BRD4 promotes immune escape of glioma cells by upregulating PD-L1 expression.

Purpose: Glioblastoma multiforme (GBM) poses significant challenges in treatment due to its aggressive nature and immune escape mechanisms. Despite recent advances in immune checkpoint blockade therapies, GBM prognosis remains poor. The role of bromodomain and extraterminal domain (BET) protein BRD4 in GBM, especially its interaction with immune checkpoints, is not well understood.

Novel mitochondrial-related gene signature predicts prognosis and immunological status in glioma.

Background: Mitochondria are the center of cellular metabolism. The relationship between mitochondria and diseases has also been studied for a long time. However, the prognostic role of mitochondrial-related genes (MRGs) in patients with glioma and their biological effects are still unclear.

TAK-242 inhibits glioblastoma invasion, migration, and proneural-mesenchymal transition by inhibiting TLR4 signaling.

Resatorvid (TAK-242), a small-molecule inhibitor of Toll-like receptor 4 (TLR4), has the ability to cross the blood-brain barrier (BBB). In this study, we explored the role of TAK-242 on glioblastoma (GBM) invasion, migration, and proneural-mesenchymal transition (PMT). RNA sequencing (RNA-Seq) data and full clinical information of glioma patients were downloaded from the Chinese Glioma Genome Atlas (CGGA) and the Cancer Genome Atlas (TCGA) cohorts and then analyzed using R language; patients were grouped based on proneural (PN) and mesenchymal (MES) subtypes.

Suberanilohydroxamic acid (SAHA), a HDAC inhibitor, suppresses the effect of Treg cells by targeting the c-Myc/CCL1 pathway in glioma stem cells and improves PD-L1 blockade therapy.

Purpose: A strong immunosuppressive tumor microenvironment (TME) represents the major barrier responsible for the failure of current immunotherapy approaches in treating Glioblastoma Multiforme (GBM). Within the TME, the regulatory T cells (Tregs) exert immunosuppressive effects on CD8 T cell - mediated anti-cancer immune killing. Consequently, targeting and inhibiting their immunosuppressive function emerges as an effective therapeutic strategy for GBM.

Metformin-induced reduction of CCR8 enhances the anti-tumor immune response of PD-1 immunotherapy in glioblastoma.

Immunotherapy strategies targeting the programmed cell death 1 (PD-1) in clinical treatments have shown limited success in controlling glioblastoma malignancies. Metformin exserts antitumor function, yet the underlying mechanisms remain unclear. Here, we investigated whether metformin could enhance the effectiveness of anti-PD-1 therapy by activating the immune system.

Retrospective analysis of 16 cases of lumbar hernia.

Background: Through a retrospective analysis of 16 cases of lumbar hernia, we discussed the anatomical basis, clinical manifestations, diagnosis, and treatment of this rare condition.

Methods: We collected medical data of 15 patients with a primary lumbar hernia and one patient with a secondary lumbar hernia treated in the General Surgery Department of Wuxi No.2 People's Hospital between January 2008 and June 2021 and analysed their demographic, preoperative, and postoperative data.

Targeting EZH2 regulates the biological characteristics of glioma stem cells via the Notch1 pathway.

Glioma is the most common malignant brain tumor, and its behavior is closely related to the presence of glioma stem cells (GSCs). We found that the enhancer of zeste homolog 2 (EZH2) is highly expressed in glioma and that its expression is correlated with the prognosis of glioblastoma multiforme (GBM) in two databases: The Cancer Genome Atlas and the Chinese Glioma Genome Atlas. Additionally, EZH2 is known to regulate the stemness-associated gene expression, proliferation, and invasion ability of GSCs, which may be achieved through the activation of the STAT3 and Notch1 pathways.

Fractalkine Enhances Hematoma Resolution and Improves Neurological Function via CX3CR1/AMPK/PPARγ Pathway After GMH.

