IDH1 mutation in Balinese glioma patients and its relationship with clinicopatological parameters." Bali Medical Journal 9, no. 3 (December 1, 2020): 819–22. http://dx.doi.org/10.15562/bmj.v9i2.2077.
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Purpose: Isocitrate dehydrogenase 1 (IDH1) mutation plays an important role in the carcinogenesis of gliomas. The most recent WHO classification of central nervous system tumors has added molecular genetic in addition to the histological features of the tumor, including status of IDH mutation in glial tumors. The purpose of this study was to determine the prevalence of IDH1 mutations in Balinese glioma patients and its association with clinicopathological features.Patients and methods: This study was conducted from 30 glioma patients at Sanglah General Hospital during January 2018 until June 2019. DNA extractions were carried out from the FFPE of tumor tissue, followed by amplification of codon 132 in exon 4 of the IDH1 gene by allele specific PCR. Relationship between IDH1 mutation status and clinicopathological features was tested with X2 with 0.05 significance.Results: The age range of patients is 14-81 years with an average age of 43.4 years (SD±17.9 years). Most patients with astrocytic tumors (25/30; 83.3%), others were oligodendroglial tumor (2/30; 6.7%) and oligoastrocytic tumor (3/30; 10%). Most patients were found with grade IV glioblastoma (18/30; 60%). Genotyping analysis showed IDH1 mutations in the majority of glioma patients (90%). Most cases (92.6%) of mutant IDH1 showed heterozygous mutations (GA genotype) while the rest showed homozygous mutations (AA genotype). There were no significant relationship between IDH1 status and age (p=0.09), sex (p=0.63) and histologic type (0.14), but there was significant relationship between IDH1 mutation status and tumor grade (p=0.01). All of IDH1 mutation were found in diffuse glioma (grade II and III gliomas and grade IV glioblastoma).Conclusion: Most of diffuse glioma (grade II-IV glioma) patients in Bali had IDH1 mutation and IDH1 mutation status has significant relationship with tumor grade. Further research about genetic abnormalities in order to improve therapeutic efficacy against IDH-mutated gliomas is needed.
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Watts, Colin, Alimu Dayimu, Tomasz Matys, Keyoumars Ashkan, Stephen Price, Michael D. Jenkinson, Gail Doughton, et al. "Refining the Intraoperative Identification of Suspected High-Grade Glioma Using a Surgical Fluorescence Biomarker: GALA BIDD Study Report." Journal of Personalized Medicine 13, no. 3 (March 13, 2023): 514. http://dx.doi.org/10.3390/jpm13030514.
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Background. Improving intraoperative accuracy with a validated surgical biomarker is important because identifying high-grade areas within a glioma will aid neurosurgical decision-making and sampling. Methods. We designed a multicentre, prospective surgical cohort study (GALA-BIDD) to validate the presence of visible fluorescence as a pragmatic intraoperative surgical biomarker of suspected high-grade disease within a tumour mass in patients undergoing 5-aminolevulinic acid (5-ALA) fluorescence-guided cytoreductive surgery. Results. A total of 106 patients with a suspected high-grade glioma or malignant transformation of a low-grade glioma were enrolled. Among the 99 patients who received 5-ALA, 89 patients were eligible to assess the correlation of fluorescence with diagnosis as per protocol. Of these 89, 81 patients had visible fluorescence at surgery, and 8 patients had no fluorescence. A total of 80 out of 81 fluorescent patients were diagnosed as high-grade gliomas on postoperative central review with 1 low-grade glioma case. Among the eight patients given 5-ALA who did not show any visible fluorescence, none were high-grade gliomas, and all were low-grade gliomas. Of the seven patients suspected radiologically of malignant transformation of low-grade gliomas and with visible fluorescence at surgery, six were diagnosed with high-grade gliomas, and one had no tissue collected. Conclusion. In patients where there is clinical suspicion, visible 5-ALA fluorescence has clinical utility as an intraoperative surgical biomarker of high-grade gliomas and can aid surgical decision-making and sampling. Further studies assessing the use of 5-ALA to assess malignant transformation in all diffuse gliomas may be valuable.
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Xuan, Chengmin, Mingwei Jin, Lei Wang, Shengbai Xue, Qi An, Qingzeng Sun, Lei Wang, and Yong Gao. "PART1 and hsa-miR-429-Mediated SHCBP1 Expression Is an Independent Predictor of Poor Prognosis in Glioma Patients." BioMed Research International 2020 (April 13, 2020): 1–12. http://dx.doi.org/10.1155/2020/1767056.
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Gliomas are the most common primary brain tumors. Because of their high degree of malignancy, patient survival rates are unsatisfactory. Therefore, exploring glioma biomarkers will play a key role in early diagnosis, guiding treatment, and monitoring the prognosis of gliomas. We found two lncRNAs, six miRNAs, and nine mRNAs that were differentially expressed by analyzing genomic data of glioma patients. The diagnostic value of mRNA expression levels in gliomas was determined by receiver operating characteristic (ROC) curve analysis. Among the nine mRNAs, the area under the ROC curve values of only CEP55 and SHCBP1 were >0.7, specifically 0.834 and 0.816, respectively. Additionally, CEP55 and SHCBP1 were highly expressed in glioma specimens and showed increased expression according to the glioma grade, and outcomes of high expression patients were poor. CEP55 was enriched in the cell cycle, DNA replication, mismatch repair, and P53 signaling pathway. SHCBP1 was enriched in the cell cycle, DNA replication, ECM receptor interaction, and P53 signaling pathway. Age, grade, IDH status, chromosome 19/20 cogain, and SHCBP1 were independent factors for prognosis. Our findings suggest the PART1-hsa-miR-429-SHCBP1 regulatory network plays an important role in gliomas.
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Mellinghoff, Ingo K., Benjamin M. Ellingson, Mehdi Touat, Elizabeth Maher, Macarena I. De La Fuente, Matthias Holdhoff, Gregory M. Cote, et al. "Ivosidenib in Isocitrate Dehydrogenase 1–Mutated Advanced Glioma." Journal of Clinical Oncology 38, no. 29 (October 10, 2020): 3398–406. http://dx.doi.org/10.1200/jco.19.03327.
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PURPOSE Diffuse gliomas are malignant brain tumors that include lower-grade gliomas (LGGs) and glioblastomas. Transformation of low-grade glioma into a higher tumor grade is typically associated with contrast enhancement on magnetic resonance imaging. Mutations in the isocitrate dehydrogenase 1 ( IDH1) gene occur in most LGGs (> 70%). Ivosidenib is an inhibitor of mutant IDH1 (mIDH1) under evaluation in patients with solid tumors. METHODS We conducted a multicenter, open-label, phase I, dose escalation and expansion study of ivosidenib in patients with m IDH1 solid tumors. Ivosidenib was administered orally daily in 28-day cycles. RESULTS In 66 patients with advanced gliomas, ivosidenib was well tolerated, with no dose-limiting toxicities reported. The maximum tolerated dose was not reached; 500 mg once per day was selected for the expansion cohort. The grade ≥ 3 adverse event rate was 19.7%; 3% (n = 2) were considered treatment related. In patients with nonenhancing glioma (n = 35), the objective response rate was 2.9%, with 1 partial response. Thirty of 35 patients (85.7%) with nonenhancing glioma achieved stable disease compared with 14 of 31 (45.2%) with enhancing glioma. Median progression-free survival was 13.6 months (95% CI, 9.2 to 33.2 months) and 1.4 months (95% CI, 1.0 to 1.9 months) for the nonenhancing and enhancing glioma cohorts, respectively. In an exploratory analysis, ivosidenib reduced the volume and growth rates of nonenhancing tumors. CONCLUSION In patients with m IDH1 advanced glioma, ivosidenib 500 mg once per day was associated with a favorable safety profile, prolonged disease control, and reduced growth of nonenhancing tumors.
