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)

A dose-intensive, cyclophosphamide (CPM)-based chemotherapy regimen was tested in 22 children with newly diagnosed metastatic or refractory neuroblastoma. The N5 protocol consisted of four courses of CPM (140 mg/kg over 2 days), doxorubicin (45 mg/m2 over 3 days), and vincristine (0.05 mg/kg/d on days 1, 2, and 9) (CAV regimen), followed by three courses of cisplatin (40 mg/m2/d) and VP16 (150 mg/m2/d) for 3 days (PVP regimen). Courses started when the neutrophil count was 500/microliters or greater and the platelet count was greater than 100,000/microliters; most courses began by day 21. Extramedullary toxicities were mild. All patients had Grade 3 to 4 myelosuppression, yet bone marrow harvested after the N5 protocol engrafted in 11 of 11 patients whose post-N5 treatments required autologous bone marrow transplantation (ABMT). Among 14 previously untreated patients, the N5 plus surgery achieved 9 complete remissions (CR) or very good partial remissions (VGPR) and 3 partial remissions (PR). An additional patient achieved CR with CAV, but experienced a recurrence in the bone marrow after PVP. The sole previously untreated patient whose bone marrow disease did not resolve received courses of the N5 at prolonged intervals (for nonmedical reasons). Among eight patients with progressive (six patients) or refractory (two patients) disease while on other, lower dose regimens, the N5 plus surgery achieved five CR/VGPR, two PR, and one minor response (MR). In conclusion, dose-intensive use of CPM has tolerable toxicity and does not preclude autografting; when administered in conjunction with other cytotoxic agents, it is highly effective against metastatic neuroblastoma and causes regressions of disease resistant to less intensive regimens. This approach plus surgery reliably achieves a minimal disease state that may be amenable to definitive ablation with relatively nontoxic therapies.
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PMID:Dose-intensive use of cyclophosphamide in ablation of neuroblastoma. 240 Sep 63

Therapeutic efficacy and toxicity were evaluated in 28 children with acute lymphoblastic leukemia, in ten with acute nonlymphoblastic leukemia (ANLL), and in 13 with metastatic neuroblastoma. All were refractory to standard chemotherapeutic agents and 25 were refractory to an investigational drug. The initial dose was 12 mg/m2/day and was based on an established maximal dose tolerated in adults. This dose was found to be intolerable in 5 of 5 children with leukemia. Similarly an initial dose of 9 mg/m2/day was intolerable in 4 of 5 patients with leukemia. The starting dose in the next 28 children with leukemia or neuroblastoma was 3 mg/m2. This drug was gradually increased to the highest tolerated dose by 3-mg/m2 increments. Fifteen children with acute lymphoblastic leukemia, 3 children with ANLL, and 2 children with neuroblastoma received the drug daily. Seven patients with ANLL and 7 patients with neuroblastoma received the drug biweekly. Seventeen patients with acute lymphoblastic leukemia, 6 patients with ANLL, and 5 patients with neuroblastoma had an adequate trial of the drug. An adequate trial was defined as a minimum of 5 weeks of therapy unless progressive disease developed. Side effects of the drug were striking and included fever, hypotension, myalgia, bone pain, arthralgia, arthritis, abdominal pain, liver toxicity, thrombocytopenia, and neurotoxicity. No complete remission occurred although interferon levels above 100 units/ml were induced in nearly 50% of the patients.
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PMID:Phase II trial of a complex polyriboinosinic-polyribocytidylic acid with poly-L-lysine and carboxymethyl cellulose in the treatment of children with acute leukemia and neuroblastoma: a report from the Children's Cancer Study Group. 241 2

