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

Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of two murine neuroblastomas (C1300, NS-20) was investigated in vivo. Five groups of mice were prepared; group 1 were fed the control diet, group 2 were fed a vitamin E-deficient diet, group 3 were fed a vitamin E-supplemented diet, group 4 were fed the control diet and plus vitamin E solution given intraperitoneally during the treatment (solvent i.p. group), and group 5 were given vitamin E in the same manner (20 mg/kg/day; vitamin E i.p. group). Cisplatin (6 mg/kg) was injected intraperitoneally into the mice of each group during the treatment. In case of the C1300 neuroblastoma, the antitumor activity of cisplatin was most enhanced in the mice receiving vitamin E i.p., and the intra-tumor vitamin E and platinum levels were significantly higher in this group than in the other groups (P less than 0.01, and P less than 0.05 respectively). In contrast, in animals transplanted with the NS-20 murine neuroblastoma, which proved to be a cisplatin-tolerant tumor in separate experiments, no combined effect of those drugs was observed, although the intra-tumor level of platinum was elevated. The possibility was that vitamin E increases the influx of cisplatin into the tumor cells and acts after incorporation of cisplatin through the plasma membrane. Vitamin E did not accentuate the cisplatin-induced renal impairment in vitamin E-loaded groups. Those results suggested that vitamin E should be considered as a co-agent of cisplatin for the treatment of neuroblastoma.
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PMID:Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of murine neuroblastoma in vivo. 320 17

A cooperative multicenter clinical study on cisplatin in children with malignant solid tumors was conducted in seventeen institutions. Of 63 children entered into the study, 18 patients were treated with cisplatin alone, 33 with a VCAP regimen (VCR, CPA, ADM and CDDP) and 12 with other combination regimens. The numbers of evaluable patients were 14, 27 and 7, respectively. Response rates for neuroblastoma were 37.5% (3/8) with cisplatin alone and 79.2% (19/24) for the VCAP regimen. Major adverse effects were gastrointestinal symptoms, bone marrow suppression and renal impairment. Hearing difficulty, electrolyte imbalance and transient elevation of transaminase were also observed. However, these adverse effects were within a tolerable range of severity. The results of this study demonstrate that cisplatin is a useful drug in the treatment of neuroblastoma.
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PMID:[Clinical evaluation of cisplatin in children with malignant solid tumors. Pediatric Cisplatin Study Group]. 367 93

To estimate the side effects of chemotherapy and the influence of age at the time of nephrectomy on renal function, we investigated renal function in 34 uninephrectomised children with neuroblastoma (NB) or Wilms' tumour (WT). The results were compared with 6 controls who underwent nephrectomy for non-malignant disease. Study of renal function was primarily based on the clearance of inulin and para-aminohippuric acid (Cin and CPAH, ml/min per 1.73 m2). No significant differences in Cin/CPAH (mean +/- SD) were found between the NB group (90 +/- 24/421 +/- 95), WT group (85 +/- 17/386 +/- 104) and the controls (93 +/- 13/430 +/- 61). Children with NB and WT were divided into two subgroups according to the theoretical nephrotoxic risk. There was no significant difference in renal function between NB or between WT subgroups. Cumulative cisplatin doses in children with NB did not affect renal function significantly. The age at time of unilateral nephrectomy (< or = 2 years vs. > 2 years) was not associated with a higher risk of renal damage in WT children, whereas in NB children the filtration fraction (Cin:CPAH) was higher in younger children (mean +/- SD: 0.243 +/- 0.023 vs. 0.191 +/- 0.041). In conclusion, uninephrectomised children with NB are supposed to have a higher risk of drug-induced renal impairment compared with those with WT. Our data do not confirm this hypothesis, since renal function was comparable to controls in both groups, except in younger patients with NB who show a high filtration fraction. Since the survival of children with NB has improved, a longer follow-up of their renal function in needed.
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PMID:Renal function following unilateral nephrectomy for neuroblastoma and Wilms' tumour. 858 14

Postoperative renal impairment was observed in 6 of 58 patients with neuroblastoma treated between November 1982 and March 1994. To clarify the clinical characteristics of these patients (renal-impairment group), they were compared with 26 patients treated during the same period who did not have renal impairment (no-impairment group). The incidence of primary retroperitoneal tumor and invasion of the hilum renalis was clearly higher in the renal-impairment group than in the group with no impairment. However, no significant difference was observed with respect to age, tumor laterality, or stage of disease. The results of postoperative biochemical examinations showed that the serum concentrations of lactic dehydrogenase were significantly higher in the renal-impairment group. In the group with renal impairment, the mean maximal body temperatures on the first, second, and third postoperative days were 38.7 degrees C, 38.6 degrees C, and 38.1 degrees C, respectively. These were higher than those of the no-impairment group. For patients with these risk factors, intraoperative prophylactic measures and early postoperative renal blood flow evaluation (in anticipation of postoperative renal impairment) are considered necessary.
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PMID:Renal impairment after surgical resection of neuroblastoma. 888 95

