Epidemiological Study of Malignant Gliomas in Korea Using Nationwide Dataset from 2007 to 2017.

BACKGROUND: The purpose of the study was to investigate the incidence, prevalence, and survival of malignant gliomas (MGs) using population-based Korean National Health Insurance Database (NHID) data. METHODS: Using the Korean NHID, we identified patients with MG as C71 codes in KCD 5-7 according to ICD-10 from January 1, 2007 to December 31, 2017. Epidemiological characteristics of MG, including annual incidence, prevalence, mortality rates, and survival rates, were collected and analyzed according to socioeconomic state (SES) and treatments received. RESULTS: We identified 45,066 newly diagnosed-MG patients from 2007 to 2017, for an age-adjusted incidence of 7.47 per 100,000 people. The mean age at diagnosis was 54 years. The male to female ratio was 1.11. Mortality and survival probability were analyzed among total subjects and in subgroups. The mortality rates were lower in female than that of male patients (hazard ratio, 0.69; 95% confidence interval, 0.67-0.71), and in younger age population and in higher income group. Patients operated had a slightly higher survival rate. The 1-, 3-, 5-, and 10-year survival rates were estimated at 63.4%, 46.2%, 39.4%, and 34.8%, respectively. This is the first population-based study to determine the incidence and prevalence of MG according to epidemiological characteristics in Korea using NHID. CONCLUSION: Our study found that female sex and high SES were factors that significantly lowered the mortality rate in MG, and younger groups and operated patients showed significantly higher survival rates.

Aquaporin 1 overexpression may enhance glioma tumorigenesis by interacting with the transcriptional regulation networks of Foxo4, Maz, and E2F families.

BACKGROUND: The glioblastoma has served as a valuable experimental model system for investigating the growth and invasive properties of glioblastoma. Aquaporin-1 (AQP1) in facilitating cell migration and potentially contributing to tumor progression. In this study, we analyzed the role of AQP1 overexpression in glioblastoma and elucidated the main mechanisms involved. METHODS: AQP1 overexpression recombinant vector was introduced into C6 rat glioma cells to construct an AQP1 overexpression C6 cell line, and its effect on cell viability and migration ability was detected by MTT and Transwell. RNA was extracted by Trizol method for gene sequencing and transcriptomics analysis, and the differentially expressed genes (DEGs) were enriched for up- and downregulated genes by Principal component analysis (PCA), and the molecular mechanism of AQP1 overexpression was analyzed in comparison with the control group using the NCBI GEO database. Statistical analysis was performed using Mann-Whitney paired two tailed t test. RESULTS: The cell viability of AQP1-transfected cell lines increased by 23% and the mean distance traveled increased by 67% compared with the control group. Quantitative analysis of gene expression showed that there were 12,121 genes with an average transcripts per million (TPM) value greater than 1. DEGs accounted for 13% of the genes expressed, with the highest correlation with upregulated genes being FOXO4 and MAZ, and the highest with downregulated genes being E2F TFs. CONCLUSIONS: AQP1 may be implicated in glioma formation by interacting with the transcriptional regulation networks involving the FOXO4, MAZ, and E2F1/2. These findings shed light on the potential significance of AQP1 in glioma pathogenesis and warrant further investigations to unravel the underlying molecular mechanisms.

Optimized risk stratification strategy for glioma patients based on the feature genes of poor immune cell infiltration patterns.

BACKGROUND: Gliomas, originating from glial cells within the brain or spinal cord, are common central nervous system tumors with varying degrees of malignancy that influence the complexity and difficulty of treatment. The current strategies, including traditional surgery, radiotherapy, chemotherapy, and emerging immunotherapies, have yielded limited results. As such, our study aims to optimize risk stratification for a more precise treatment approach. We primarily identify feature genes associated with poor immune cell infiltration patterns through various omics algorithms and categorize glioma patients based on these genes to enhance the accuracy of patient prognosis assessment. This approach can underpin individualized treatment strategies and facilitate the discovery of new therapeutic targets. METHODS: We procured datasets of gliomas and normal brain tissues from TCGA, CGGA, and GTEx databases. Clustering was conducted using the input of 287 immune cell feature genes. Hub genes linked with the poor prognosis subtype (C1) were filtered through WGCNA. The TCGA dataset served as the discovery cohort and the CGGA dataset as the external validation cohort. We constructed a prognostic model related to feature genes from poor immune cell infiltration patterns utilizing LASSO-Cox regression. Comprehensive analyses of genomic heterogeneity, tumor stemness, pathway relevance, immune infiltration patterns, treatment response, and potential drugs were conducted for different risk groups. Gene expression validation was performed using immunohistochemistry (IHC) on 98 glioma samples and 11 normal brain tissue samples. RESULTS: Using the filtered immune cell-related genes, glioma patients were stratified into C1 and C2 subtypes through clustering. The C1 subtype exhibited a worse prognosis, with upregulated genes primarily enriched in immune response, extracellular matrix, etc., and downregulated genes predominantly enriched in neural signal transduction and neural pathway-related aspects. Seven advanced algorithms were used to elucidate immune cell infiltration patterns of different subtypes. In addition, WGCNA identified hub genes from poor immune infiltration patterns, and a prognostic model was constructed accordingly. High-risk patients demonstrated shorter survival times and higher risk scores as compared to low-risk patients. Multivariate Cox regression analysis revealed that, after adjusting for confounding clinical factors, risk score was a vital independent predictor of overall survival (OS) (P < 0.001). The established nomogram, which combined risk scores with WHO grade and age, accurately predicted glioma patient survival rates at 1, 3, and 5 years, with AUCs of 0.908, 0.890, and 0.812, respectively. This risk score enhanced the nomogram's reliability and informed clinical decision-making. We also comprehensively analyzed genomic heterogeneity, tumor stemness, pathway relevance, immune infiltration patterns, treatment response, and potential drugs for different risk groups. In addition, we conducted preliminary validation of the potential PLSCR1 gene using IHC with a large sample of gliomas and normal brain tissues. CONCLUSION: Our optimized risk stratification strategy for glioma patients has the potential to improve the accuracy of prognosis assessment. The findings from our omics research not only enhance the understanding of the functions of feature genes related to poor immune cell infiltration patterns but also offer valuable insights for the study of glioma prognostic biomarkers and the development of individualized treatment strategies.

