Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is a well-known finding in some patients with neuroblastoma. However, it has not previously been described in association with the use of Imipramine. We report the occurrence of severe hypertension (blood pressure 190/160) in a 4-year-old girl with neuroblastoma who was given Imipramine to control a behavior disorder. It was determined later that this patient's tumor was recurring at the time of her hypertensive episode. Since she had no blood pressure elevation at initial diagnosis and none following discontinuation of the Imipramine (when she was in florid relapse), we believe that this drug rather than her underlying disease alone caused her hypertension. The mechanism for this reaction is believed to be increased levels of vasoactive catecholamines due to interference of their physiologic inactivation by Imipramine. From this experience, we urge extreme caution in the use of tricyclic antidepressants in children with active neuroblastoma.
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PMID:Hypertension in neuroblastoma induced by imipramine. 343 80

Dysembryoplastic neuroepithelial tumor (DNT) is a clinicopathologically unique group of tumors, mostly located in the temporal lobe, associated with intractable complex partial seizure in young patients. We report two unusual cases with multifocal involvement of diverse sites in the central nervous system. Case 1 is that of a 50-year-old man with 9-year history of grand mal seizures, who died of acute myocardial infarction. Case 2 is that of a 10-year-old girl with intractable complex partial seizures and behavioral disorder. Postmortem examination in case 1 showed multifocal tumor in the left temporal lobe, third ventricle, and basal ganglia. Magnetic resonance imaging in case 2 showed tumor in the right temporal lobe, both thalami, right cerebellar hemisphere, and pons. Histologically, both tumors were characterized by a multinodular appearance with a predominant component of alveolar arrangement of oligodendroglial-like cells around delicate capillaries, with mucoid matrix containing floating ganglion cells. There were also astrocytic nodules resembling pilocytic astrocytoma in case 1, and a gangliocytoma-like area merging with surrounding cortical dysplasia in case 2. Ultrastructural examination showed ganglionic differentiation in the oligodendroglial-like cells in case 2. They possessed dense core neurosecretory granules and many slender neuritic processes with microtubules arranged in parallel and terminating in synaptic junctions. The periventricularly located tumor with nodular extension to the periphery suggests an origin from subependymal germinal matrix with nests of primitive neuroblasts arrested in their embryonal migration. DNTs are related to ganglioglioma based on their common location and clinical behavior and on the presence of both ganglionic and astrocytic cells. They are also related to pilocytic astrocytoma by morphological and behavioral similarity. Together with cerebral neuroblastoma and central neurocytoma, they form a spectrum of tumors harboring small neuronal cells. The differentiation of DNT from oligodendroglioma is important so as to avoid unnecessarily aggressive therapy.
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PMID:Dysembryoplastic neuroepithelial tumor. A tumor with small neuronal cells resembling oligodendroglioma. 817 75

Although the pathogenic mechanisms of Parkinson's disease (PD) remain unclear, ample empirical evidence suggests that oxidative stress is involved in the pathogenesis of this disease. The nuclear factor E2-related factor 2 (Nrf2) is known to activate several antioxidant response element (ARE)-driven antioxidative genes that prevents oxidative stress in vitro and in vivo. Moreover, it was documented that hydralazine is a potent Nrf2 activator. In this study, we tested whether hydralazine can attenuate 1-Methyl-4-phenylpyridinium (MPP+) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- induced neurotoxicity in vitro and in vivo by activating Nrf2 and its downstream network of antioxidative genes. We found that treatment with hydralazine attenuated MPP+ or H2O2-induced loss of cell viability in human neuroblastoma cell line (SH-SY5Y). In addition, hydralazine significantly promoted the nuclear translocation of Nrf2, and upregulated the expression of its downstream antioxidative genes. Further, knockout of Nrf2 abolished the protection conferred by hydralazine on MPP+ -induced cell death. Similar findings were observed in vivo. Before, during, and after MPTP 30 mg/kg (i.p.) administration for 7 days, the mice were given hydralazine (Hyd) 51.7 mg/kg per day by oral gavage for 3 weeks. Oral administration of hydralazine ameliorated oxidative stress, MPTP-induced behavioral disorder, and loss of neurons of dopaminergic system in the substantia nigra (SN) and striatum, all of which were attributed to its ability to activate the Nrf2-ARE pathway. Hydralazine increased the migration of Nrf2 to the nucleus in dopaminergic neurons, enhanced the expression of its downstream antioxidative genes. Together, these datasets show that the Nrf2-ARE pathway mediates the protective effects of hydralazine on Parkinson's disease.
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PMID:Hydralazine Protects Nigrostriatal Dopaminergic Neurons From MPP+ and MPTP Induced Neurotoxicity: Roles of Nrf2-ARE Signaling Pathway. 3094 26