Hypercalcemia is a potential dosage-related adverse effect of 13-cis-retinoic acid in patients with neuroblastoma. Severe hypercalcemia requiring dosage reduction has been reported in children receiving 13-cis-retinoic acid 200 mg/m2/day and in those with concurrent renal impairment receiving 160 mg/m2/day. A 12-year-old girl without renal dysfunction, diagnosed with neuroblastoma, developed severe hypercalcemia requiring several hospitalizations while receiving 13-cis-retinoic acid 160 mg/m2/day. Her hypercalcemia resolved with hydration, diuretic therapy, and temporary discontinuation of 13-cis-retinoic acid. Despite a 50% dosage reduction to 80 mg/m2/day, severe hypercalcemia recurred with the next treatment cycle. Further treatment with 13-cis-retinoic acid was made tolerable by shortening the duration of the remaining cycles. Serum calcium levels should be monitored in patients with neuroblastoma who receive 13-cis-retinoic acid.
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PMID:Hypercalcemia induced by 13-cis-retinoic acid in a patient with neuroblastoma. 1201 65

We retrospectively analysed the outcomes of children transplanted for high-risk neuroblastoma (NB) at a single institution predominantly transplanted with total body irradiation and chemotherapy. The aims of this study were to determine the prognostic impact of clinical and biological features and to document long-term health outcomes. Forty patients were transplanted with a single unpurged autograft. Fourteen patients died from disease progression and two from late complications of treatment. Twenty-three patients are alive at a median of 4.6 years from diagnosis. Kaplan-Meier estimates of overall survival at 2, 5 and 10 years are 76+/-7.0, 60.2+/-8.4 and 54.7+/-9.3% following transplant. Response to induction therapy was significantly associated with survival (P<0.01). Long-term complications included growth (100%) and pubertal failure (83%), hearing impairment (73%), orthopaedic complications (63%), renal impairment (47%) and thyroid abnormalities (36%). Intrinsic and acquired resistance to chemotherapy remains the major obstacle to improving outcomes in high-risk NB. Although patients with chemo-sensitive disease are less likely to experience a relapse, substantial therapy-related toxicities result in poor long-term health outcomes for survivors.
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PMID:Long-term outcomes in children with high-risk neuroblastoma treated with autologous stem cell transplantation. 1791 65

Treatment with (131)I-metaiodobenzylguanidine (MIBG) has been introduced to the management of neuroendocrine tumors (NET) nearly 30 years ago. It provides efficient internal radiotherapy of chromaffin tumors (neuroblastoma, pheochromocytoma, and paraganglioma), but also of carcinoid and other less frequent tumors. Although for various NET types the role of this treatment form decreased by the emergence of peptide receptor radionuclide therapy, (131)I-MIBG still remains the primary radiopharmaceutical for targeting chromaffin tumors with outstanding efficiency. Results in neuroblastoma with overall response rates around 30% in refractory or recurrent diseases have been improved by combinations with chemotherapy, radiosensitizers, and autologous stem cell support. For adult chromaffin tumors, that is, pheochromocytoma and/or paraganglioma, (131)I-MIBG therapy is currently the most efficient nonsurgical therapeutic modality and applies for inoperable, disseminated disease. The antisecretory effect with powerful palliation of symptomatic disease (response rate: 75%-90%) should also be considered when judging treatment benefit. The results in carcinoid tumors are less pronounced, primarily achieving arrest of tumor growth, and most importantly effective functional control. With the presence of peptide receptor radionuclide therapy, (131)I-MIBG remains the alternative radionuclide in this tumor entity, for example, for patients with renal impairment. Another worthwhile mentioning indication-although less prevalent-are metastatic medullary thyroid carcinomas, especially if functioning. These patients are good candidates for this treatment form in the absence of reasonable surgical options and presence of diagnostic MIBG uptake. This article outlines the current status, results, and methodological improvements of (131)I-MIBG therapy.
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PMID:131I-metaiodobenzylguanidine therapy of neuroblastoma and other neuroendocrine tumors. 2011 83