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)

Altered structure and regulation of the c-myc proto-oncogene have been associated with a variety of human tumours and derivative cell lines, including Burkitt's lymphoma, promyelocytic leukaemia and small cell lung cancer (SCLC). The N-myc gene, first detected by its homology to the second exon of the c-myc gene, is amplified and/or expressed in tumours or cell lines derived from neuroblastoma, retinoblastoma and SCLC. Here we describe a third myc-related gene (L-myc) cloned from SCLC DNA with homology to a small region of both the c-myc and N-myc genes. Human genomic DNA shows an EcoRI restriction fragment length polymorphism (RFLP) of L-myc defined by two alleles (10.0- and 6.6-kilobase (kb) EcoRI fragments), neither associated disproportionately with SCLC. Mouse and hamster DNAs exhibit a 12-kb EcoRI L-myc homologue, which indicates conservation of the gene in mammals. Gene mapping studies assign L-myc to human chromosome region 1p32, a location distinct from that of either c-myc or N-myc but associated with cytogenetic abnormalities in certain human tumours. This L-myc sequence is amplified 10-20-fold in four SCLC cell line DNAs and in one SCLC tumour specimen taken directly from a patient. Either the 10.0- or 6.6-kb allele can be amplified and in heterozygotes only one of the two alleles was amplified in any SCLC genome. SCLC cell lines with amplified L-myc sequences express L-myc-derived transcripts not seen in SCLC with amplified c-myc or N-myc genes. In addition, some SCLCs without amplification also express L-myc-related transcripts. Together, these findings suggest an enlarging role for myc-related genes in human lung cancer and provide evidence for the concept of a myc family of proto-oncogenes.
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PMID:L-myc, a new myc-related gene amplified and expressed in human small cell lung cancer. 299 22

Two human retinoblastoma cell lines (Y79 and McA) were evaluated for the presence of binding sites for human beta-endorphin (beta h-EP). Using tritiated beta h-EP (3H-beta h-EP) and synthetic beta-EP analogues, it was possible to demonstrate binding sites for 3H-beta h-EP with an ED50 of 3.5 nM in Y79 cells and 8 nM in McA cells respectively. The non-opioid segment [beta h-EP-(6-31)] retained about 20% relative potency in Y79 and 40% in McA in displacing the tritiated hormone when compared with beta h-EP. Camel beta-EP had a relative potency of less than 1% and beta h-EP-(1-27) was inactive in both cells in doses as high as 4 microM. Taken together with previous reports on similar binding sites in human neuroblastoma and glioblastoma cell lines, it appears that cell lines of neural origin have binding sites for the COOH-terminal of human beta-EP.
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PMID:Human retinoblastomas have binding sites for the COOH-terminal segment of human beta-endorphin. 300 97

The human N-myc gene is related to the c-myc proto-oncogene, and has been shown to have transforming potential in vitro. Many studies have reported amplification of N-myc in human neuroblastoma and retinoblastoma cell lines. In primary tumors, amplification of the gene was found to correlate directly with behavior of the tumor. Specific restriction fragments of a partial complementary DNA clone of N-myc from LA-N-5 human neuroblastoma cells were placed into a bacterial expression vector for the purpose of producing antigens representative of the N-myc protein. Rabbits immunized with these antigens produced antisera that recognized a protein of 62-64 kilodaltons in neuroblastoma cells. By several criteria, this protein appears to be part of the same proto-oncogene family as the c-myc protein. Moreover, the antisera to fragments of this protein were capable of histochemically identifying malignant cells in clinical specimens.
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PMID:Identification and characterization of the protein encoded by the human N-myc oncogene. 300 39