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Wang, Zengliang, Yirizhati Aili, Yongxin Wang, Nuersimanguli Maimaitiming, Hu Qin, Wenyu Ji, Guofeng Fan, and Bo Li. "The RPL4P4 Pseudogene Is a Prognostic Biomarker and Is Associated with Immune Infiltration in Glioma." Oxidative Medicine and Cellular Longevity 2022 (August 9, 2022): 1–28. http://dx.doi.org/10.1155/2022/7967722.
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Objective. Research over the past decade has suggested important roles for pseudogenes in gliomas. Our previous study found that the RPL4P4 pseudogene is highly expressed in gliomas. However, its biological function in gliomas remains unclear. Methods. In this study, we analyzed clinical data on patients with glioma obtained from The Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA), the Genotype-Tissue Expression (GTEx), and the GEPIA2 databases. We used the R language for the main analysis. Correlations among RPL4P4 expression, pathological characteristics, clinical outcome, and biological function were evaluated. In addition, the correlations of RPL4P4 expression with immune cell infiltration and glioma progression were analyzed. Finally, wound healing, Transwell, and CCK-8 assays were performed to analyze the function of RPL4P4 in glioma cells. Result. We found that RPL4P4 is highly expressed in glioma tissues and is associated with poor prognosis, IDH1 wild type, codeletion of 1p19q, and age. Multivariate analysis and the nomogram model showed that high RPL4P4 expression was an independent risk factor for glioma prognosis and had better prognostic prediction power. Moreover, high RPL4P4 expression correlated with immune cell infiltration, which showed a significant positive association with M2-type macrophages. Finally, RPL4P4 knockdown in glioma cell lines caused decreased glioma cell proliferation, invasion, and migration capacity. Conclusion. Our data suggest that RPL4P4 can function as an independent prognostic predictor of glioma. It also shows that RPL4P4 expression correlates with immune cell infiltration and that targeting RPL4P4 may be a new strategy for the treatment of glioma patients.
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Gao, Huasong, Bin Yu, Yaohua Yan, Jianhong Shen, Sanhu Zhao, Jianhong Zhu, Wenxin Qin, and Yilu Gao. "Correlation of expression levels of ANXA2, PGAM1, and CALR with glioma grade and prognosis." Journal of Neurosurgery 118, no. 4 (April 2013): 846–53. http://dx.doi.org/10.3171/2012.9.jns112134.
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Object Biomarkers for the diagnosis and prognosis of gliomas are lacking. To elucidate new diagnostic and prognostic targets, a routine method is used to evaluate differences between the protein profile of normal and tumor cells. The object of the current study was to investigate novel differentially expressed proteins and their roles in gliomas. Methods Differences in the protein profile were compared using 2D polyacrylamide gel electrophoresis using C6 glioma cells and rat astrocytes. The mRNA and protein expression of ANXA2, PGAM1, and CALR were analyzed in glioma tissues and normal brain tissues. The expression of ANXA2 in the U87 glioma cell line was interrupted using short interfering RNA duplexes, and the role of ANXA2 in the migration and invasiveness of glioma cells was assessed. The expression of ANXA2, PGAM1, and CALR was examined further by immunohistochemical analysis using 130 glioma samples obtained in patients, and their prognostic roles in gliomas were evaluated using Kaplan-Meier and Cox regression analyses. Results Significantly higher expression levels of ANXA2 and PGAM1 and a lower level of CALR were found in glioma samples than in the normal brain samples. ANXA2, PGAM1, and CALR expression correlated with the grade and survival of patients with gliomas. Multivariate analysis further revealed that ANXA2 was an independent prognostic marker for glioma. After ANXA2 expression was suppressed using short interfering RNA, U87 cells had decreased migratory and invasive capabilities in vitro. Conclusions Protein expression alterations in ANXA2, PGAM1, and CALR were found in gliomas, and ANXA2 provided a novel prognostic value.
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Qi, Ying, Xinyu Yang, Chunxia Ji, Chao Tang, and Liqian Xie. "Identification of an IL-4-Related Gene Risk Signature for Malignancy, Prognosis and Immune Phenotype Prediction in Glioma." Brain Sciences 12, no. 2 (January 29, 2022): 181. http://dx.doi.org/10.3390/brainsci12020181.
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Background: Emerging molecular and genetic biomarkers have been introduced to classify gliomas in the past decades. Here, we introduced a risk signature based on the cellular response to the IL-4 gene set through Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis. Methods: In this study, we provide a bioinformatic profiling of our risk signature for the malignancy, prognosis and immune phenotype of glioma. A cohort of 325 patients with whole genome RNA-seq expression data from the Chinese Glioma Genome Atlas (CGGA) dataset was used as the training set, while another cohort of 667 patients from The Cancer Genome Atlas (TCGA) dataset was used as the validating set. The LASSO model identified a 10-gene signature which was considered as the optimal model. Results: The signature was confirmed to be a good predictor of clinical and molecular features involved in the malignancy of gliomas. We also identified that our risk signature could serve as an independently prognostic biomarker in patients with gliomas (p < 0.0001). Correlation analysis showed that our risk signature was strongly correlated with the Tregs, M0 macrophages and NK cells infiltrated in the microenvironment of glioma, which might be a supplement to the existing incomplete innate immune mechanism of glioma phenotypes. Conclusions: Our IL-4-related gene signature was associated with more aggressive and immunosuppressive phenotypes of gliomas. The risk score could predict prognosis independently in glioma, which might provide a new insight for understanding the IL-4 involved mechanism of gliomas.
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Hajri, Rami, Marie Nicod-Lalonde, Andreas F. Hottinger, John O. Prior, and Vincent Dunet. "Prediction of Glioma Grade and IDH Status Using 18F-FET PET/CT Dynamic and Multiparametric Texture Analysis." Diagnostics 13, no. 15 (August 5, 2023): 2604. http://dx.doi.org/10.3390/diagnostics13152604.
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Mutations in isocitrate dehydrogenase (IDH) represent an independent predictor of better survival in patients with gliomas. We aimed to assess grade and IDH mutation status in patients with untreated gliomas, by evaluating the respective value of 18F-FET PET/CT via dynamic and texture analyses. A total of 73 patients (male: 48, median age: 47) who underwent an 18F-FET PET/CT for initial glioma evaluation were retrospectively included. IDH status was available in 61 patients (20 patients with WHO grade 2 gliomas, 41 with grade 3–4 gliomas). Time–activity curve type and 20 parameters obtained from static analysis using LIFEx© v6.30 software were recorded. Respective performance was assessed using receiver operating characteristic curve analysis and stepwise multivariate regression analysis adjusted for patients’ age and sex. The time–activity curve type and texture parameters derived from the static parameters showed satisfactory-to-good performance in predicting glioma grade and IDH status. Both time–activity curve type (stepwise OR: 101.6 (95% CI: 5.76–1791), p = 0.002) and NGLDM coarseness (stepwise OR: 2.08 × 1043 (95% CI: 2.76 × 1012–1.57 × 1074), p = 0.006) were independent predictors of glioma grade. No independent predictor of IDH status was found. Dynamic and texture analyses of 18F-FET PET/CT have limited predictive value for IDH status when adjusted for confounding factors. However, they both help predict glioma grade.
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Sabedot, Thais S., Tathiane M. Malta, James Snyder, Kevin Nelson, Michael Wells, Ana C. deCarvalho, Abir Mukherjee, et al. "A serum-based DNA methylation assay provides accurate detection of glioma." Neuro-Oncology 23, no. 9 (February 9, 2021): 1494–508. http://dx.doi.org/10.1093/neuonc/noab023.
