Objectives We aimed to evaluate risk factors of sis-VADAs recurrence after reconstructive treatment based on 113 reconstructed lesions. Methods A total of 111 patients (M:F = 68:43; median age, 47 years) with 113 sis-VADAs underwent reconstruction from October 2000 to March 2011, using stent(s) and coils. Treatments and predictors of recurrence were retrospectively analysed. Results Fifty-eight sis-VADAs underwent single-stent treatment, and the remaining 55 sis-VADAs underwent treatment with 2-4 overlapping stents. Follow-up angiography was available for 94 sis-VADAs 12 -78 months, with recurrence in ten patients, including seven angiographic recurrences and three post-treatment haemorrhagic recurrences. A higher rate of post-treatment recurrence was observed in the single stent group than in the multiple stents group (p = 0.010). The interaction between stent (s) implantation and immediate occlusion degree (odds ratio [OR] =3.152; 95 % confidence interval [CI], 1.293-7.686; p = 0.012), between stent (s) implantation and the posterior inferior cerebellar artery (PICA) involvement (OR = 4.607; 95 % CI, 1.172-18.113; p = 0.029), and between PICA involvement and immediate occlusion degree (OR = 5.018; 95 % CI, 1.263-19.933; p = 0.022) affect recurrence in the reconstructed sis-VADAs. Conclusions This single centre cohort study indicated that the interaction effect between stent (s) implantation, PICA involvement, and immediate occlusion degree were closely associated with recurrence after reconstructive treatment of sis-VADA. Key Points • The interaction between stent (s) and immediate occlusion degree affect aneurysmal recurrence • The interaction between stent and PICA involvement affect aneurysmal recurrence • The interaction between PICA involvement and immediate occlusion degree affect aneurysmal recurrence

Background: Glioma is a lethal brain cancer and lacking effective therapies. Challenges include no effective therapeutic target, intra- and intertumoral heterogeneity, inadequate effective drugs, and an immunosuppressive microenvironment, etc. Deciphering the pathogenesis of gliomas and finding out the working mechanisms are urgent and necessary for glioma treatment. Identification of prognostic biomarkers and targeting the biomarker genes will be a promising therapy. Methods: From our RNA-sequencing data of the oxidative phosphorylation (OXPHOS)-inhibition sensitive and OXPHOS-resistant cell lines, we found that the scaffolding protein caveolin 1 (CAV1) is highly expressed in the resistant group but not in the sensitive group. By comprehensive analysis of our RNA sequencing data, Whole Genome Bisulfite Sequencing (WGBS) data and public databases, we found that CAV1 is highly expressed in gliomas and its expression is positively related with pathological processes, higher CAV1 predicts shorter overall survival. Results: Further analysis indicated that (1) the differentiated genes in CAV1-high groups are enriched in immune infiltration and immune response; (2) CAV1 is positively correlated with tumor metastasis markers; (3) the methylation level of CAV1 promoters in glioma group is lower in higher stage than that in lower stage; (4) CAV1 is positively correlated with glioma stemness; (5) higher expression of CAV1 renders the glioma cells’ resistant to oxidative phosphorylation inhibitors. Conclusion: Therefore, we identified a key gene CAV1 and deciphered its function in glioma progression and prognosis, proposing that CAV1 may be a therapeutic target for gliomas. Graphical

Background: Glioma is the most lethal and most aggressive brain cancer, and currently there is no effective treatment. Cancer immunotherapy is an advanced therapy by manipulating immune cells to attack cancer cells and it has been studied a lot in glioma treatment. Targeting the immune checkpoint CD47 or blocking the CD47-SIRPα axis can effectively eliminate glioma cancer cells but also brings side effects such as anemia. Glutaminyl-peptide cyclotransferase-like protein (QPCTL) catalyzes the pyroglutamylation of CD47 and is crucial for the binding between CD47 and SIRPα. Further study found that loss of intracellular QPCTL limits chemokine function and reshapes myeloid infiltration to augment tumor immunity. However, the role of QPCTL in glioma and the relationship between its expression and clinical outcomes remains unclear. Deciphering the role of QPCTL in glioma will provide a promising therapy for glioma cancer immunotherapy.Methods: QPCTL expression in glioma tissues and normal adjacent tissues was primarily analyzed in The Cancer Genome Atlas (TCGA) database, and further validated in another independent cohort from the Gene Expression Omnibus (GEO) database, Chinese Glioma Genome Atlas (CGGA), and Human Protein Atlas (HPA). The relationships between QPCTL expression and clinicopathologic parameters and overall survival (OS) were assessed using multivariate methods and Kaplan-Meier survival curves. And the proteins network with which QPCTL interacted was built using the online STRING website. Meanwhile, we use Tumor Immune Estimation Resource (TIMER) and Gene Expression Profiling Interactive Analysis (GEPIA) databases to investigate the relationships between QPCTL expression and infiltrated immune cells and their corresponding gene marker sets. We analyzed the Differentially Expressed Genes (DEGs) including GO/KEGG and Gene Set Enrichment Analysis (GSEA) based on QPCTL-high and -low expression tumors.Results: In contrast to normal tissue, QPCTL expression was higher in glioma tumor tissue (p < 0.05). Higher QPCTL expression was closely associated with high-grade malignancy and advanced tumor stage. Univariate and multivariate analysis indicated the overall survival of glioma patients with higher QPCTL expression is shorter than those with lower QPCTL expression (p < 0.05). Glioma with QPCTL deficiency presented the paucity of infiltrated immune cells and their matching marker sets. Moreover, QPCTL is essential for glioma cell proliferation and tumor growth and is a positive correlation with glioma cell stemness.Conclusion: High QPCTL expression predicts high grades of gliomas and poor prognosis with impaired infiltration of adaptive immune cells in the tumor microenvironment as well as higher cancer stemness. Moreover, targeting QPCTL will be a promising immunotherapy in glioma cancer treatment.