Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acid extracts from mouse Neuroblastoma x rat Glioma hybrid cells have been purified by means of Sep-Pak C-18 and fractionated by high performance liquid chromatography. Each fraction has been submitted to a sensitive beta-endorphin radioimmunoassay and an immunoreactivity peak at camel beta-endorphin retention time was found.
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PMID:beta-Endorphin in neuroblastoma x glioma hybrid cells. 315 80

Neuroblastoma cell lines have been reported to contain two proopiomelanocortin (POMC) mRNA transcripts. We have now shown by immunocytochemistry and radioimmunoassay (RIA) that a number of neuroectodermally derived cell lines contain immunoreactive beta-endorphin although cell concentrations were not characteristic of any tumour type. To explore further the functional significance of beta-endorphin expression, we analysed neuroblastoma cell lines having intermediate (I), substrate adherent (S) and neuronal (N) phenotypes. No differences in cell beta-endorphin content were detected. However, the expression of POMC mRNA and of immunoreactive beta-endorphin was reduced within a few hours of treatment of these cell lines with retinoic acid. Culture of the cell lines in the presence of beta-endorphin resulted in small but significant increases in growth. Although the POMC gene is in the same chromosomal segment as N-myc, which is normally amplified in neuroblastoma, no corresponding amplification of POMC could be demonstrated. The data suggest that POMC gene products may contribute to the autocrine/paracrine growth of neuroectodermal tumours.
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PMID:Modulation of POMC expression in human neuroectodermal cells. 828 Jan 57

Neuroblastoma is predominantly a paediatric neoplasm of the sympathetic nervous system. Despite the aggressive nature of the disease, spontaneous regression is frequently observed in infants diagnosed under the age of 12 months; especially with a specific stage referred to as stage 4s. Discovering the conditions, the elements, the mechanism and the indices behind this regression phenomenon could have therapeutic potential for prevention and cure. A review of the literature has implicated adrenocorticotropin hormone in both the aetiology and spontaneous regression of neuroblastoma. Manipulation of adrenocorticotropin hormone may offer hope for prevention and cure. Ingestible products such as retinoic acid, glycyrrhizic acid, salsolinol and ketoconazole acting in concert, could represent instrumental tools in a therapeutic manipulation process.
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PMID:Adrenocorticotropic hormone in the aetiology and regression of neuroblastoma. 1220 96

Opsoclonus-myoclonus syndrome (OMS) is a rare, autoimmune neurological disorder that is poorly recognized and undertreated. Neuroblastoma is found in one half of the cases. Because of the high incidence of spontaneous regression of neuroblastoma, it is unknown whether not finding a tumor means there was none. To define demographic trends and the standard of care in the first large series of OMS, 105 children were recruited over a 13-year period in a retrospective questionnaire survey. Children with and without a tumor differed little in viral-like prodrome and neurological symptoms. Earliest neurological symptoms were staggering and falling, leading to a misdiagnosis of acute cerebellitis. Later symptoms included body jerks, drooling, refusal to walk or sit, speech problems, decreased muscle tone, opsoclonus, and inability to sleep. Tumor resection alone did not provide adequate therapy for most. Adrenocorticotropic hormone (ACTH), prednisone, and intravenous immunoglobulin were used with equal frequency, but ACTH was associated with the best early response. More than one half of the children had relapses. Residual behavioral, language, and cognitive problems occurred in the majority. The delay in diagnosis (11 weeks) and initiation of treatment (17 weeks) is unacceptably long.
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PMID:Neuroepidemiologic trends in 105 US cases of pediatric opsoclonus-myoclonus syndrome. 1557 22

Neuroblastoma x glioma hybrid cells (NG108CC15) were examined for the presence of ?-endorphin-like material. In order to differentiate this ?-endorphin-like material from crude cell extract, a procedure for immunoaffinity chromatography was developed. The monoclonal antibody 3-E7 employed possesses the unique property of recognizing the N-terminal sequence of virtually all endogenous opioid peptides, but not their precursors. By means of this immunoaffinity procedure about 90% of exogenous ?-endorphin was recovered from 10 ml phosphate buffered saline samples. Affinity chromatography served as first-step purification of crude NG108CC15 cell extract for the separation and concentration of ?-endorphin-like material. The eluate of the immunoaffinity gel was subjected either to Sephadex gel filtration or to high pressure liquid chromatography. Under either condition, immunoreactive ?-endorphin which eluted with synthetic ?-endorphin was detected. The concentration in six different batches varied from 4 to 17 fmol/10(8) cells. This would be 10-200-fold lower than that observed for the enkephalins or dynorphin A/?-neo-endorphin. It is concluded that the utilization of the monoclonal antibody 3-E7 for a first-step purification of cell extracts was an essential pre-requisite for the separation of ?-endorphin-like material from the hybrid cells. The presence of enkephalin-like material, of dynorphin A/?-neo-endorphin-like material and of ?-endorphin immunoreactive material suggests that NG108CC15 cells are able to generate opioid peptides related to the precursors pre-proenkephalin A, pre-proenkephalin B and pro-opiomelanocortin.
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PMID:Affinity purification of ?-endorphin-like material from NG108CC15 hybrid cells by means of the monoclonal ?-endorphin antibody 3-E7. 2049 21