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)

Human retinoblastoma contains clusters of cells immunoreactive for methionine-enkephalin and methionine-enkephalin-arginine-phenylalanine. Some tumour cells also exhibited methionine-enkephalin-arginine-glycine-leucine-like immunoreactivity. The results are in agreement with those obtained with similar testing of neuroblastoma cell cultures. It is concluded that some human retinoblastoma cells are capable of synthesizing preproenkephalin A or parts of this molecule.
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PMID:Immunohistochemical evidence for preproenkephalin A synthesis in human retinoblastoma. 638 22

Intensive chemotherapy followed by infusion of cryopreserved autologous bone marrow (ABMR) was used in the treatment of 22 children with advanced tumours. In nine this was their initial therapy; in eight it was used after partial or complete remission had been achieved with standard therapy; and in five, after relapse had occurred. Recovery of marrow function occurred in 20 patients with a mean time of 13.2 and 18.2 days to recovery of neutrophils (greater than 0.5 X 10(9)/l) in newly diagnosed and previously treated patients respectively. Platelet count recovery to greater than 50 X 10(9)/l occurred in a mean time of 13.4 days in newly diagnosed and 20.4 days in previously treated patients. Control of extensive local tumour was obtained in three of three evaluable patients with abdominal non-Hodgkin's lymphoma (NHL). Metastatic bony and marrow disease was controlled in two of two patients with retinoblastoma. In Ewing's sarcoma, temporary control of widespread metastatic disease occurred in one patient. In the other, eradication of extensive local mass disease at the primary site had been achieved. Poor response to treatment has been seen in seven of eight patients with Stage III or IV rhabdomyosarcoma, three patients with neuroblastoma and four of five patients with recurrent disease. Apart from the anticipated bone marrow toxicity, the major complications were severe mucositis, anaphylaxis following bone marrow infusion and haemorrhagic cystitis. The presence of herpes simplex infection appeared to aggravate mucosal complication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experience with high dose multiagent chemotherapy and autologous bone marrow rescue in the treatment of twenty-two children with advanced tumours. 639 55

Screening of a partial cDNA library prepared from the human neuroblastoma cell line BE(2)-C with genomic DNA probes containing sequences representative of the amplified domain of that cell line allowed us to identify cloned transcripts from an active gene within the domain. The gene BE(2)-C-59 is amplified ca. 150-fold and encodes a 3.0- and a 1.5-kilobase RNA transcript, both of which are overproduced in BE(2)-C cells. A survey of a large variety of human tumor cell types indicated that this gene is amplified to varying degrees in all neuroblastoma cell lines and a retinoblastoma cell line that exhibit obvious cytological manifestations of DNA sequence amplification, i.e., homogeneously staining regions and double-minute chromosomes. The BE(2)-C-59 gene is not amplified, however, in other nonrelated tumor types, even those containing amplified DNA. Although the functional significance of this specific gene amplification in neuroblastoma cells remains unknown, an indication that it may relate to the malignant phenotype of these cells follows from the remainder of our data which show that the amplified BE(2)-C-59 gene shares partial homology with both the second and third exons, but not the first exon, of the human c-myc oncogene.
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PMID:Expression of the amplified domain in human neuroblastoma cells. 654 47

Incidence rates of cancer among children aged 0-14 for the period 1970-79 have been generated with the use of data from the Greater Delaware Valley (GDV) Pediatric Tumor Registry. This population-based registry covers a 31-county area and has a pediatric base population of 2 million. During the period, approximately 2,300 cases of childhood cancer were diagnosed in the region. Incidence rates for all histologic types combined are similar to rates from other large surveys conducted in the United States and Western Europe. However, certain histology-specific rates in the GDV vary by race. In the GDV nonwhites relative to whites have higher rates of Wilms' tumor, soft tissue sarcomas other than rhabdomyosarcoma, and retinoblastoma. These contrasts are supported by surveys in African populations showing relatively higher rates of these tumors among African black children. GDV whites exceed nonwhites in incidence of acute leukemia, neuroblastoma, and Ewing's sarcoma. African black children also experience low rates of these tumors. The frequency of central nervous system tumors is similar for GDV whites and nonwhites, despite reports of a rarity of these neoplasms in African blacks. Variations in incidence rates reveal population subgroups with particular tumor susceptibilities and may provide clues as to the relative influence of heredity and environment on patterns observed.
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PMID:Incidence of childhood cancer: experience of a decade in a population-based registry. 657 21

The true survival rates for the various forms of childhood cancer are best determined from a population-based study rather than from the results of clinical trials. Population-based survival rates have been calculated for four periods between 1956 and 1980 in Queensland. There was a significant improvement in survival for children who developed cancer after 1973 compared with those diagnosed before this date. There has however been no significant improvement in the survival rate for childhood cancer overall, or for acute lymphoblastic leukaemia since 1973. Over the 25 year period significant trends in survival rates were seen in acute lymphoblastic leukaemia, non-Hodgkin's lymphoma, Hodgkin's disease, Wilms' tumour, medulloblastoma, and retinoblastoma. No such trend was seen for acute non-lymphoblastic leukaemia, neuroblastoma, rhabdomyosarcoma, juvenile or anaplastic astrocytoma, brain stem glioma, histiocytosis X, or bone tumours. There is a need for continuing research into better methods of treatment of childhood cancer.
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PMID:Childhood cancer survival trends in Queensland 1956-80. 658 17

