Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a woman who had a total resection of a cardiac myxoma followed 8 months later by a hemorrhage in the right frontal lobe secondary to extravascular metastasis of the myxoma. Six years later, after an asymptomatic follow-up, she developed a recurrence of left-sided seizures and an enhancing mass in the same location as the previous tumor. At operation, a malignant astrocytoma was demonstrated. Cardiac myxoma is a true neoplasm with benign histology, which may be associated with heart failure, systemic illness, or peripheral embolization. The neurological manifestations of embolization may include no symptoms, acute or delayed infarction, and intravascular proliferation with aneurysmal dilatation and potential for hemorrhage. The development of extravascular metastatic tumor deposits has been reported previously in only three histologically verified cases. Once the integrity of the blood vessel wall is destroyed by the tumor, a portal of entry is established for tumor cell proliferation in the brain parenchyma. There is no known association between a metastatic cardiac myxoma and a malignant glioma in the literature. Several possibilities for the occurrence of these two neoplasms are discussed.
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PMID:Malignant astrocytoma six years after the resection of a cerebral metastatic cardiac myxoma: case report. 161 97

The impaired inotropic responsiveness of myocardial tissue to catecholamines in congestive heart failure has been ascribed to downregulation of beta-adrenergic receptors. It has been reported recently that resistance to catecholamines is related to a defect in the guanine nucleotide binding protein that couples the beta-adrenergic receptor to adenylate cyclase. Studies of beta-adrenergic receptors were carried out using three different experimental protocols: (a) the interactions of the atypical agonists pindolol and celiprolol with beta-adrenergic receptors from C6 glioma cells (40% beta 1, 60% beta 2) were compared with those of the full agonist isoproterenol; (b) the ability of pindolol, celiprolol, and isoproterenol to induce downregulation and sequestration of beta-adrenergic receptors in wild-type S49 lymphoma cells was compared with the responses observed with a mutant line of S49 cells (cyc-, which lack Gs activity); and (c) the differential response of patients with heart failure and age-matched control subjects to exercise-induced changes in the density of beta-adrenergic receptors and isoproterenol-stimulated adenylate cyclase activity on circulating lymphocytes was investigated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of downregulation of beta-adrenergic receptors: perspective on the role of beta-adrenergic receptors in congestive heart failure. 247 5

Four examples of astrocytic tumorettes (microscopic to minute foci of glioma) are described herein. They include one malignant astrocytoma and three low grade astrocytomas. The first patient, who died of heart failure, was found incidentally to havour a small malignant astrocytoma at the time of autopsy. The other three patients with astrocytomas of low grade in malignancy, ranged from 18 to 25 years in age, and presented with intractable seizures. Electroencephalography defined a temporal lobe focus in all three patients. Subsequently, all three underwent a unilateral temporal lobectomy with resection of the epileptic focus. Careful histological examinations on the removed tissues from each patient revealed that each of them had a minute astrocytoma. The histogenesis of benign and malignant astrocytomas and the importance of surgical exploration in the management of the patients with intractable seizure disorders are discussed.
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PMID:Astrocytic tumorette: microscopic to minute foci of glioma unexpectedly found in autopsy or surgical specimens. 345 65

A newborn is described who presented with heart failure from a posterior dural arteriovenous malformation and had a coexisting congenital medulloblastoma. There have been sporadic reports of arteriovenous malformation and brain neoplasms in older children and adults, and these have generally been glial tumors. This is the first known case of a combined congenital primitive neuroectodermal tumor and arteriovenous malformation in an infant.
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PMID:Posterior dural arteriovenous malformation and medulloblastoma in an infant: case report. 842 41

Because both imipramine and citalopram have been commonly used to treat depression, which commonly occurs in glioma patients, it would be interesting to conduct large epidemiological studies to investigate the actual benefit that these two drugs would provide for malignant glioma patients when delivered during their glioma treatment. Such large-scale epidemiological studies have recently revealed the actual benefit provided by digoxin, a Na+/K+ ATPase inhibitor used to treat heart failure, in prostate cancer patients treated for both prostate cancer and heart failure.
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PMID:Voltage-dependent K+ channels as oncotargets in malignant gliomas. 2269 12