Background: Hematoma clearance has been a proposed therapeutic strategy for hemorrhagic stroke. This study investigated the impact of CX3CR1 (CX3C chemokine receptor 1) activation mediated by r-FKN (recombinant fractalkine) on hematoma resolution, neuroinflammation, and the underlying mechanisms involving AMPK (AMP-activated protein kinase)/PPARγ (peroxisome proliferator-activated receptor gamma) pathway after experimental germinal matrix hemorrhage (GMH).

Methods: A total of 313 postnatal day 7 Sprague Dawley rat pups were used.

G9a promotes immune suppression by targeting the Fbxw7/Notch pathway in glioma stem cells.

Aim: Immunotherapy for glioblastoma multiforme (GBM) is limited because of a strongly immunosuppressive tumor microenvironment (TME). Remodeling the immune TME is an effective strategy to eliminate GBM immunotherapy resistance. Glioma stem cells (GSCs) are inherently resistant to chemotherapy and radiotherapy and involved in immune evasion mechanism.

Heat shock protein 27 deficiency promotes ferrous ion absorption and enhances acyl-Coenzyme A synthetase long-chain family member 4 stability to promote glioblastoma cell ferroptosis.

Background: Glioblastoma is one of the malignant tumors of the central nervous system with high lethality, high disability and low survival rate. Effective induction of its death is one of the existing challenges. In recent studies, heat shock protein 27 (HSP27) has been shown to be associated with ferroptosis; therefore, targeting HSP27 may be a potential therapeutic approach for GBM.

General Characteristics and Promotion Properties of Circular PLOD2 in Patients with Glioma.

Background: Circular RNAs are closed endogenous RNAs that are involved in the progression of diverse tumors. Even with the most advanced combined treatments, patients with glioblastoma multiforme have a median survival time of <15 months. This study aimed to investigate the roles of circular PLOD2 (circPLOD2) in glioma tumorigenesis and tumor development and to clarify its tumor-promoting effects by bioinformatics analysis and molecular experiments.

Experimental study of selective MGMT peptides mimicking TMZ drug resistance in glioma.

Background: Glioblastoma (GBM) is a very frequent primary tumour in the cerebrospinal nervous system. Temozolomide (TMZ) is the first-line treatment for patients with GBM. However, some of GBM patients do not respond to TMZ.

[Retracted] miR‑218‑5p inhibits the stem cell properties and invasive ability of the A2B5CD133 subgroup of human glioma stem cells.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that Fig. 5 on p. 874 contained a series of DAPI panels within the figure that looked unexpectedly similar in appearance, with the similarities also evident in the second and 'Merge' data columns; moreover, of especial note, the similarities in the 'DAPI' panels for the Blank control experiments shown in Fig.

[Corrigendum] Downregulation of RNF138 inhibits cellular proliferation, migration, invasion and EMT in glioma cells via suppression of the Erk signaling pathway.

Following the publication of the above paper, during a routine examination of the raw data the authors noticed errors in Fig. 5 in the published version of the article. Essentially, in Fig.

Anti-VEGFR2 monoclonal antibody(MSB0254) inhibits angiogenesis and tumor growth by blocking the signaling pathway mediated by VEGFR2 in glioblastoma.

Angiogenesis is a key physiological process that plays a key role in glioblastoma (GBM) progression and displays therapeutic resistance to antiangiogenic therapies. In this study, we aimed to identify whether vascular endothelial growth factor receptor 2(VEGFR2)monoclonal antibodies(mab)could inhibit tumorigenicity and the formation of vascular mimicry (VM) in GBM. The bioinformatic analysis from TCGA, CGGA, and TCPA databases and Immunohistochemistry (IHC) revealed that VEGFR2 is highly expressed in glioma tissues and results in a poor prognosis and is positively associated with VM markers (CD34 and PAS).

Glioma Stem Cells Upregulate CD39 Expression to Escape Immune Response through SOX2 Modulation.

