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)

Bromoacetylcholine (30 mg/kg intratumor one to three times per day) and bromoacetate (12 mg/kg intratumor two times per day) inhibited neuroblastoma in A/J mice efficiently and prolonged the lifespan of these animals at least 200%. Since the neuroblastoma-inoculated A/J mice are considered to be comparable to human neuroblastoma, the cytolytic action of bromoacetylcholine and bromoacetate on murine neuroblastoma warrants further studies on patients. The fact that these tumors were cured in adult mice is very important because older children and adults with neuroblastoma have the poorest prognosis.
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PMID:Treatment of neuroblastoma in mice with bromoacetylcholine and bromoacetate. 64 17

The effect of bromoacetylcholine on mouse neuroblastoma C-1300 was investigated in cell culture as well as in A/J mice. In vitro, bromoacetylcholine (1 X 10(-5) M) was a potent cytolytic agent and produced an additive effect in combination with vincristine (3 X 10(-9) M). Since the choline acetyltransferase inhibitor, dimethylaminoethyl chloroacetate, does not inhibit neuroblastoma efficiently in vitro, the potent cytolytic action of bromoacetylcholine is probably not due to its choline acetyltransferase inhibitory action. Furthermore, the neuroblastoma inhibitory effect of bromoacetylcholine was not affected by atropine. Therefore, the inhibitory action is not related to the interaction of bromoacetylcholine with muscarinic receptors either. In in vivo experiments, 1, 10, or 30 mg/kg of bromoacetylcholine was injected directly into the tumors three times daily for 6 weeks. Bromoacetylcholine at 10 and 30 mg/kg gave significant protection of A/J mice from the death induced by neuroblastoma inoculation, and the lifespan was prolonged significantly with these bromoacetylcholine treatments.
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PMID:Cytolysis of neuroblastoma cells in vitro and treatment of neuronal tumors in vivo with bromoacetylcholine. 87 86

Because neuroblastoma cells in vitro are sensitive to changes in glucose levels in growth media, the effects of glucose levels and dietary carbohydrate on the sensitivity of neuroblastoma cells to chemotherapy were studied. In vitro, 20 microM bromoacetylcholine, 3mM 1,3-diaminopropane, and 5 mM 5-fluorouracil were added to the growth medium of strain N2a neuroblastoma cells cultured in Dulbecco's modified Eagle medium with high glucose (4.5 g/L, HG), normal glucose (1.0 g/L, NG), or low glucose (0.1 g/L, LG). Diaminopropane and 5-fluorouracil had some cytotoxic effect on cells in all media. Bromoacetylcholine killed cells in all media, but at a concentration of 20 microM was most effective in LG medium. Mice (A/Jax) were inoculated with neuroblastoma cells for in vivo studies. Mice could not tolerate a carbohydrate-free diet, while a high-carbohydrate diet caused no change in survival time. When mice on a high carbohydrate diet were treated with cyclophosphamide (100 mg/kg, ip) or 5-fluorouracil (125 mg/kg, ip) they died faster than drug-treated mice on a normal diet. Oral chlorpropamide or cimetidine did not prolong survival time. Analysis of blood glucose levels showed neuroblastoma significantly lowered blood glucose levels (p less than 0.05), while chlorpropamide had no significant effect. It is proposed that manipulation of plasma glucose to lower levels will not be effective in enhancing the chemotherapy of neuroblastoma.
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PMID:Effects of glucose on neuroblastoma in vitro and in vivo. 365 98