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Abstract Background The detection of somatic mutations in cell-free DNA (cfDNA) from liquid biopsy has emerged as a noninvasive tool to monitor the follow-up of cancer patients. However, the significance of cfDNA clinical utility remains uncertain in patients with brain tumors, primarily because of the limited sensitivity cfDNA has to detect real tumor-specific somatic mutations. This unresolved challenge has prevented accurate follow-up of glioma patients with noninvasive approaches. Methods Genome-wide DNA methylation profiling of tumor tissue and serum cfDNA of glioma patients. Results Here, we developed a noninvasive approach to profile the DNA methylation status in the serum of patients with gliomas and identified a cfDNA-derived methylation signature that is associated with the presence of gliomas and related immune features. By testing the signature in an independent discovery and validation cohorts, we developed and verified a score metric (the “glioma-epigenetic liquid biopsy score” or GeLB) that optimally distinguished patients with or without glioma (sensitivity: 100%, specificity: 97.78%). Furthermore, we found that changes in GeLB score reflected clinicopathological changes during surveillance (eg, progression, pseudoprogression, and response to standard or experimental treatment). Conclusions Our results suggest that the GeLB score can be used as a complementary approach to diagnose and follow up patients with glioma.
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Mitsuka, Kentaro, Tomoyuki Kawataki, Eiji Satoh, Takayuki Asahara, Toru Horikoshi, and Hiroyuki Kinouchi. "Expression of Indoleamine 2,3-Dioxygenase and Correlation With Pathological Malignancy in Gliomas." Neurosurgery 72, no. 6 (February 19, 2013): 1031–39. http://dx.doi.org/10.1227/neu.0b013e31828cf945.
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Abstract BACKGROUND: Indoleamine 2,3-dioxygenase (IDO) is a tryptophan catabolic enzyme involved in immune tolerance and tumor immune escape processes. Recently, IDO expression has been found to correlate with the prognosis of malignant tumors, but the implication of IDO in glioma progression remains unknown. OBJECTIVE: To investigate the relationship between IDO expression and histological malignancy in gliomas. METHODS: IDO expression was examined in a total of 75 surgical specimens obtained from 68 patients with glioma using immunohistochemical staining. The 75 specimens included 15 diffuse astrocytomas, 21 anaplastic astrocytomas, and 39 glioblastomas. Six of 39 glioblastomas were secondary glioblastomas, transforming from grade II or III gliomas that had been determined at the first surgery. IDO expression rate was compared in each histological grade, and patient survival was analyzed. RESULTS: Expression of IDO was found in 72 of 75 gliomas at varying intensities. Stronger expression of IDO was more likely to be observed in malignant gliomas compared with low-grade gliomas. IDO expression in the 6 cases of secondary glioblastoma was stronger than in the initial low-grade glioma. Survival analysis using the Kaplan-Meier method revealed that grade IV patients with strong IDO expression had significantly worse overall survival rates (P = .04) than patients with weak IDO expression. CONCLUSION: IDO is expressed more strongly in both primary and secondary glioblastoma tissue than low-grade glioma and may affect clinical outcome. If IDO promotes glioma cells to escape from the immune system, IDO may be a crucial therapeutic target for malignant gliomas.
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Joe, Dorothy, Jose Lavrador, Francesco Vergani, Richard Gullan, Ranjeev Bhangoo, Keyoumars Ashkan, and Gerald Finnerty. "033 Audit on the diagnostic pathway of patients with glioma mimics." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 12 (November 14, 2019): A18.4—A19. http://dx.doi.org/10.1136/jnnp-2019-abn-2.60.
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BackgroundConditions such as primary CNS lymphoma (PCNSL) or demyelinating/inflammatory diseases may present with similar clinical and neuroradiological features to gliomas. These ‘glioma mimics’ are commonly diagnosed with brain biopsy, but this is not always possible. We aim to optimize the contribution of less invasive investigations to the diagnostic pathway.MethodRetrospective review of the diagnostic process of glioma mimics between September to November 2018 in a tertiary Neuro–oncology unit.ResultsThe Neuro-oncology MDT gave 558 opinions excluding post –operative reviews. Twelve cases were identified as glioma mimics. 6/12 were new cases. Further investigations in five new cases took 2.5 – 11 weeks to complete. Two patients deteriorated during diagnostic workup and had expedited brain biopsies which confirmed PCNSL. One proceeded with chemotherapy and one was referred to palliative care.ConclusionDiagnostic tests prior to brain biopsy were not performed in all glioma mimic cases. This was because test results excluding brain biopsy were not available to start treatment before the patient deteriorated clinically. We anticipate that the frequency of glioma mimics will increase due to the greater use of immunomodulatory therapies. A dedicated protocol to achieve rapid diagnosis of glioma mimics is imperative to facilitate early, appropriate treatment.
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Wang, Jialin, Zhendong Liu, Cheng Zhang, Hongbo Wang, Ang Li, Binfeng Liu, Xiaoyu Lian, et al. "Abnormal expression of HOXD11 promotes the malignant behavior of glioma cells and leads to poor prognosis of glioma patients." PeerJ 9 (February 8, 2021): e10820. http://dx.doi.org/10.7717/peerj.10820.
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Background Homeobox D11 (HOXD11) plays an important role in a variety of cancers, but its precise role in gliomas remains unclear. This study aimed to explore the relationship between HOXD11 and gliomas by combining bioinformatics methods with basic experimental validation. Materials and methods Obtain gene expression information and clinical information of glioma and non-tumor brain tissue samples from multiple public databases such as TCGA (666 glioma samples), CGGA (749 glioma samples), GEPIA(163 glioblastoma samples and 207 normal control samples), GEO (GSE4290 and GSE15824). Nine cases of glioma tissue and five cases of normal control brain tissue were collected from the clinical department of Henan Provincial People’s Hospital for further verification. A series of bioinformatic analysis methods were used to confirm the relationship between HOXD11 expression and overall survival and clinical molecular characteristics of patients with glioma. RT-qPCR was used to verify the change of expression level of HOXD11 in glioma cells and tissues. MTT assay, colony formation assay, wound-healing assay, immunofluorescence staining, flow cytometry and western blotting were used to detect the effect of HOXD11 on the biological behavior of glioma cell line U251. Results The high expression of HOXD11 was significantly related to age, World Health Organization (WHO) grade, chemotherapy status, histological type, and even 1p19q codeletion data and isocitrate dehydrogenase (IDH) mutation. HOXD11, as an independent risk factor, reduces the overall survival of glioma patients and has diagnostic value for the prognosis of glioma. Gene Set Enrichment Analysis (GSEA) showed that HOXD11 was significantly enriched in cell signaling pathway such as cell cycle, DNA replication and so on. Finally, we confirmed that the knockout of HOXD11 can inhibit the proliferation and invasion of U251 glioma cells, and change the biological behavior of tumor cells by preventing the progression of cell cycle. Conclusions HOXD11 may be used as a candidate biomarker for the clinical application of targeted drug and prognostic assessment treatment of glioma. In addition, This study will help to explore the pathological mechanism of glioma.
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Cheng, Tong, Manyu Xu, Hui Zhang, Bing Lu, Xiaojing Zhang, Ziheng Wang, and Jianfei Huang. "KLHDC8A Expression in Association with Macrophage Infiltration and Oxidative Stress Predicts Unfavorable Prognosis for Glioma." Oxidative Medicine and Cellular Longevity 2022 (September 19, 2022): 1–14. http://dx.doi.org/10.1155/2022/2694377.