A Phase II study of poly(I,C)-LC was performed in 28 children and adolescents with acute lymphoblastic leukemia (ALL), 10 with acute nonlymphoblastic leukemia (ANLL), and 13 with metastatic neuroblastoma. All were refractory to standard chemotherapeutic agents and 25 to an investigational drug. Initial doses of 12 mg/m2 and 9 mg/m2 were intolerable. However, 9 mg/m2 was tolerable in the majority of patients when the drug was started at 3 mg/m2 and increased by 3 mg/m2 increments. Fifteen children with ALL, three with ANLL, and two with neuroblastoma received the drug daily. Seven patients with ANLL and seven children with neuroblastoma received the drug biweekly. Twenty-eight patients received an adequate trial, which was defined as a minimum of 5 weeks at the maximal tolerated dose, unless there was progressive disease at the maximal tolerated dose. Side effects of the drug were striking, and included fever, hypotension, myalgia, bone pain, arthralgia, arthritis, abdominal pain, liver toxicity, thrombocytopenia, and neurotoxicity. No complete remissions occurred in spite of interferon levels above 100 U in nearly 50% of patients.
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PMID:Phase II trial of poly(I,C)-LC, an interferon inducer, in the treatment of children with acute leukemia and neuroblastoma: a report from the Children's Cancer Study Group. 241 84

Treatment of neuroblastoma is an unsolved problem of pediatric oncology. In spite of highly intensified chemotherapy, the long-term survival rate of children with a metastatic neuroblastoma is below 10%. We therefore used 131I-metaiodobenzylguanidine (MIBG) for the first time to treat children with a neuroblastoma in relapse or primary unresponsiveness to chemotherapy. We had previously demonstrated that MIBG is useful for the scintigraphic imaging of neuroblastoma lesions and had investigated the cytotoxicity and uptake of MIBG in various neuroblastoma cell lines. We treated 6 children with neuroblastoma in a total of 19 courses. Three of the children suffered from a relapse of neuroblastoma; 3 had never gained a remission. Four of the 6 children lost their bone pain and fever during the first 3 days. In 5 of the 6 children the solid tumor as well as the bone marrow infiltration responded to MIBG treatment, with responses ranging from transitory decrease of the tumor mass to complete disappearance of abdominal tumors. We also witnessed a stabilization of osteolytic lesions, a decrease in elevated serum catecholamines, and a decrease in bone marrow infiltration. Five of the 6 children died of tumor progression 55-249 days after the first MIBG treatment.
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PMID:Clinical experiences in the treatment of neuroblastoma with 131I-metaiodobenzylguanidine. 248 76

Magnetic resonance imaging (MRI) was compared with iodine-131-labeled monoclonal antibody scanning for ability to detect bone marrow metastases in the spine, pelvis, and femurs of children with disseminated neuroblastoma. The five patients in this study had received high-dose chemotherapy and radiation, either with (N = 2) or without (N = 3) bone marrow transplants. MRI disclosed marrow abnormalities at all sites detected with the radiolabeled antibody, which is highly specific for neuroblastoma. However, several diffuse and multifocal marrow changes apparent on MR scans were not present on scintigrams, indicating that MRI is probably less specific than monoclonal antibody imaging. Both methods were more useful than conventional radiography, computed tomography, and 99mTc-MDP bone scans for identifying sites of marrow involvement by neuroblastoma.
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PMID:Comparison of radiolabeled monoclonal antibody and magnetic resonance imaging in the detection of metastatic neuroblastoma in bone marrow: preliminary results. 260 20

Therapy of disseminated neuroblastoma remains an unsolved problem in pediatric oncology. Therefore, new therapeutic approaches have to be developed for this malignancy. In this paper, we investigated the possibility of the in vitro generation and expansion of lymphokine-activated killer (LAK) cells in patients with disseminated neuroblastoma. Although the patients had very low Natural Killer (NK) activity, it was possible to induce LAK activity in peripheral mononuclear lymphocytes (PMNC) by incubation with Interleukin-2 (IL-2). Moreover, the PMNCs could be expanded up to 50-fold in the presence of Interleukin-2 while maintaining or even increasing their LAK activity. The target cells were neuroblastoma cell lines and, in one case, autologous neuroblastoma cells. Additionally, it was possible to induce LAK cell activity against autologous neuroblastoma cells in bone marrow-derived mononuclear cells.
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PMID:In vitro induction of lymphokine-activated killer (LAK) activity in patients with neuroblastoma. 264 3

