ArticleEpilepsia2012
Overexpression of ADK in human astrocytic tumors and peritumoral tissue is related to tumor-associated epilepsy.
Article in Epilepsia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 87 citations in OpenAlex.
- Adenosine Signaling in Primary and Metastatic Brain Tumors: Immune Suppression, Tumor Progression, and Therapeutic Opportunities.Molecular neurobiology · 2026Review
- Therapeutic Potential Target of Adenosine for Epilepsy: Focusing on Its Interaction with the Molecular Epileptogenic Network.Biomolecules · 2026Review
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- Research progress in glioma-related epilepsy (Review).Biomedical reports · 2025Article
- The molecular landscape of glioblastoma-associated epilepsy.Journal of molecular medicine (Berlin, Germany) · 2025Review
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- Clinico-genetic Analysis of Adenosine Signaling Pathway in Drug-Resistant Epilepsy.Annals of Indian Academy of Neurology · 2025Article
- Multi-omics technologies and molecular biomarkers in brain tumor-related epilepsy.CNS neuroscience & therapeutics · 2024Review
- NLRs and inflammasome signaling in opioid-induced hyperalgesia and tolerance.Inflammopharmacology · 2024Review
- Upregulated PPP1R14B is connected to cancer progression and immune infiltration in kidney renal clear cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- Aberrant adenosine signaling in patients with focal cortical dysplasia.Molecular neurobiology · 2023Article
- Neuroinflammation in epileptogenesis: from pathophysiology to therapeutic strategies.Frontiers in immunology · 2023Review
- The Interaction Between Sleep and Epilepsy.Current neurology and neuroscience reports · 2022Review
- ATP and Adenosine Metabolism in Cancer: Exploitation for Therapeutic Gain.Pharmacological reviews · 2022Review
- NLRP3 Inflammasome Activation Enhances ADK Expression to Accelerate Epilepsy in Mice.Neurochemical research · 2022Article
- Adenosine Kinase on Deoxyribonucleic Acid Methylation: Adenosine Receptor-Independent Pathway inFrontiers in pharmacology · 2022Review
- Metabolic Aspects of Adenosine Functions in the Brain.Frontiers in pharmacology · 2021Review
- Adenosine and Ketogenic Treatments.Journal of caffeine and adenosine research · 2020Review
- Epigenetics and epilepsy prevention: The therapeutic potential of adenosine and metabolic therapies.Neuropharmacology · 2020Review
- Loss of FBXO9 Enhances Proteasome Activity and Promotes Aggressiveness in Acute Myeloid Leukemia.Cancers · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
purposeAdenosine kinase (ADK), a largely astrocyte-based metabolic enzyme, regulates adenosine homeostasis in the brain. Overexpression of ADK decreases extracellular adenosine and consequently leads to seizures. We hypothesized that dysfunction in the metabolism of tumor astrocytes is related to changes in ADK expression and that those changes might be associated with the development of epilepsy in patients with tumors.
methodsWe compared ADK expression and cellular distribution in surgically removed tumor tissue (n = 45) and peritumoral cortex (n = 20) of patients with glial and glioneuronal tumors to normal control tissue obtained at autopsy (n = 11). In addition, we compared ADK expression in tumor patients with and without epilepsy. To investigate ADK expression, we used immunohistochemistry and Western blot analysis. ADK activity measurement was performed in surgical specimens of astrocytomas World Health Organization (WHO) grade III (n = 3), peritumoral cortex (n = 3), and nonepileptic cortex (n = 3). KEY
findingsImmunohistochemistry predominantly showed cytoplasmic labeling in tumors and peritumoral tissue containing infiltrating tumor cells. ADK immunoreactivity was significantly stronger in tumor and peritumoral tissue compared to normal white matter and normal cortex, especially in astrocytoma WHO grade III, as confirmed by Western blot analysis and ADK activity measurements. Importantly, we found a significantly higher expression of ADK in the peritumoral infiltrated tissue of patients with epilepsy than in patients without epilepsy. SIGNIFICANCE: These results suggest a dysregulation of ADK in astrocytic brain tumors. Moreover, the upregulation of ADK observed in peritumoral infiltrated tissue of glioma patients with epilepsy supports the role of this enzyme in tumor-associated epilepsy.
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