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)

Poor results with 131I-meta-iodobenzylguanidine (MIBG) therapy have been obtained in two children with stage IV neuroblastoma treated after partial surgery and unsatisfactory combination chemotherapy. Both patients' response to treatment (four and three 1-month-spaced courses, respectively; cumulative administration of 11.9 and 9.2 GBq) has been characterized by a low isotope concentration in the primary tumor and in the multiple bone metastases and by bone marrow uptake with final severe hematological toxicity. A slight decrease in the primary tumor's volume was observed in one patient at a cumulative dose of 85 Gy; there was no change in the other's at 42 Gy. At an initial, greater isotope concentration delivering 103 Gy, some bone metastases displayed a sharp decrease in uptake that persisted in the successive courses. For both patients a progressive spreading of new tumor localisation in the bones and finally in the soft tissues was observed.
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PMID:131I-metaiodobenzylguanidine treatment in neuroblastoma: report of two cases. 365 11

Seven patients with neuroblastoma (six children and one adult) were treated with therapeutic doses of high specific activity 131I-metaiodobenzylguanidine (131I-MIBG). Six patients were in stage IV and unresponsive to conventional treatment. One patient, in stage III, was treated at diagnosis, an approach never previously reported. Single doses of 131I-MIBG varying from 70 to 184 mCi split into two parts were administered by slow i.v. infusion (4 to 8 hours) at 2- to 4-day intervals. The following results were obtained in the six evaluable patients: two patients showed transient stabilization of the disease; three had an objective response, with shrinking of the primary tumor and/or regression of the metastatic lesions. Of these three patients, two suffered relapses at 2 and 7 months, respectively, from the first course of MIBG. The third patient, in whom the residual disease almost completely disappeared following MIBG therapy, is still alive in complete remission after autologous bone marrow transplantation with a follow-up of 14 months. The single patient treated at diagnosis showed a dramatic response to a relatively low dosage of MIBG, with histologically proved disappearance of the tumor mass. Our data indicate that MIBG may be useful in the treatment of neuroblastoma unresponsive to conventional chemotherapy. The complete response observed in the patient treated at diagnosis suggests that the full potentiality of MIBG therapy should be explored in untreated patients.
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PMID:Treatment of neuroblastoma with 131I-metaiodobenzylguanidine. 365 12

Additional histopathological and immunocytological studies were completed on the serially transplanted Warren rat pheochromocytoma. Special efforts were made to characterize features of the primary tumor common to pheochromocytomas, as well as features of the primary tumor commonly found in neuroblastoma. In summary this study found evidence for a composite primary tumor exhibiting a dual differentiative expression of both pheochromocytoma and neuroblastoma. We feel this reflects a possibility that this primary tumor arose from a common progenitor cell in the neural crest.
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PMID:Further studies of a transplantable rat pheochromocytoma. 368 79

In 1979/80 meta-iodobenzylguanidine (MIBG) was introduced as a radiopharmaceutical agent with high affinity to the adrenal medulla. It could be shown, that scintigraphic imaging with 131J labeled MIBG is a sensitive and highly specific method for localization of pheochromocytoma. In this connection we could demonstrate in 1983 that neuroblastoma can be visualized scintigraphically with MIBG as well. Until now 13 patients were examined with 131J-MIBG by our group: In 10 children with histologically proven neuroblastoma we found a specific enrichment in the tumor area. Besides the primary tumor local recurrence and metastases to bones, bone marrow and brain were detected. There was no neuroblastoma manifestation without MIBG uptake. In 3 patients with tumors other than neuroblastoma no uptake of MIBG was noticed. The results agree with those of other studies: If the physiological pattern of distribution is taken into consideration and if the proper imaging technique is adapted, 131J-MIBG scintigraphy is a highly sensitive and specific method for staging, monitoring of disease and follow-up of neuroblastoma.
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PMID:[Scintigraphic diagnosis of neuroblastoma using meta-iodobenzylguanidine]. 372 86

A case of trabecular carcinoma of the skin that resulted in prequarter amputation of the arm for local tumor aggressiveness is presented. The tumor was originally diagnosed as metastatic, most probably neuroblastoma, leading to inadequate local resection that resulted in recurrence with extensive regional nodal metastases. The importance of recognizing trabecular carcinoma as a primary tumor of the skin with a potential for recurrence and metastasis is underscored, primarily since initial total excision with adequate margins of resection has proven in most instances to be curative.
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PMID:Trabecular carcinoma of the skin simulating metastatic disease. 372 97