In order to evaluate the frequency, clinical and radiological aspects and prognosis of central nervous system metastases in children's neuroblastoma, the 258 children presenting with neuroblastoma, and registered from January 1982 to August 1987, were studied. Among them, 7 patients (2.7%), of which 6 had an initially metastatic neuroblastoma, presented with a secondary neuro-meningeal involvement. Parenchyma involvement (4 cases) occurred after a mean period of time of 21 months and marked the relapses. The disease recurs later on, even when locally controlled by surgical excision and local irradiation. Meningeal involvements (3 cases) occurred after a mean delay of 12.7 months, in patients with full tumoral evolutivity, and were responsible for rapid death. The clinical presentation of these metastases differs from that in adults by the rapidity of setting up of the signs and the frequency of intracranial hypertension. CT scan allows approaching diagnosis in the majority of the cases. These data are compared with those in the literature, where 30 cases were reported: they show a high patients' average age and the worse prognosis.
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PMID:[Secondary metastatic neuromeningeal localization of neuroblastoma in children]. 265 63

One hundred and sixty six bone marrow aspirates from children with abdominal neuroblastoma were independently examined for the presence of neuroblastoma cells by conventional haematological staining techniques and by indirect immunofluorescence using one or more of five monoclonal antibodies. Results using the two methods were evaluated by comparison with the results of bone marrow, bone and lymph node biopsy specimens taken at the same time, and in the light of the child's clinical course. One antibody, UJ13A, was found to have 98.5% specificity and 85.7% sensitivity, compared with sensitivities for conventional staining of 50% for aspirate alone and of aspirate or trephine biopsy specimen of 71.4%. The remaining antibodies UJ127/11, UJ223/8, UJ181/4 and UJ167/11, with specificities in the range 94-99%, were found to have sensitivities in the range 47-61%, lower than the sensitivity of conventionally stained aspirate or trephine biopsy specimen. Routine immunofluorescence staining with monoclonal antibody UJ13A should increase the sensitivity of detection of metastatic neuroblastoma.
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PMID:Monoclonal antibodies for detecting bone marrow invasion by neuroblastoma. 265 92

We have developed a long term marrow culture assay for the study of advanced bone marrow metastatic neuroblastoma. In this in vitro system the hemopoietic growth (GM-CFU) is not affected by the presence of tumor cells. The neuroblastoma cells grow and differentiate partially when in contact with the stromal layer, arresting the culture. We present culture and histological data suggesting that the solid tumors interact specifically with the stromal layer of marrow origin.
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PMID:Long term bone marrow culture in metastatic neuroblastoma. 270 74

An acutely ill 6-month-old female infant presented with massive hepatomegaly, accompanied by severe anemia with peripheral normoblastemia and thrombocytopenia. Bone marrow examination revealed erythroid hyperplasia with gross erythroid dysplasia, reduced granulocytic precursors, and virtually absent megakaryocytes. The bone marrow also contained completely necrotic cells occurring in clumps as well as singly. The appearances suggested bone marrow involvement by neuroblastoma. Accordingly, combination chemotherapy was instituted and laparotomy was performed as soon as her clinical condition had improved. Left adrenalectomy was carried out, because a small adrenal nodule of ganglioneuroma was present. Liver biopsy showed expansion of portal tracts by loose fibrous connective tissue containing hemosiderin deposits and some degenerate cellular debris, consistent with areas of involuted metastatic neuroblastoma. Complete recovery followed, and subsequent bone marrow examination was entirely normal. It is thought that the dyserythropoiesis probably resulted from the release of toxic metabolites from regressing neuroblastoma.
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PMID:Transient dyserythropoiesis occurring during the involutionary phase of stage IV-S neuroblastoma. 271 38


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