Previous studies had revealed that DNA with partial similarity to the myc oncogene (N-myc) is frequently amplified in human neuroblastoma cell lines and neuroblastoma tumors. We show here for one patient that N-myc amplification is confined to the neuroblastoma tumor and is not present in normal tissue. N-myc mRNA approximately equal to 4.0 kilobases in size is detectable in neuroblastoma cell lines and tumors and in a retinoblastoma cell line. By contrast, appreciable amounts of this RNA were not present in a number of cell lines derived from other human tumors and in fibroblasts from a normal individual and from a neuroblastoma patient. Low levels of N-myc RNA were found in human and murine neuroblastoma cell lines lacking amplification of this gene, up to 80-fold greater levels in all cell lines carrying amplified N-myc. In situ hybridization to sections of neuroblastoma tumors revealed high expression of N-myc predominantly in undifferentiated neuroblasts. We hypothesize that amplification and consequent elevated expression of N-myc may be related to malignant progression.
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PMID:Enhanced expression of the human gene N-myc consequent to amplification of DNA may contribute to malignant progression of neuroblastoma. 658 38

Metastatic behavior of neuroblastic tumors was analyzed to determine whether the secondary distribution of tumor was random, or whether the pattern of metastases was predictable and related to tumor type. The authors reviewed the 64 patients subjected to complete autopsy who had metastases from a neuroblastoma, retinoblastoma, medulloblastoma, or pinealoblastoma. The organ and tissue distribution of metastases was recorded in relation to location of primary tumor, type of therapy, survival, and presence of central nervous system metastases. Data were analyzed using chi-square contingency tables, correlation coefficients, and cluster analysis. The results indicate that: (1) the development of central nervous system metastases from neuroblastoma correlates with the pattern of extracentral nervous system metastases; (2) the pattern of tumor metastases is altered by chemotherapy and/or radiation; and (3) regardless of the site of origin, neuroblastic tumors behave in a uniform manner with a nonrandom metastatic distribution in particular tissues within the central nervous system. Cluster analysis demonstrated patterns of neuroblastoma tumor metastases which were consistent with both Hutchison and Pepper syndromes. The findings suggest that a random distribution, as might be secondary to blood flow, does not account for metastatic patterns, but rather that there are preferential patterns of growth, possibly reflecting trophic tendencies in neoplasms.
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PMID:Nonrandom distribution of metastases in neuroblastic tumors. 687 32

The reactivities of mouse monoclonal antibodies directed against human neuroblastoma and peripheral melanoma associated antigens, with human retinoblastoma and choroidal melanoma cell lines were tested. Segregation of antigenic determinants according to each tumor class and cell line were observed. Three retinoblastoma cell lines and one fresh tumor explant showed determinants detected by two human neuroblastoma antisera, while the choroidal melanoma showed one determinant present on a peripheral melanoma but not neuroblastomas nor retinoblastomas, suggesting certain potential distinctive tumor related determinants.
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PMID:Ocular tumors react with anti-neuroblastoma monoclonal antibodies. 687 79

Three cases of postirradiation osteosarcoma which presented in childhood are reported and the pertinent literature reviewed. The children had been treated in each instance before the age of 3 years for an astrocytoma, retinoblastoma, and neuroblastoma, respectively. An average latent interval of 9.5 years lapsed before the osteosarcomas were diagnosed. Two of the tumors occurred in unusual sites, the cervical vertebrae and maxilla but were within the fields of prior irradiation. The tumors were predominantly sclerotic and were high-grade osteosarcomas. Only one patient has remained free of disease after treatment. One tumor-related death has occurred and the third patient has had two wedge resections of pulmonary metatases.
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PMID:Postirradiation osteosarcoma in childhood. A clinicopathologic study of three cases and review of the literature. 693 66

Twenty-nine children with tumours that had failed to respond to conventional therapy have been treated with AMSA. There were 16 patients with haematological malignancies in whom treatment was initiated at 25 mg/m2 for 3 days, increasing to 150 mg/m2 for 5 days. There were one complete and four partial remissions in these patients, all of whom had received at least 500 mg AMSA/m2. Thirteen children with solid tumours were treated. They received single doses of 120 mg/m2 initially, increasing to 100 mg/m2 for 5 days. No complete or partial responses occurred, but some antitumour activity was noted in neuroblastoma and retinoblastoma. Dose-related severe bone marrow toxicity occurred, but gastrointestinal and other toxicity was mild. An additional patient with T cell lymphoma, who received AMSA prior to a successful autologous bone marrow transplant, is described. AMSA is an active drug in childhood leukaemia. Further studies at the maximum tolerated dose are needed to assess enough patients with any single solid tumour type. In particular, the response of neuroblastoma warrants further study. Investigation of the use of AMSA either prior to bone marrow transplantation in leukaemia or in association with autologous marrow transplant in neuroblastoma and other solid tumours may be of value.
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PMID:Phase I and II study of AMSA in childhood tumours. 695 93


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