Neuron-specific enolase (NSE) in sera of 3 patients with neuroblastoma (Stage IV) were measured by radioimmunoassay, as compared with urinary catecholamine metabolites (vanillyl-mandelic acid (VMA) and homovanillic acid (HVA] during the course of chemotherapy, radiation, and second look operation. In Case 1 (Stage IV B) and Case 3 (Stage IV A), NSE-level on admission was found to be elevated to 51.0 ng/ml and 25.5 ng/ml, respectively. VMA and HVA were also elevated. In Case 2 (Stage IV A), NSE on admission was elevated to 128.0 ng/ml., HVA was high, but VMA was within normal range. From 1 to 3 weeks after chemotherapy and radiation, high levels of urinary VMA and/or HVA in patients promptly decreased within normal range. The size of primary tumor masses either showed no marked change or slightly decreased by radiological examinations. After intensive chemotherapy, high levels of serum NSE decreased within normal range. At that time, second look operations were carried out. The size of primary tumors was reduced (3.6 X 2.7 X 2.1 cm in average) and almost all masses had scarred over. These data suggest that serum NSE levels correlate very well with residual tumor burdens.
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PMID:Serum neuron-specific enolase as a marker useful for monitoring the effectiveness of therapy in patients with neuroblastoma--as compared with urinary catecholamine metabolites. 373 14

Two cases of primary retroperitoneal benign teratoma, in which Tc-99m MDP localized in the primary tumor are presented. Localization of bone-imaging agents in neuroblastoma has been reported but, extraosseous localization of bone-imaging agents in teratomas has not been confirmed.
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PMID:Extraosseous localization of technetium-99m MDP in benign cystic teratoma. 374 14

Bone marrow examination at the time of diagnosis of neuroblastoma was performed in 48 new cases prior to instituting therapy. Bone marrow involvement by neuroblastoma was present in 20 patients (approximately 42%). In this study the trephine biopsy was a more reliable technique than marrow aspiration in establishing the presence of metastatic disease, but in a single case the trephine biopsy was negative with metastatic cells present in the aspirate. Myelofibrosis secondary to metastatic neuroblastoma was a frequent finding, being the predominant feature in 6 cases. Bone marrow involvement by neuroblastoma was usually associated with the presence of a primary adrenal tumor and occurred only infrequently with extra-adrenal primary origin. Bone marrow involvement was usually present at the time of presentation in case where the primary tumor was located in the adrenal gland.
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PMID:Bone marrow changes in neuroblastoma. 376 7

Of a total of 1561 patients registered in the Intergroup Rhabdomyosarcoma Study (IRS) as of May 1983, 78 patients (5%) were younger than 1 year of age. These infants did not differ from the older children (1-20 years of age) in male/female ratio, clinical grouping, or survival rates. Infants younger than 1 year of age had a significantly greater frequency of undifferentiated sarcoma, 18% versus 7% in older children (P less than 0.005). Infants also had a significantly greater proportion of cancers with botryoid pathology, 10% versus 4% in older children (P less than 0.005). When reviewed by the newly proposed IRS cytopathologic classification, there was no difference in pathologic types between the two age groups. Infants younger than 1 year of age had a higher rate of bladder-prostate-vagina primary tumor sites than older children, 24% versus 10% (P less than 0.05). In addition, infants tended to receive less of the prescribed doses of chemotherapy and radiation therapy than older children, and to develop more toxicity to treatment than older children. Despite these differences, the overall survival curve for the two age groups appears to be similar. In contrast to Wilms' tumor and neuroblastoma, in which age (less than 1 year) is a favorable prognostic factor, age does not appear to be an important prognostic factor in rhabdomyosarcoma.
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PMID:Infants younger than 1 year of age with rhabdomyosarcoma. 377 10

Multivariate analysis on an unselected patient population consisting of all 253 children treated for neuroblastoma in Denmark during 1943 to 1980 shows that stage, age, and treatment given are independent prognostic variables. Calendar year of diagnosis, sex of the patient, and site of primary tumor were not significant prognostic factors. Further analysis shows that multimodal treatment with surgery, irradiation, and chemotherapy, especially in patients older than 1 year of age with Stage II disease, has influenced the survival significantly. The fact that age at diagnosis and the administration of chemotherapy have independent prognostic significance can be explained by the theory that all neuroblastomas are virtually congenital; therefore, the difference in age at diagnosis largely reflects the difference in growth rates of the tumor. Thus, according to this theory, age may be a measure of the probability of micrometastases in addition to the clinical extent or stage of the disease, as it represents the duration of the disease. Additional chemotherapy may thus have eradicated these micrometastases in the older children, since the age influence on Stage II disease disappeared when multimodal treatment was given in this study. The implications for treatment policy are discussed in view of this theory.
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PMID:Prognostic factors in neuroblastomas treated in Denmark from 1943 to 1980. A statistical estimate of prognosis based on 253 cases. 377 18


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