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Background. The tumor immune microenvironment (TME) is associated with cancer progression and immune escape. Although KLHDC8A has been reported in glioma in vitro, the expression and clinical significance of this gene in clinical samples are unknown. Methods. The Cancer Genome Atlas and Chinese Glioma Genome Atlas databases were used to evaluate the mRNA expression level of KLHDC8A and its significance in the glioma TME. Tissue microarray-based multiple immunohistochemical staining was conducted to determine KLHDC8A protein levels and characterize the immune signature of tumor-infiltrating immune cells in gliomas. Results. Tumor cells and tumor-associated macrophages expressed KLHDC8A. The expression of KLHDC8A was higher in glioma tissues than in normal brain tissues and was associated with patient clinical characteristics. Gliomas exhibited a high abundance of macrophages, neutrophils, regulatory T cells, and the immune checkpoint PD-L1, as well as high KLHDC8A expression. Cox regression analysis showed that KLHDC8A+CD68+ macrophages and KLHDC8A predicted unfavorable survival in patients with glioma. Finally, protein-protein interaction network analysis showed that the KLHDC8A expression was associated with hypoxia and oxidative stress. Conclusions. KLHDC8A is a potential marker for the clinical diagnosis of glioma. The immune characteristics of macrophages play a crucial role in predicting patients with glioma, providing a new avenue for targeted glioma therapy.
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Lim, Jaejoon, Youngjoon Park, Minjun Kim, Juwon Ahn, KyuBum Kwack, and Kyunggi Cho. "TMIC-03. UPREGULATION OF THE NLRC4 INFLAMMASOME CONTRIBUTES TO POOR PROGNOSIS IN GLIOMA PATIENTS." Neuro-Oncology 21, Supplement_6 (November 2019): vi247. http://dx.doi.org/10.1093/neuonc/noz175.1037.
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Abstract Inflammation in tumor microenvironments is implicated in the pathogenesis of tumor development. In particular, inflammasomes, which modulate innate immune functions, are linked to tumor growth and anticancer responses. However, the role of the NLRC4 inflammasome in gliomas remains unclear. Here, we investigated whether the upregulation of the NLRC4 inflammasome is associated with the clinical prognosis of gliomas. We analyzed the protein expression and localization of NLRC4 in glioma tissues from 11 patients by immunohistochemistry. We examined the interaction between the expression of NLRC4 and clinical prognosis via a Kaplan-Meier survival analysis. The level of NLRC4 protein was increased in brain tissues, specifically, in astrocytes, from glioma patients. NLRC4 expression was associated with a poor prognosis in glioma patients, and the upregulation of NLRC4 in astrocytomas was associated with poor survival. Furthermore, hierarchical clustering of data from the Cancer Genome Atlas dataset showed that NLRC4 was highly expressed in gliomas relative to that in a normal healthy group. Our results suggest that the upregulation of the NLRC4 inflammasome contributes to a poor prognosis for gliomas and presents a potential therapeutic target and diagnostic marker.
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den Hartog, Sanne J., Anja van der Kolk, Annette Bruggink, Tatjana Seute, Pieter Wesseling, and Joyce Wilbers. "Pathology-proven extradural (“distant”) metastases of gliomas in adults in the Netherlands between 1971 and 2018: a systematic case series." Neuro-Oncology Practice 8, no. 3 (January 22, 2021): 317–24. http://dx.doi.org/10.1093/nop/npab006.
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Abstract Background Diffuse gliomas are the most frequent primary tumors originating in the central nervous system parenchyma. Although the majority of these tumors are highly malignant, extradural metastases (EDM) are extremely rare. We aimed to perform a systematic review of patients with pathology-proven EDM of diffuse gliomas in the Netherlands. Methods From the Nationwide Network and Registry of Histo- and Cytopathology in the Netherlands information on all cases with EDM between 1971 and October 2018 was retrieved. Patients aged < 18 years or with a diagnosis of ependymoma or continuous tumor growth from intradural to extradural were excluded. Demographics, initial tumor diagnosis, treatment characteristics, location of the EDM, and survival data were collected. IDH1 R132H immunohistochemistry was performed on cases in which a paraffin block of the metastatic tumor could be retrieved. Results Twenty-five patients with diffuse glioma and pathology-proven EDM were identified. Median age at diagnosis of glioma was 46 years (IQR: 35-59); 21 patients (84%) were male. Histopathologic diagnosis was glioblastoma in 17 patients (68%) and lower-grade tumor in eight patients. In 3 out of 12 patients of which a paraffin block could be retrieved immunohistochemistry revealed an IDH1-mutant glioma. Most frequent EDM locations were bone/bone marrow (14/25 patients; 56%), and lymph nodes (6/25 patients; 24%). Conclusion EDM of diffuse glioma are rare. They occur most frequently in patients with glioblastoma, however, they can also originate from lower-grade, IDH-mutant gliomas. In daily practice, EDM of diffuse glioma should be considered in patients with tumefactive lesions of the bone or lymph nodes.
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Nguyen, Anthony V., Jose M. Soto, Sarah-Marie Gonzalez, Jennifer Murillo, Eric R. Trumble, Frank Y. Shan, and Jason H. Huang. "H3G34-Mutant Gliomas—A Review of Molecular Pathogenesis and Therapeutic Options." Biomedicines 11, no. 7 (July 15, 2023): 2002. http://dx.doi.org/10.3390/biomedicines11072002.
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The 2021 World Health Organization Classification of Tumors of the Central Nervous System reflected advances in understanding of the roles of oncohistones in gliomagenesis with the introduction of the H3.3-G34R/V mutant glioma to the already recognized H3-K27M altered glioma, which represent the diagnoses of pediatric-type diffuse hemispheric glioma and diffuse midline glioma, respectively. Despite advances in research regarding these disease entities, the prognosis remains poor. While many studies and clinical trials focus on H3-K27M-altered-glioma patients, those with H3.3-G34R/V mutant gliomas represent a particularly understudied population. Thus, we sought to review the current knowledge regarding the molecular mechanisms underpinning the gliomagenesis of H3.3-G34R/V mutant gliomas and the diagnosis, treatment, long-term outcomes, and possible future therapeutics.
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Riviere-Cazaux, C., and T. Burns. "OS01.6.A Through the Looking Glass: CSF Proteomics for Glioma Monitoring and Response Assessment." Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii10. http://dx.doi.org/10.1093/neuonc/noac174.031.
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Abstract Background The development of novel glioma therapies necessitates rapid, longitudinal, and individualized feedback from each patient's tumor. Due in part to the relative inaccessibility of dynamic gliomas, little information is available regarding mechanisms of in situ therapeutic response and resistance which may be needed to iteratively develop candidate therapies and combinations thereof. To address this challenge, we are performing glioma biomarker discovery by serial cerebrospinal fluid (CSF) sampling from Ommaya reservoirs to determine how the CSF proteome can reveal early longitudinal intelligence regarding glioma status, biology, and therapeutic response. Material and Methods Global proteomic analysis of CSF was performed on the Somalogic platform -- an aptamer-based technology for highly sensitive and specific analyses of over 7,000 proteins. Discovery analysis comprised of the top-500 ranked proteins in CSF from seven patients with high-grade gliomas (HGG) versus non-glioma controls. The top-500 HGG proteins were then preliminarily filtered to include only proteins that met two additional criteria: 1) decrease with lower tumor burden as defined by tumor resection, and 2) increase with greater tumor burden as defined by recurrence in individual paired patient samples. Results Proteomic enrichment analysis revealed a conserved HGG CSF proteomic signature defined by 79 proteins, including ones known to be over-expressed in solid tumor malignancies, such as retinoblastoma binding protein 4, heat shock protein 90, and sorcin. When queried in an independent validation cohort, the HGG proteomic signature was consistently enriched across 13 gliomas diverse in primary versus recurrent status, subtype, and grade, when compared to control CSF samples. In two patients for whom CSF was available prior to and immediately after resections, proteins in the HGG signature decreased as indicated by a lower tumor burden. Interestingly, the glioma CSF proteomic signature was highly enriched for blood-associated proteins (as defined by two paired sets of CSF samples with low vs. high hemoglobin), despite these patients' samples containing little-to-no hemoglobin proteins. Conclusion Global CSF proteomics acquired from longitudinal neurosurgical access to unique gliomas has the promise to yield biomarkers which may be used to gain insights regarding glioma biology, tumor burden, and evolution throughout a patient's disease and treatment course.