Glioblastoma multiforme is the most lethal and aggressive astrocytoma among primary brain tumors in adults. However, most glioblastoma cells have been reported to be resistant to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Here, we have shown that digitoxin (DT), a clinically approved cardiac glycoside for heart failure, can induce TRAIL-mediated apoptosis of glioblastoma cells. DT in noncytotoxic doses (20 nmol/l) can increase TRAIL-induced apoptosis in TRAIL-resistant U87MG glioblastoma cells. Treatment with DT led to apoptosis and a robust reduction in the levels of the antiapoptotic protein survivin by inducing its proteasomal degradation; however, it did not affect the levels of many other apoptosis regulators. Moreover, silencing survivin with small interfering RNAs sensitized glioma cells to TRAIL-induced apoptosis, underscoring the functional role of survivin depletion in the TRAIL-sensitizing actions of DT. We demonstrate that inactivation of survivin and death receptor 5 expression by DT is sufficient to restore TRAIL sensitivity in resistant glioma cells. Our results suggest that combining DT with TRAIL treatments may be useful in the treatment of TRAIL-resistant glioma cells.
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PMID:Digitoxin sensitizes glioma cells to TRAIL-mediated apoptosis by upregulation of death receptor 5 and downregulation of survivin. 2404 65

Cardiac glycosides induce apoptotic effects on glioma cells, but whether cardiac glycosides protect against risk for glioma is unknown. We therefore explored the relation between glycoside use and glioma risk using a large and validated database. We performed a case-control analysis using the Clinical Practice Research Datalink involving 2005 glioma cases diagnosed between 1995 and 2012 that were individually matched to 20,050 controls on age, gender, general practice, and number of years of active history in the database. Conditional logistic regression analysis was used to evaluate the association between cardiac glycosides and the risk of glioma adjusting for body mass index and smoking. We also examined use of common heart failure and arrhythmia medications to differentiate between a specific glycoside effect and a generic effect of treatment for congestive heart failure or arrhythmia. Cardiac glycoside use was inversely related to glioma incidence. After adjustment for congestive heart failure, arrhythmia, diabetes, and common medications used to treat those conditions, the OR of glioma was 0.47 (95% CI 0.27-0.81, Bonferroni-corrected p value = 0.024) for use versus non-use of cardiac glycosides, based on 17 exposed cases. In contrast, no associations were noted for other medications used to treat congestive heart failure or arrhythmias. The OR of glioma in people with congestive heart failure was 0.65 (95% CI 0.40-1.04), and for arrhythmia it was 1.01 (95% CI 0.78-1.31). These data indicate that cardiac glycoside use is independently associated with reduced glioma risk.
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PMID:Use of cardiac glycosides and risk of glioma. 2672 Dec 42

Carbon monoxide (CO) is well-known as toxic gas and intrinsic signaling molecule such as neurotransmitter and blood vessel relaxant. Recently, it has been reported that low concentration of CO exerts therapeutic actions under various pathological conditions including liver failure, heart failure, gastric cancer, and cardiac arrest. However, little has been known about the effect of CO in neurodegenerative diseases like Parkinson's disease (PD). To test whether CO could exert a beneficial action during oxidative cell death in PD, we examined the effects of CO on 6-hydroxydopamine (6-OHDA)-induced cell death in C6 glioma cells. Treatment of CO-releasing molecule-2 (CORM-2) significantly attenuated 6-OHDA-induced apoptotic cell death in a dose-dependent manner. CORM-2 treatment decreased Bax/Bcl2 ratio and caspase-3 activity, which had been increased by 6-OHDA. CORM-2 increased phosphorylation of NF-E2-related factor 2 (Nrf2) which is a transcription factor regulating antioxidant proteins. Subsequently, CORM-2 also increased the expression of heme oxygenase-1 and superoxide dismutases (CuZnSOD and MnSOD), which were antioxidant enzymes regulated by Nrf2. These results suggest that CO released by CORM-2 treatment may have protective effects against oxidative cell death in PD through the potentiation of cellular adaptive survival responses via activation of Nrf2 and upregulation of heme oxygenase-1, leading to increasing antioxidant defense capacity.
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PMID:Carbon Monoxide Ameliorates 6-Hydroxydopamine-Induced Cell Death in C6 Glioma Cells. 2942 49