Topic: gliomas

Gliomas are brain tumors formed by networks of connected tumor cells, nested in and interacting with neuronal networks. Neuronal activities interfere with tumor growth and occurrence of seizures affects glioma prognosis, while the developing tumor triggers seizures in the infiltrated cortex. Oncometabolites produced by tumor cells and neurotransmitters affect both the generation of epileptic activities by neurons and the growth of glioma cells through synaptic-related mechanisms, involving both GABAergic / Chloride pathways and glutamatergic signaling. From a clinical sight, epilepsy occurrenc

Introduction: Early diagnosis and classification of brain tumours are crucial to enable decisive early treatment and improve patient outcomes. Misdiagnosed brain malignancies can result in incorrect medical interventions, reducing patient survival. Computer-aided diagnostic systems incorporated with artificial intelligence techniques can be used as a robust clinical decision support system to improve brain tumour diagnosis. Aim: We aim to develop an artificial intelligence algorithm to classify MRI images into different brain tumours. Methodology: We used 7022 T1-weighted MRI scans compri

Gliomas, the heterogeneous primary brain tumors lacking efficient treatment, interact with their tumor microenvironment (TME) and the central nervous system (CNS) resident cells to support their own survival and growth. Deeper knowledge on these interactions is needed to improve treatment, and therefore glioma models incorporating components of human TME are of great interest. The aim of this work was to develop a three-dimensional (3D) in vitro coculture model for assessing physical and functional neuro-glioma interactions. For that, human glioblastoma cell line LN229/GFP-derived spheroids we

Gliomas constitute a heterogeneous group of primary brain cancers, being glioblastoma (GBM) the most prevalent and aggressive form. Despite intensive research, current biomarkers and therapies are still not applied in a personalized manner, and do not prevent recurrency. H3.3 is a non-canonical, replication-independent histone H3 variant which alterations have gain- and loss-of-function effects in pediatric and adult GBM, respectively. The canonical replication-dependent H3.1/H3.2 variants remain largely unexplored in gliomas. We examined these variants in surgical resections of two independen

Social cognition refers to a range of processes that allow us to make sense of others' behaviors and engage in daily interactions. A key network supporting social cognition is the mirror neuron system (MNS), a set of fronto-parietal regions that allows inferring others' intentions through action observation. The MNS exhibits considerable plasticity based on an individual's motor repertoire, but little is known about its potential for reorganization in the presence of brain damage. To address this gap, we investigated the adaptive capacity of the MNS in patients with gliomas affecting key netwo

WNT signaling is aberrantly activated in human tumors including gliomas. Promoter methylation and expression of WNT pathway’s negative regulators, DKK1 and DKK3, and positive, GSK3β, together with two signaling antagonists, SFRP1 and SFRP3, were investigated in human gliomas. Gliomas, paired blood and FFPE slides were collected with patients’ consents and classified according to WHO guidelines. Methylation-specific-PCR was used for promoter analyses, while immunohistochemistry and semi-quantitative score for consequent protein expressions. Different promoter methylation frequencies were observ

Introduction:The glycoprotein clusterin (CLU) plays a pivotal role in vital cellular functions, including cell proliferation and DNA damage repair. Its frequent overexpression in tumor cells, particularly in gliomas, positions it as a promising therapeutic target. This study aims to investigate the impact of CLU dysregulation on glioma cell lines and explore its therapeutic potential. Methods:Two human astrocytic cell lines, CCF-STTG1 astrocytoma cells, and SV-40 immortalized normal human astrocytes, were utilized in our investigation. CLU expression was suppressed using transient siRNA transf