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1.
Front Immunol ; 12: 679425, 2021.
Article in English | MEDLINE | ID: covidwho-1344264

ABSTRACT

Gliomas are the most common primary brain tumors in adults. Despite the fact that they are relatively rare, they cause significant morbidity and mortality. High-grade gliomas or glioblastomas are rapidly progressing tumors with a very poor prognosis. The presence of an intrinsic immune system in the central nervous system is now more accepted. During the last decade, there has been no major progress in glioma therapy. The lack of effective treatment for gliomas can be explained by the strategies that cancer cells use to escape the immune system. This being said, immunotherapy, which involves blockade of immune checkpoint inhibitors, has improved patients' survival in different cancer types. This novel cancer therapy appears to be one of the most promising approaches. In the present study, we will start with a review of the general concept of immune response within the brain and glioma microenvironment. Then, we will try to decipher the role of various immune checkpoint inhibitors within the glioma microenvironment. Finally, we will discuss some promising therapeutic pathways, including immune checkpoint blockade and the body's effective anti-glioma immune response.


Subject(s)
Brain Neoplasms/drug therapy , Brain Neoplasms/pathology , Glioma/drug therapy , Glioma/pathology , Immune Checkpoint Inhibitors/therapeutic use , Tumor Microenvironment/drug effects , Biomarkers, Tumor , Brain/drug effects , Brain/immunology , Brain/metabolism , Brain/pathology , Brain Neoplasms/etiology , Brain Neoplasms/mortality , Disease Susceptibility , Glioma/etiology , Glioma/mortality , Humans , Immune Checkpoint Inhibitors/administration & dosage , Immune Checkpoint Inhibitors/adverse effects , Immune Checkpoint Proteins/genetics , Immune Checkpoint Proteins/metabolism , Molecular Targeted Therapy , Prognosis , Treatment Outcome , Tumor Microenvironment/genetics , Tumor Microenvironment/immunology
2.
Int J Mol Sci ; 22(13)2021 Jun 29.
Article in English | MEDLINE | ID: covidwho-1304666

ABSTRACT

Epilepsy can be both a primary pathology and a secondary effect of many neurological conditions. Many papers show that neuroinflammation is a product of epilepsy, and that in pathological conditions characterized by neuroinflammation, there is a higher probability to develop epilepsy. However, the bidirectional mechanism of the reciprocal interaction between epilepsy and neuroinflammation remains to be fully understood. Here, we attempt to explore and discuss the relationship between epilepsy and inflammation in some paradigmatic neurological and systemic disorders associated with epilepsy. In particular, we have chosen one representative form of epilepsy for each one of its actual known etiologies. A better understanding of the mechanistic link between neuroinflammation and epilepsy would be important to improve subject-based therapies, both for prophylaxis and for the treatment of epilepsy.


Subject(s)
Disease Susceptibility , Epilepsy/etiology , Inflammation/complications , Animals , Biomarkers , Brain Neoplasms/complications , Brain Neoplasms/etiology , Brain Neoplasms/pathology , Combined Modality Therapy , Disease Management , Epilepsy/diagnosis , Epilepsy/metabolism , Epilepsy/therapy , Genetic Predisposition to Disease , Humans , Inflammation/etiology , Neurodegenerative Diseases/complications , Neurodegenerative Diseases/etiology , Neurodegenerative Diseases/pathology , Symptom Assessment , Treatment Outcome
3.
Balkan Med J ; 37(1): 208-214, 2020 06 01.
Article in English | MEDLINE | ID: covidwho-826668