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Cinarer, Gokalp, and Bulent Gursel Emiroglu. "Classification of brain tumours using radiomic features on MRI." New Trends and Issues Proceedings on Advances in Pure and Applied Sciences, no. 12 (April 30, 2020): 80–90. http://dx.doi.org/10.18844/gjpaas.v0i12.4989.
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Glioma is one of the most common brain tumours among the diagnoses of existing brain tumours. Glioma grades are important factors that should be known in the treatment of brain tumours. In this study, the radiomic features of gliomas were analysed and glioma grades were classified by Gaussian Naive Bayes algorithm. Glioma tumours of 121 patients of Grade II and Grade III were examined. The glioma tumours were segmented with the Grow Cut Algorithm and the 3D feature of tumour magnetic resonance imaging images were obtained with the 3D Slicer programme. The obtained quantitative values were statistically analysed with Spearman and Mann–Whitney U tests and 21 features with statistically significant properties were selected from 107 features. The results showed that the best performing among the algorithms was Gaussian Naive Bayes algorithm with 80% accuracy. Machine learning and feature selection techniques can be used in the analysis of gliomas as well as pathological evaluations in glioma grading processes.
Keywords: Radiomics, glioma, naive bayes.
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Kadiyala, Padma, Felipe Nunez, Maria Garcia-Fabiani, Fernando Nunez, Dan Li, Anna Schwendeman, Pedro Lowenstein, and Maria Castro. "IMMU-03. SUPPRESSION OF ONCOMETABOLITE 2-HYDROXYGLUTRATE PRODUCED BY MUTANT IDH1 GLIOMA WITH AGI-5198 ENHANCES THE EFFICACY OF RADIOTHERAPY AND IMMUNE CHECKPOINT BLOCKADE ELICITING IMMUNOLOGICAL MEMORY." Neuro-Oncology 21, Supplement_6 (November 2019): vi119. http://dx.doi.org/10.1093/neuonc/noz175.497.
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Abstract Patients with mutant IDH1 gliomas survive ~3.8 year longer than patients harboring wildtype IDH1 glioma, irrespective of histology or genetic lesions, making mutant IDH1 an essential prognostic indicator. Mutant IDH1 gliomas are highly infiltrative with a high incidence of relapse. We are studying a low grade glioma subtype, genetically characterized by inactivating mutations in α-thalassemia/mental retardation syndrome X-linked (ATRX) gene, TP53 and gain of function mutations in isocitrate dehyrdogenase 1 (mIDH1). Mutation in IDH1 converts α-ketoglutrate (αKG) to 2-hydroxyglutarate (2HG), an oncometabolite that inhibits histone and DNA demethylases, leading to a hypermethylated tumor phenotype [1]. This leads to epigenetic reprograming of the tumor transcriptome. The role of 2HG as an immune regulator in the mIDH1 glioma tumor microenvironment remains to be elucidated. Herein, we investigate whether 2HG produced by mIDH1 glioma in the tumor microenvironment mediating antitumor immunity. We used mIDH1 inhibitor AGI-5198 to abrogate the neomorphic enzymatic activity of IDH1R132H in a transplantable mIDH1 glioma mouse model. Animals were implanted with mIDH1 tumor neurospheres and they were systemically administered with AGI-5198. Our results indicate that pharmacological inhibition of IDH1R132H enzymatic function significantly prolongs the median survival (MS) of mIDH1 glioma bearing mice (~1.5-fold vs controls); eliciting strong antitumor activity, eradicating 40% of the established mIDH1 gliomas. Our results also demonstrate that antitumor immunity induced by 2HG inhibition is enhanced when combined with standard of care (temozolomide and radiation) and anti-PDL1 immune checkpoint blockade. In addition, when the long-term survivors (>90 days) were rechallenged with mIDH1 tumor cells in the contralateral hemisphere, without further treatment, all the mice remained tumor free, indicating the development of anti-glioma immunological memory. Collectively, these findings support the clinical testing of AGI-5198 as an adjuvant therapy and a novel immunotherapeutic strategy for treating patients with mIDH1 glioma.
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Guo, Lydia, Ryan Rilinger, Akshay Sharma, Mina Lobbous, and Matthew Grabowski. "SDPS-45 PROGNOSTIC CHARACTERIZATION OF GENETIC MARKERS IN GLIOMA-ASSOCIATED EPILEPSY." Neuro-Oncology Advances 5, Supplement_3 (August 1, 2023): iii25. http://dx.doi.org/10.1093/noajnl/vdad070.099.
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Abstract BACKGROUND High-grade gliomas are often associated with seizures, which impair quality of life and cause deleterious neurocognitive effects. Few molecular markers characterized in high-grade gliomas have prognostic capacity for glioma-associated epilepsy. Mutations in isocitrate-dehydrogenase 1 (IDH1) have been associated with glioma-associated epilepsy (Chen et al. Neurology 2017;88(19):1805–13), but other genetic and cell proliferation markers in glioma biopsies have inconclusive connections with glioma-associated epilepsy. Current AAN guidelines advise against prophylactic administration of anti-seizure medications in patients with newly diagnosed brain tumors. We sought to characterize common molecular markers in high-grade glioma-associated epilepsy. METHODS We retrospectively reviewed 241 patients diagnosed with grade IV gliomas between 2018 and 2021 at our institution. Analysis of genetic biomarkers in tumor biopsies included chromosome 1p/19q deletion, ki-67 expression, p53 expression, MGMT methylation, IDH1 mutation, and EGFR amplification. Multiple logistic regressions were utilized to examine the association between genetic biomarkers and seizure incidence at three intervals: preoperative, postoperative, and six months post-surgery. Other variables examined were age, tumor location (lobe, laterality, eloquence), and treatment type (radiation therapy, chemotherapy, immunotherapy). RESULTS Of 241 patients analyzed, 104 (43%) patients experienced seizures. EGFR amplification in high-grade gliomas was associated with preoperative seizures (β = .92, p = .013) but was not associated with postoperative seizures nor seizures six months post-surgery. Chromosome 1p/19q deletion, ki-67 expression, p53 expression, MGMT methylation, and IDH1 mutation were all not associated with seizure incidence. CONCLUSION The study results indicate that EGFR amplification is associated with preoperative seizures, suggesting EGFR to promote glioma epileptiform activity. As EGFR amplification is characteristic of the classical subtype of glioblastoma, these results further suggest that the pathogenesis of glioma-associated epilepsy is likely related to specific molecular tumor characteristics. These preliminary results will be expanded upon with further analyses that increase sample size and include next-generation sequencing RESULTS
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Fries, Georg, Axel Perneczky, and Oliver Kempski. "Glioblastoma-associated circulating monocytes and the release of epidermal growth factor." Journal of Neurosurgery 85, no. 4 (October 1996): 642–47. http://dx.doi.org/10.3171/jns.1996.85.4.0642.
