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Purpose: Glioblastoma is a malignant brain tumor which has one of the poorest prognosis. It is not clear if toxic environmental factors can influence its aggressiveness. Recently, it was suggested that brain cancer patients with heavy cell phone use showed reduced survival. Here we aimed to assess the effect of controlled brain averaged specific absorption rate (BASAR) from heavy use of cell phone radiofrequency electromagnetic fields (RF-EMF) on in vivo C6 brain tumors in Wistar rats.
Methods: C6 cells grafted male rats were exposed to GSM 900 MHz signal at environmental BASAR, 0 (sham), 0.25 or 0.5 W/kg (5 days a week, 45 min a day in restraint), or were cage controls (no restraint). At death, tumor volume and immunohistochemistry for CD31, cleaved caspase (CC) 3 and Ki67 were assessed to examine vascularization, apoptosis and cellular divisions, respectively. Moreover, immune cell invasion, necrosis and mitotic index were determined.
Results: Results showed no BASAR effect on survival (31 days post-graft median), tumor volume, mitotic index, vascularization, infiltration, necrosis or cell division. However, results suggested a BASAR-dependent reduction of immune cell invasion and apoptosis.
Conclusions: Our data suggested an action of RF-EMF by reducing immune cell invasion and glioblastoma cell apoptosis, at probably too low amplitude to impact survival. Further replication studies are needed to confirm these observations.
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http://dx.doi.org/10.1007/s11060-018-03012-y | DOI Listing |
Future Oncol
September 2025
Department of General Surgery, Institute of General Surgery, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou University, Yangzhou, China.
Immune checkpoint therapy has demonstrated significant potential in the treatment of various solid tumors. Among these, tumor-induced immunosuppression mediated by programmed cell death protein 1 (PD-1) represents a critical checkpoint. PD-1/programmed death-ligand 1 (PD-L1) inhibitors have been proven to exhibit substantial efficacy in solid tumors such as melanoma and bladder cancer.
View Article and Find Full Text PDFRev Med Liege
September 2025
Service de Diabétologie, Nutrition et Maladies métaboliques, CHU Liège, Belgique.
Type 1 diabetes (T1D) is an autoimmune chronic disease that leads to the destruction of pancreatic beta cells and thus requires lifelong insulin therapy. Constraints and adverse events associated to insulin therapy are well known as well as the risk of long-term complications linked to chronic hyperglycaemia. Symptomatic T1D is preceded by a preclinical asymptomatic period, which is characterized by the presence of at least two auto-antibodies against beta cell without disturbances of blood glucose control (stage 1) or, in addition to immunological biomarkers, by the presence of mild dysglycaemia reflecting a defect of early insulin secretion (stage 2).
View Article and Find Full Text PDFJ Neurochem
September 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Microglia, the resident immune cells of the central nervous system (CNS), are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), and Parkinson's disease (PD). 14-3-3 proteins act as molecular hubs to regulate protein-protein interactions, which are involved in numerous cellular functions, including cellular signaling, protein folding, and apoptosis. We previously revealed decreased 14-3-3 levels in the brains of human subjects with neurodegenerative diseases.
View Article and Find Full Text PDFCNS Neurosci Ther
September 2025
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Aims: Sustained neuroinflammation following ischemic stroke impedes post-injury tissue repairment and neurological functional recovery. Developing innovative therapeutic strategies that simultaneously suppress detrimental inflammatory cascades and facilitate neurorestorative processes is critical for improving long-term rehabilitation outcomes.
Methods: We employed a microglia depletion-repopulation paradigm by administering PLX5622 for 7 days post-ischemia; followed by a 7-day withdrawal period to allow microglia repopulation.
Brain Behav
September 2025
School of Pharmacy and Medical Technology, Putian University, Putian, China.
Background: Recent research has started to uncover an important connection between immune system activity and cognitive abilities. Although correlative associations have been documented, the causal mechanisms connecting specific immune cell subpopulations to cognitive capabilities remain insufficiently characterized. Our research aimed to determine directional relationships between distinct immune cell subtypes and cognitive function, potentially identifying targets for immunomodulatory interventions.
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