ABSTRACT

Background: Brain metastasis is a major cause of cancer death in patients with lung cancer. Sirtuin 1 and hsa-miR-217 have been identified to mediate the development of non-small cell lung cancer. Aims: To investigate the roles of hsa-miR-217, its target sirtuin 1, and the P53/KAI1 axis in the brain metastasis from non-small cell lung cancer. Study Design: Cell culture study. Methods: Human pulmonary adenocarcinoma brain metastasis cell line PC-14/B were incubated and treated with constructed lentiviral plasmids expressing miR-217 and/or sirtuin 1. BEAS-2B cell line was used as a control. The targeted regulation of miR-217 to sirtuin 1was examined using a dual-luciferase reporter assay. Cell proliferation, migration, invasion, and related protein expression were detected to examine the effect of the miR-217/sirtuin 1 expression on metastasis. Results: PC-14/B cells expressed higher sirtuin 1 and lower P53 and KAI1 compared with BEAS-2B control cells (p<0.05). Sirtuin 1 was a direct target of miR-217. MiR-217 expression suppressed PC-14/B cell invasion (p=0.004), migration (p=0.001), and proliferation (p<0.05), whereas sirtuin 1 overexpression reversed all processes. sirtuin 1 expression inhibited P53, KAI1/CD82, matrix metalloproteinase-9, and ß-catenin but upregulated E-cadherin protein. MiR-217 overexpression induced reverse changes. Conclusion: Hsa-miR-217 and its target sirtuin 1 acted as metastasis suppressor and promoter gene in non-small cell lung cancer, respectively. The hsa-miR-217/sirtuin 1/P53/KAI1 metastasis regulatory pathway showed novel and crucial roles in brain metastasis from non-small cell lung cancer. This axis might be a potential target for the treatment of brain metastasis of lung cancer.


Subject(s)
Carcinoma, Non-Small-Cell Lung/drug therapy , Kangai-1 Protein/drug effects , MicroRNAs/pharmacology , Sirtuin 1/drug effects , Tumor Suppressor Protein p53/drug effects , Brain Neoplasms/etiology , Brain Neoplasms/physiopathology , Brain Neoplasms/prevention & control , Carcinoma, Non-Small-Cell Lung/physiopathology , Cell Culture Techniques/methods , Cell Proliferation/drug effects , Humans , MicroRNAs/therapeutic use , Signal Transduction/drug effects
4.
Med Hypotheses ; 144: 110009, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-611692

ABSTRACT

The outbreak of Novel Coronavirus 2019 (COVID-19) represents a global threat to the public healthcare. The viral spike (S) glycoprotein is the key molecule for viral entry through interaction with angiotensin converting enzyme 2 (ACE2) receptor molecules present on the cell membranes. Moreover, it has been established that COVID-19 interacts and infects brain cells in humans via ACE2. Therefore in the light of these known facts we hypothesized that viral S protein molecule may bind to the other overexpressed receptor molecules in glioma cells and may play some role in glioma tumorogenesis. Thus we leverage docking analysis (HEX and Z-DOCK) between viral S protein and epidermal growth factor receptors (EGFR), vascular endothelial growth factor receptors (VEGFR) and hepatocyte growth factor receptors (HGFR/c-MET) to investigate the oncogenic potential of COVID-19. Our findings suggested higher affinity of Viral S protein towards EGFR and VEGFR. Although, the data presented is preliminary and need to be validated further via molecular dynamics studies, however it paves platform to instigate further investigations on this aspect considering the aftermath of COVID-19 pandemic in oncogenic perspective.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , Brain Neoplasms/etiology , COVID-19/complications , Glioma/etiology , Neoplasm Proteins/metabolism , Proto-Oncogene Proteins c-met/metabolism , Receptors, Vascular Endothelial Growth Factor/metabolism , SARS-CoV-2/pathogenicity , Spike Glycoprotein, Coronavirus/metabolism , Virus Internalization , Angiotensin-Converting Enzyme 2/chemistry , Angiotensin-Converting Enzyme 2/genetics , Brain/virology , Brain Neoplasms/genetics , Brain Neoplasms/metabolism , Cell Transformation, Neoplastic , ErbB Receptors/chemistry , ErbB Receptors/metabolism , Glioma/genetics , Glioma/metabolism , Humans , Models, Molecular , Molecular Docking Simulation , Neoplasm Proteins/genetics , Nerve Tissue Proteins/chemistry , Nerve Tissue Proteins/metabolism , Protein Binding , Protein Conformation , Proto-Oncogene Proteins c-met/chemistry , Receptors, Vascular Endothelial Growth Factor/chemistry , SARS-CoV-2/metabolism , Up-Regulation
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