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✓ Monocytes/macrophages frequently infiltrate malignant gliomas and play a central role in the tumor-associated immune response as they process tumor antigen and present it to T-lymphocytes. Findings have accumulated that peripheral blood monocytes leaving the cerebral circulation become microglial cells and vice versa and that monocytes/macrophages may stimulate malignant tumor growth by some unknown mechanism. Most malignant gliomas express growth factor receptors, for example epidermal growth factor receptor (EGFR). The aim of this study was to determine whether peripheral blood monocytes of glioma patients release EGF, the appropriate ligand of gliomacell membrane-bound EGFR. Long-term cultured peripheral blood monocytes from 14 patients with malignant gliomas were compared to those from 12 controls (seven with nontumorous disease and five healthy individuals). Using an enzyme-linked immunosorbent assay for EGF, the EGF content of cell culture supernatants was determined at Days 7, 21, and 100 of culture. The EGF content (mean ± standard error) of supernatants was 5.9 ± 0.2 pg/ml/103 glioma monocytes versus 1.3 ± 0.1 pg/ml/103 control monocytes at Day 7 of culture, 22.9 ± 0.8 pg/ml/103 glioma monocytes versus 1.8 ± 0.9 pg/ml/103 control monocytes at Day 21 of culture, and 23.4 ± 0.7 pg/ml/103 glioma monocytes, and below detection levels for control monocytes at Day 100 of culture. Steroid treatment of glioma patients did not influence the EGF release of cultured monocytes. These data indicate that glioblastoma-associated peripheral blood monocytes may be distinct from those of healthy individuals. Moreover, this study indicates that subtypes of glioma-associated peripheral blood monocytes may support immunosuppression and promote growth of malignant glioma by releasing unusually high amounts of EGF.
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Yeo, Kee Kiat, Sanda Alexandrescu, Chantel Cacciotti, Emily Krzykwa, Jessica Clymer, Christine Chordas, Mary Ann Zimmerman, Susan Chi, Katherine Warren, and Karen Wright. "LGG-03. INCIDENCE AND OUTCOME OF PEDIATRIC IDH-MUTANT GLIOMA." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii366—iii367. http://dx.doi.org/10.1093/neuonc/noaa222.388.
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Abstract INTRODUCTION The incidence of IDH mutations in pediatric glioma is unclear. Recent publications suggest rates ranging between 0–20%. Therapy poses challenges as it is unclear if the biology and prognosis of pediatric IDH-mutant gliomas are identical to adults. METHODS We performed an IRB approved, systematic retrospective search for IDH-mutant gliomas in the Dana-Farber Cancer Institute/Boston Children’s Hospital database between 2009–2018, analyzing incidence, demographics, histology, co-occurring genetic alterations and outcome. RESULTS We identified 575 patients with glioma, ages 0–21 years. Of these, 394 underwent biopsy/resection (0–9 years:n=204; 10–21 years:n=190), with 294 genetic testing. Fifteen of 294 tumors (5%) were IDH1-mutant. Among patients 0–9 years and 10–21 years, 1/156 (0.6%) and 14/138 (10%) had IDH1-mutant tumors, respectively. Among patients 10–21 year old, 13/115 low-grade gliomas were IDH1-mutant (11%). High-grade gliomas accounted for the remaining 23, with one IDH1-mutant glioma (4%). Most common co-occurring genetic alterations for diffuse astrocytoma (n=12) were TP53 (n=9) and ATRX (n=2). Three patients with IDH1-mutant oligodendrogliomas had 1p/19q deletion. Eleven IDH1-mutant patients were evaluable for outcomes with median follow-up of five years. Five-year radiation-free, progression-free and overall survival for patients with low-grade histology were 76% and 100%, respectively. One patient with high-grade glioma recurred 1.2 years after upfront chemo-radiation and died soon after recurrence. CONCLUSION IDH-mutant gliomas comprise a small proportion of pediatric gliomas. Incidence rate is higher in the second decade of life. Comparative analyses between pediatric IDH-mutant gliomas and adult historical cohorts are currently underway, evaluating outcomes, radiation therapy and frequency of malignant transformation.
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Wang, Hesong, Yanyan Feng, Yuxiang Zhang, Ting Wang, Heng Xu, Yuxing Zhi, Yuyin Feng, Lichun Tian, and Kai Yuan. "Siglec10—An immunosuppressor and negative predictor of survival prognosis in gliomas." Frontiers in Genetics 13 (November 16, 2022). http://dx.doi.org/10.3389/fgene.2022.873655.
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Glioma is a type of tumor occurring in the central nervous system. In recent decades, specific gene mutations and molecular aberrations have been used to conduct the glioma classification and clinical decisions. Siglec10 is a member of the sialic acid-binding immunoglobulin superfamily. In this study, we investigated the expression and functions of siglec10 in gliomas. We analyzed the siglec10 expression in glioma patients with immunohistochemical (IHC) staining and evaluated the survival prognosis. The high siglec10 expression had a shorter survival prognosis than the low siglec10 expression in patients, especially in malignant gliomas. Bioinformatic datasets, including TCGA and CGGA, validated the IHC results and discovered the expression of siglec10 was higher in the malignant subtype than a benign subtype of gliomas. So, siglec10 is associated with the poor prognosis of gliomas. Furthermore, the related mechanisms of siglec10 in gliomas were investigated by functional enrichment analysis, including GSEA, GO, and KEGG analysis. Siglec10 was correlated with inflammatory mediators, inflammatory cells, and inflammatory pathways in gliomas. Siglec10 might take part in the immune response in the tumor microenvironment to induce glioma’s progression and metastasis. This study showed siglec10 was a biomarker in glioma, and it might be the potential target of glioma immunotherapy in the future.
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Zhou, Kaijia, Tao Jiang, Yanwei Liu, Zheng Zhao, Lijie Huang, and Guanzhang Li. "FXYD2 mRNA expression represents a new independent factor that affects survival of glioma patients and predicts chemosensitivity of patients to temozolomide." BMC Neurology 21, no. 1 (November 9, 2021). http://dx.doi.org/10.1186/s12883-021-02476-2.
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Abstract Purpose Glioma is the most common primary intracranial tumor. Owing to the poor prognosis associated with high-grade gliomas, there is an urgent need to identify biomarkers related to prognosis and treatment sensitivity. Here, we analyze the expression of FXYD2 mRNA in gliomas, and explore its clinical prognostic value and significance in this disease. Methods Clinical features, FXYD2 mRNA expression levels, and survival data were analyzed for 516 glioma patients from the Chinese Glioma Genome Map Project, 481 from the cancer genome map datbase and 268 from the molecular braintumor database. The expression patterns for FXYD2 mRNA were compared using the chi-square test, and overall survival (OS) of glioma patients was evaluated according to FXYD2 mRNA expression levels. The factors affecting glioma survival were evaluated by Cox univariate and multivariate regression analysis. Results FXYD2 mRNA expression was related to the grade of gliomas. The higher the level, the lower the expression. Meanwhile related to the pathological classification of gliomas. Oligodendroglioma, IDH-mutant and 1p/19q-codeleted was higher than Astrocytoma, IDH-mutant, higher than Glioblastoma, IDH-wildtype. Moreover, temozolomide (TMZ) chemotherapy was found to be an independent factor affecting survival in patients with high FXYD2 mRNA expression, but not in patients with low expression. Conclusion FXYD2 mRNA expression represents a new independent factor affecting the survival of glioma patients and may serve as an independent prognostic indicator to predict the sensitivity of gliomas to TMZ.
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Sprugnoli, Giulia, Laura Rigolo, Meghan Faria, Parikshit Juvekar, Yanmei Tie, Simone Rossi, Nicola Sverzellati, Alexandra J. Golby, and Emiliano Santarnecchi. "Glioma BOLD connectivity profile and its relationship to patients’ survival." Neuro-Oncology Advances, September 25, 2022. http://dx.doi.org/10.1093/noajnl/vdac153.