High expression of cluster of differentiation 276 indicates poor prognosis in glioma.

BACKGROUND: Glioma is the central nervous system tumor with the highest incidence rate and the molecular detection of gliomas has been the focus of research. This study aimed to investigate the guiding effect of cluster of differentiation 276 (CD276) expression on the clinical prognosis of glioma. METHODS: The TCGA and CGGA databases were used to study whether CD 276 can be used as an independent prognostic factor for gliomas. Immunohistochemistry was used to detect the expression of CD276, isocitrate dehydrogenase-1 (IDH1), matrix metallopeptidase 9 (MMP9), p53, and Ki-67, and 1p/19q co-deletion was detected by fluorescence in situ hybridization (FISH). The effects of CD276 RNA interference (RNAi) on cell invasion, cell cycle and the expression of ß-catenin, tumor necrosis factor receptor 1 (TNFR1), and MMP9 were observed. Furthermore, the biological effects of CD276 gene knockout on intracranial transplanted tumors in nude mice were studied. RESULTS: CD276 expression was positively correlated with the extracellular matrix, collagen decomposition, and cell adhesion molecules. Immunohistochemistry and FISH showed that CD276 expression positively correlated with the glioma grade, p53 mutation, Ki-67 proliferation, and MMP9 expression; however, it negatively correlated with IDH1 mutation, 1p/19q co-deletion, and the survival rate. CD276 RNAi in U87 cells inhibited cell proliferation, migration, and invasion, but had no effect on the cell cycle. CD276 inhibited the expression of ß-catenin, TNFR1, and MMP9 in U87 cells at the mRNA and protein levels. In vivo experiments showed that the tumor formation and invasion of the CD276 small interfering RNA glioma cell line in nude mice were reduced and the survival time was prolonged. CONCLUSIONS: The present study demonstrated that high expression of CD276 in gliomas indicates a poor prognosis.

Research progress on radiation-resistant and radiation-sensitive proteomics in glioma stem cells / 中华放射肿瘤学杂志

After multidisciplinary treatment including radiotherapy, the median survival of patients with glioblastoma multiforme (GBM) remains approximately 1 year. The heterogeneity of the genome and proteome of glioblastoma stem cells (GSC) is the fundamental factor affecting the prognosis. Proteomics-based sensitization of key radioresistance proteins is expected to improve the prognosis of GBM patients. In this article, literature review was conducted from PubMed and other databases in the previous 10 years to systematically discuss the research progress on various commonly used protein quantitative techniques, tools for data processing analysis and the application in radioresistance and radiosensitization of GSCs.

Research progress on radiation-resistant and radiation-sensitive proteomics in glioma stem cells / 中华放射肿瘤学杂志

After multidisciplinary treatment including radiotherapy,the median survival of patients with glioblastoma multiforme (GBM) remains approximately 1 year.The heterogeneity of the genome and proteome of glioblastoma stem cells (GSC) is the fundamental factor affecting the prognosis.Proteomics-based sensitization of key radioresistance proteins is expected to improve the prognosis of GBM patients.In this article,literature review was conducted from PubMed and other databases in the previous 10 years to systematically discuss the research progress on various commonly used protein quantitative techniques,tools for data processing analysis and the application in radioresistance and radiosensitization of GSCs.

Spontaneous rupture of adrenal haemangioma mimicking abdominal aortic aneurysm rupture.

Serious bleeding from a ruptured adrenal mass limits preoperative diagnostics and can necessitate urgent laparotomy to control blood loss. A 45-year old man underwent an emergency laparotomy due to severe retroperitoneal haemorrhage causing hypovolaemia. Detailed retroperitoneal dissection after splenectomy and clamping of the abdominal aorta revealed bleeding from a ruptured haemangioma of the left adrenal gland. Following a left adrenalectomy, the patient returned to a stable haemodynamic state. Adrenal haemangiomas are rare, but may cause spontaneous life-threatening haemorrhage.

A Case of Arteriovenous Hemangioma showing Darier's Sign / 대한피부과학회지

We experienced a case of arteriovenous hemangioma showing Dariers sign on the forehead of a 43-year-old man. He presented with a single, 1 * 1.5cm sized, violaceous, asymptomatic nodule with a history of an intermittent wheal at the lesional site. This skin lesion showed Dariers sign clinically and proliferation of mast cells histopathologically with the punch biopsy specirnen suggesting urticaria pig- mentosa. Howerer, we could diagnose it as a arteriovenous hemangioma on complete excision, as the specimen showed arteriovenous proliferation with increased mast cells in a perivascular pattern. This case showed confusing clinical signs and showed the importance of complete excision for the diagnosis of a small skin tumor especially when a vascular proliferating tumor is suspected.