Ectonucleotidase CD39 hydrolyzing extracellular ATP (eATP) functions as a key modulator of immune response in the tumor microenvironment, yet the role of CD39 in contributing tumor stem cells in a more immunosuppressive microenvironment remains elusive. Here we report that the upregulation of CD39 is crucial for the decrease of extracellular ATP concentration around glioma stem cells (GSCs) to maintain an immunosuppressive microenvironment. Adriamycin (ADM) is able to promote the release of ATP, which recruits dendritic cells (DCs) to phagocytose GSCs.

Previously Unrecognized Nonreproducible Antibody-Probe Interactions.

Antibody-antigen (Ab-Ag) interactions are canonically described by a model that exclusively accommodates noninteraction (0) or reproducible interaction (RI) states, yet this model is inadequate to explain often-encountered nonreproducible signals. Here, by monitoring diverse experimental systems using a peptide-protein hybrid microarray, we observed that Ab-probe interactions comprise a substantial proportion of nonreproducible antibody-based results. This enabled our discovery and capacity to reliably identify nonreproducible Ab-probe interactions (NRIs), as well as our development of a powerful explanatory model ("0-NRI-RI-Hook four-state model") that is mAb concentration-dependent, regardless of specificity, which ultimately shows that both nonspecific interactions and NRIs are not predictable yet certain to happen.

Spatial Dissection of Invasive Front from Tumor Mass Enables Discovery of Novel microRNA Drivers of Glioblastoma Invasion.

Diffuse invasion is the primary cause of treatment failure of glioblastoma (GBM). Previous studies on GBM invasion have long been forced to use the resected tumor mass cells. Here, a strategy to reliably isolate matching pairs of invasive (GBM ) and tumor core (GBM ) cells from the brains of 6 highly invasive patient-derived orthotopic models is described.

USP7 inhibition induces apoptosis in glioblastoma by enhancing ubiquitination of ARF4.

Background: Glioblastomas (GBMs) are grade IV central nervous system tumors characterized by a poor prognosis and a short median overall survival. Effective induction of GBM cell death is difficult because the GBM cell population is genetically unstable, resistant to chemotherapy and highly angiogenic. In recent studies, ubiquitin-specific protease 7 (USP7) is shown to scavenge ubiquitin from oncogenic protein substrates, so effective inhibition of USP7 may be a potential key treatment for GBM.

LncRNA-PVT1 indicates a poor prognosis and promotes angiogenesis via activating the HNF1B/EMT axis in glioma.

Recent studies identified that long non-coding RNAs (lncRNAs) exhibited critical roles in tumor migration and invasion. However, the roles of lncRNAs in glioma remain unclear. The aim of this study was to uncover the underlying mechanisms of glioma progression and provide potential therapeutic targets for its treatment in clinic.

Clinical study of apatinib plus temozolomide for the treatment of recurrent high-grade gliomas.

Objectives: Recurrent high-grade glioma, a malignant tumor of the brain or spinal cord associated with poor prognosis with a median survival of <6 months. Recurrent high-grade glioma does not have standard treatment even if some strategies have some effect in recurrent gliomas. Apatinib, as a tyrosine kinase inhibitor shown to be effective in treating the lung and gastric cancer.

TSHZ3 functions as a tumor suppressor by DNA methylation in colorectal cancer.

Objective: Teashirt zinc finger homeobox 3 (TSHZ3) is currently reported to be aberrantly expressed in several tumors, but the detailed functions and epigenetic mechanisms of TSHZ3 in colorectal cancer (CRC) remain unclear.

Materials And Methods: In this study, the TSHZ3 expression in 118 CRC and normal adjacent tissues (NATs) was evaluated, and the methylation status of the TSZH3 promoter region in CRC tissues and cell lines was also analyzed.

Results: The results of PCR analysis showed that TSHZ3 was significantly down-regulated in CRC tissues, and patients with low TSHZ3 levels had a poorer 5-year overall survival (OS) rate.