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Abstract Background Presence of residual neurovascular activity within glioma lesions have been recently demonstrated via functional MRI (fMRI) along with active electrical synapses between glioma cells and healthy neurons that influence survival. In this study, we aimed to investigate whether gliomas demonstrate synchronized neurovascular activity with the rest of the brain, by measuring Blood Oxygen Level Dependent (BOLD) signal synchronization, i.e. functional connectivity-FC, while also testing whether the strength of such connectivity might predict patients’ overall survival (OS). Methods Resting-state fMRI scans of patients who underwent presurgical brain mapping were analysed (total sample, n=54; newly diagnosed patients, n=18; recurrent glioma group, n=36). A seed to voxel analysis was conducted to estimate the FC signal profile of the tumor mass. A regression model was then built to investigate the potential correlation between tumor FC and individual OS. Finally, an unsupervised, cross-validated clustering analysis was performed including tumor FC and clinical OS predictors (e.g., KPS, tumor volume, genetic profile) to verify the performance of tumor FC in predicting OS with respect to validated radiological, demographic, genetic and clinical prognostic factors. Results In both newly diagnosed and recurrent gliomas patients a significant pattern of BOLD synchronization between the solid tumor and distant brain regions was found. Crucially, glioma-brain functional connectivity positively correlated with variance in individual survival in both newly diagnosed patients (r=0.90-0.96; p<0.001; R 2=81-92%) and in the recurrent glioma group (r=0.72; p<0.001; R 2=52%), outperforming standard clinical, radiological and genetic predictors. Conclusions Results suggest glioma’s synchronization with distant brain regions should be further explored as a possible diagnostic and prognostic biomarker.
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Zhu, Hua, Xinyao Hu, Shi Feng, Lijuan Gu, Zhihong Jian, Ning Zou, and Xiaoxing Xiong. "Predictive value of PIMREG in the prognosis and response to immune checkpoint blockade of glioma patients." Frontiers in Immunology 13 (July 15, 2022). http://dx.doi.org/10.3389/fimmu.2022.946692.
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Glioma is the most common primary brain tumor in the human brain. The present study was designed to explore the expression of PIMREG in glioma and its relevance to the clinicopathological features and prognosis of glioma patients. The correlations of PIMREG with the infiltrating levels of immune cells and its relevance to the response to immunotherapy were also investigated. PIMREG expression in glioma was analyzed based on the GEO, TCGA, and HPA databases. Kaplan–Meier survival analysis was used to examine the predictive value of PIMREG for the prognosis of patients with glioma. The correlation between the infiltrating levels of immune cells in glioma and PIMREG was analyzed using the CIBERSORT algorithm and TIMRE database. The correlation between PIMREG and immune checkpoints and its correlation with the patients’ responses to immunotherapy were analyzed using R software and the GEPIA dataset. Cell experiments were conducted to verify the action of PIMREG in glioma cell migration and invasion. We found that PIMREG expression was upregulated in gliomas and positively associated with WHO grade. High PIMREG expression was correlated with poor prognosis of LGG, prognosis of all WHO grade gliomas, and prognosis of recurrent gliomas. PIMREG was related to the infiltration of several immune cell types, such as M1 and M2 macrophages, monocytes and CD8+ T cells. Moreover, PIMREG was correlated with immune checkpoints in glioma and correlated with patients’ responses to immunotherapy. KEGG pathway enrichment and GO functional analysis illustrated that PIMREG was related to multiple tumor- and immune-related pathways. In conclusion, PIMREG overexpression in gliomas is associated with poor prognosis of patients with glioma and is related to immune cell infiltrates and the responses to immunotherapy.
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Lv, Kun, Xin Cao, Rong Wang, Peng Du, Junyan Fu, Daoying Geng, and Jun Zhang. "Neuroplasticity of Glioma Patients: Brain Structure and Topological Network." Frontiers in Neurology 13 (May 13, 2022). http://dx.doi.org/10.3389/fneur.2022.871613.
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Glioma is the most common primary malignant brain tumor in adults. It accounts for about 75% of such tumors and occurs more commonly in men. The incidence rate has been increasing in the past 30 years. Moreover, the 5-year overall survival rate of glioma patients is < 35%. Different locations, grades, and molecular characteristics of gliomas can lead to different behavioral deficits and prognosis, which are closely related to patients' quality of life and associated with neuroplasticity. Some advanced magnetic resonance imaging (MRI) technologies can explore the neuroplasticity of structural, topological, biochemical metabolism, and related mechanisms, which may contribute to the improvement of prognosis and function in glioma patients. In this review, we summarized the studies conducted on structural and topological plasticity of glioma patients through different MRI technologies and discussed future research directions. Previous studies have found that glioma itself and related functional impairments can lead to structural and topological plasticity using multimodal MRI. However, neuroplasticity caused by highly heterogeneous gliomas is not fully understood, and should be further explored through multimodal MRI. In addition, the individualized prediction of functional prognosis of glioma patients from the functional level based on machine learning (ML) is promising. These approaches and the introduction of ML can further shed light on the neuroplasticity and related mechanism of the brain, which will be helpful for management of glioma patients.
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Liu, Fangkun, Jing Huang, Xuming Liu, Quan Cheng, Chengke Luo, and Zhixiong Liu. "CTLA-4 correlates with immune and clinical characteristics of glioma." Cancer Cell International 20, no. 1 (January 6, 2020). http://dx.doi.org/10.1186/s12935-019-1085-6.
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Abstract Background CTLA-4 is a well-studied immune checkpoint protein that negatively regulates T cell-mediated immune responses. However, the expression of CTLA-4 in glioma and the effects of CTLA-4 on prognosis in patients with glioma have not yet been examined. Methods We investigated the protein level of CTLA-4 in human glioma samples, extracted genetic and clinical data from 1024 glioma patients to characterize CTLA-4 expression and its relationship with immune functions in gliomas. R language was used for statistical analysis. Results Higher CTLA-4 expression was found in patients with higher grade, isocitrate dehydrogenase (IDH)-wild-type, and mesenchymal-molecular subtype gliomas than in patients with lower grade, IDH-mutant, and other molecular subtype gliomas. Further analysis showed that there was a strong positive correlation between CTLA-4 and the specific marker gene expression of immune cells, including CD8+ T cells, regulatory T cells, and macrophages in both databases, suggesting that higher CTLA-4 expression in the glioma microenvironment induced greater immune cell infiltration compared with that in gliomas with lower CTLA-4 expression. We further explored the associations between CTLA-4 and other immune-related molecules. Pearson correlation analysis showed that CTLA-4 was associated with PD-1, CD40, ICOS, CXCR3, CXCR6, CXCL12 and TIGIT. Patients with glioma with lower CTLA-4 expression exhibited significantly longer overall survival. Thus, these findings suggested that increased CTLA-4 expression conferred a worse outcome in glioma. Conclusions In summary, our findings revealed the expression patterns and clinical characteristics of CTLA-4 in glioma and may be helpful for expanding our understanding of antitumor immunotherapy in gliomas.
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Ge, Honglin, Guangfu Di, Zheng Yan, Dongming Liu, Yong Liu, Kun Song, Kun Yang, et al. "Does epilepsy always indicate worse outcomes? A longitudinal follow-up analysis of 485 glioma patients." World Journal of Surgical Oncology 20, no. 1 (September 19, 2022). http://dx.doi.org/10.1186/s12957-022-02772-2.
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Abstract Background Epilepsy is one of the most common glioma complications, and the two may be connected in more ways than we understand. We aimed to investigate the clinical features of glioma-associated epilepsy and explore the risk factors associated with it. Methods We collected clinical information from 485 glioma patients in the Nanjing Brain Hospital and conducted 4 periodic follow-up visits. Based on the collected data, we analyzed the clinical characteristics of glioma patients with or without epilepsy and their relationship with survival. Results Among glioma patients, younger people were more likely to have epilepsy. However, epilepsy incidence was independent of gender. Patients with grade II gliomas were most likely to develop epilepsy, while those with grade IV gliomas were least likely. There was no difference in Karnofsky Performance Status scores between patients with glioma-associated epilepsy and those without epilepsy. Additionally, epilepsy was independently associated with longer survival in the World Health Organization grade IV glioma patients. For grades II, III, and IV tumors, the 1-year survival rate of the epilepsy group was higher than that of the non-epilepsy group. Conclusions Epilepsy did not lead to worse admission performance and correlated with a better prognosis for patients with grade IV glioma.
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Liu, Li-qiang, Li-fei Feng, Cheng-rui Nan, and Zong-mao Zhao. "CREB3L1 and PTN expressions correlate with prognosis of brain glioma patients." Bioscience Reports 38, no. 3 (May 22, 2018). http://dx.doi.org/10.1042/bsr20170100.
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The present study was conducted to investigate the clinical significance of cAMP responsive element binding protein 3 like 1 (CREB3L1) and pleiotrophin (PTN) expression in prognosis of patients with brain gliomas. Human brain tissue samples were collected from normal glial tissues (control), low- and high-grade glioma tissues. CREB3L1 and PTN expression levels in cells were assessed by immunohistochemistry (IHC), and population distribution of the CREB3L1- and PTN-presenting patients was examined. The CREB3L1 and PTN mRNA expression levels in three types of the brain cells was determined by RT-PCR. Survival rates for population of the CREB3L1- and PTN-presenting patients were examined. CREB3L1+ cell counts were decreased with increased PTN+ cells in the low-grade and high-grade glioma tissues as compared with the control. Population proportion of the CREB3L1+-presenting patients decreased from the control to the high-grade glioma and the population of the PTN+-presenting patients increased in low- and high-grade gliomas as compared with the control (both P<0.05). The decrease in the CREB3L1 mRNA expression was associated with the increase in the PTN mRNA expression in the low- and high-grade gliomas (P<0.05). Survival time for patients with CREB3L1− and PTN+ gliomas was shorter than patients with CREB3L1+ and PTN− gliomas in the investigated cohorts (both P<0.05). There was a relationship between the expression levels of both proteins and survival time. CREB3L1 and PTN expression levels serve as biomarkers with utility in grading gliomas. Absence of CREB3L1 and presence of PTN in brain glioma cells correlate with survival time of the glioma patients.
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Liu, Zhendong, Wang Zhang, Xingbo Cheng, Hongbo Wang, Lu Bian, Jialin Wang, Zhibin Han, et al. "Overexpressed XRCC2 as an independent risk factor for poor prognosis in glioma patients." Molecular Medicine 27, no. 1 (May 29, 2021). http://dx.doi.org/10.1186/s10020-021-00316-0.
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Abstract Background XRCC2, a homologous recombination-related gene, has been reported to be associated with a variety of cancers. However, its role in glioma has not been reported. This study aimed to find out the role of XRCC2 in glioma and reveal in which glioma-specific biological processes is XRCC2 involved based on thousands of glioma samples, thereby, providing a new perspective in the treatment and prognostic evaluation of glioma. Methods The expression characteristics of XRCC2 in thousands of glioma samples from CGGA and TCGA databases were comprehensively analyzed. Wilcox or Kruskal test was used to analyze the expression pattern of XRCC2 in gliomas with different clinical and molecular features. The effect of XRCC2 on the prognosis of glioma patients was explored by Kaplan–Meier and Cox regression. Gene set enrichment analysis (GSEA) revealed the possible cellular mechanisms involved in XRCC2 in glioma. Connectivity map (CMap) was used to screen small molecule drugs targeting XRCC2 and the expression levels of XRCC2 were verified in glioma cells and tissues by RT-qPCR and immunohistochemical staining. Results We found the overexpression of XRCC2 in glioma. Moreover, the overexpressed XRCC2 was associated with a variety of clinical features related to prognosis. Cox and meta-analyses showed that XRCC2 is an independent risk factor for the poor prognosis of glioma. Furthermore, the results of GSEA indicated that overexpressed XRCC2 could promote malignant progression through involved signaling pathways, such as in the cell cycle. Finally, doxazosin, quinostatin, canavanine, and chrysin were identified to exert anti-glioma effects by targeting XRCC2. Conclusions This study analyzed the expression pattern of XRCC2 in gliomas and its relationship with prognosis using multiple datasets. This is the first study to show that XRCC2, a novel oncogene, is significantly overexpressed in glioma and can lead to poor prognosis in glioma patients. XRCC2 could serve as a new biomarker for glioma diagnosis, treatment, and prognosis evaluation, thus bringing new insight into the management of glioma.
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Chen, Chia-Hua, Kuo-Chen Wei, Wei-Chao Liao, You-Yu Lin, Hsiu-Chi Chen, Li-Ying Feng, Chiung-Hui Liu, et al. "Prognostic value of an APOBEC3 deletion polymorphism for glioma patients in Taiwan." Journal of Neurosurgery, September 1, 2022, 1–13. http://dx.doi.org/10.3171/2022.7.jns2250.
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OBJECTIVE The molecular pathogenesis of malignant gliomas, characterized by diverse tumor histology with differential prognosis, remains largely unelucidated. An APOBEC3 deletion polymorphism, with a deletion in APOBEC3B, has been correlated to risk and prognosis in several cancers, but its role in glioma is unclear. The authors aimed to examine the clinical relevance of the APOBEC3 deletion polymorphism to glioma risk and survival in a glioma patient cohort in Taiwan. METHODS The authors detected deletion genotypes in 403 glioma patients and 1365 healthy individuals in Taiwan and correlated the genotypes with glioma risk, clinicopathological factors, patient survival, and patient sex. APOBEC3 gene family expression was measured and correlated to the germline deletion. A nomogram model was constructed to predict patient survival in glioma. RESULTS The proportion of APOBEC3B−/− and APOBEC3B+/− genotypes was higher in glioblastoma (GBM) patients than healthy individuals and correlated with higher GBM risk in males. A higher percentage of cases with APOBEC3B− was observed in male than female glioma patients. The presence of APOBEC3B−/− was correlated with better overall survival (OS) in male astrocytic glioma patients. No significant correlation of the genotypes to glioma risk and survival was observed in the female patient cohort. Lower APOBEC3B expression was observed in astrocytic glioma patients with APOBEC3B−/− and was positively correlated with better OS. A 5-factor nomogram model was constructed based on male patients with astrocytic gliomas in the study cohort and worked efficiently for predicting patient OS. CONCLUSIONS The germline APOBEC3 deletion was associated with increased GBM risk and better OS in astrocytic glioma patients in the Taiwan male population. The APOBEC3B deletion homozygote was a potential independent prognostic factor predicting better survival in male astrocytic glioma patients.
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Zhang, Hao, Jialin He, Ziyu Dai, Zeyu Wang, Xisong Liang, Fengqiong He, Zhiwei Xia, et al. "PDIA5 is Correlated With Immune Infiltration and Predicts Poor Prognosis in Gliomas." Frontiers in Immunology 12 (February 16, 2021). http://dx.doi.org/10.3389/fimmu.2021.628966.
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Gliomas are the most common and lethal primary malignant tumor of the brain. Routine treatment including surgical resection, chemotherapy, and radiotherapy produced limited therapeutic effect, while immunotherapy targeting the glioma microenvironment has offered a novel therapeutic option. PDIA5 protein is the member of PDI family, which is highly expressed in glioma and participates in glioma progression. Based on large-scale bioinformatics analysis, we discovered that PDIA5 expression level is upregulated in aggressive gliomas, with high PDIA5 expression predicting poor clinical outcomes. We also observed positive correlation between PDIA5 and immune infiltrating cells, immune related pathways, inflammatory activities, and other immune checkpoint members. Patients with high PDIA5 high-expression benefited from immunotherapies. Additionally, immunohistochemistry revealed that PDIA5 and macrophage biomarker CD68 were upregulated in high-grade gliomas, and patients with low PDIA5 level experienced favorable outcomes among 33 glioma patients. Single cell RNA sequencing exhibited that PDIA5 was in high level presenting in neoplastic cells and macrophages. Cell transfection and co-culture of glioma cells and macrophages revealed that PDIA5 in tumor cells mediated macrophages exhausting. Altogether, our findings indicate that PDIA5 overexpression is associated with immune infiltration in gliomas, and may be a promising therapeutic target for glioma immunotherapy.