Opioid receptor sites were detectable in 4 out of 9 human neuroblastoma cell lines tested, in the human retinoblastoma line Y79 NHT C10 and in the mouse neuroblastoma line Neuro 2A. All of these cell lines expressed delta sites, while only one coexpressed mu sites (SK-N-SH). Together with delta sites previously found in rodent neuroblastoma lines, these results suggest that the expression of delta sites is under less stringent control than that of mu and chi sites. A large number of delta sites (greater than 10,000 sites per cell) is expressed in IMR-32 and NMB neuroblastoma lines. Agonist binding was sensitive to Na+ and guanine nucleotides. The delta sites in IMR-32 and NMB cells were further characterized with delta selective ligands and [3H]DADL tracer. Their delta binding affinities were identical to those of the mu and delta cell line SK-N-SH; therefore the presence of mu sites does not appear to affect the binding behavior of the delta sites by any potential interaction among the binding proteins. Further, close correlations were found when comparing ligand binding in the human neuroblastoma cell lines with those of mouse neuroblastoma cells and rodent brain, an indication that the delta receptor is highly preserved among different species.
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PMID:Delta opioid receptors in human neuroblastoma cell lines. 301 81

A cytogenetic analysis of primitive neuroectodermal tumor (PNET) cell lines was undertaken. PNET are presumed to be embryologically related to, but clinically and histologically distinct from, other tumors of neuroectodermal origin, including neuroblastoma and retinoblastoma. No single chromosome abnormality was found in all five of the tumors studied. In three of the five cases, however, additional 1q material [either as extra chromosome #1 or i(1q)] was found in all cells, and in two of the five, monosomy 13 was noted in all cells; the possible significance of these findings is discussed.
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PMID:Primitive neuroectodermal tumor cell lines: chromosomal analysis of five cases. 302 11

Association with family history of cancer of each site was examined for each type of childhood malignancies using data of National Childhood Malignancy Registry in Japan as materials (n = 16,555). 2,926 cases were with cancer family history. Family history of same type of malignancy was found significantly in excess for leukemia, a malignant lymphoma, brain tumor, neuroblastoma and retinoblastoma. When observed by cell type, association with family history of leukemia was most striking in acute myeloid leukemia. Median age at first diagnosis of retinoblastoma was 11 months earlier when family history of retinoblastoma existed. Family history of leukemia and history of exposure to prenatal radiation exposure was found to enhance relative risk for childhood leukemia when combined, suggesting existence of genetic environment interaction. Mode of interaction was interpreted as multiplicative.
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PMID:[Interaction of cancer family history and environmental factors in the risk of cancer--with special reference to childhood malignancies]. 303 33

There are no documented cases of long-term, disease-free survival in retinoblastoma (RB) metastatic to the bone marrow. The following study details successful outcome in a 3-year-old child with extensive marrow replacement 7 months postenucleation in an otherwise untreated group V RB. Therapy consisted of combinations of vincristine, doxorubicin, and cyclophosphamide for 3 months. After demonstrating cross-reactivity by a panel of six monoclonal neuroblastoma (NB) antibodies with the patient's RB cells, her marrow was purged by using microsphere-linked monoclonal antibodies, and then reinfused as rescue therapy after ablative doses of etoposide and cyclophosphamide. The authors conclude that short-term induction therapy followed by marrow ablative combination chemotherapy and immunomagnetically purged autologous marrow rescue can (1) effect successful outcome in widely metastatic RB, and (2) eliminate the risk of therapy-induced second malignancies.
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PMID:Metastatic retinoblastoma successfully treated with immunomagnetic purged autologous bone marrow transplantation. 305 86

Ifosfamide was given to 61 patients with malignant solid tumors diagnosed before the age of 21 years. In this phase II study, all patients received 1.6 g/m2/day X 5 iv over 15 minutes followed by mesna at a dose of 400 mg/m2 iv at 15 minutes and 4 and 6 hours after ifosfamide. Responses were observed in five of 15 patients with osteosarcoma, two of ten with neuroblastoma, two of six with Wilms' tumor, two of five with rhabdomyosarcoma, four of eight with other soft tissue sarcomas, one of one with retinoblastoma, one of two with germ cell tumors, one of one with B-cell lymphoma, and one of one with a primitive neuroectodermal tumor. Fifty-nine of 61 patients had received prior alkylating agent therapy which included cyclophosphamide, cisplatin, mechlorethamine, melphalan, or dacarbazine. Fourteen of 19 responses developed in patients whose tumors were resistant to treatment with cyclophosphamide. A patient with malignant Schwannoma who had received no prior chemotherapy developed a complete response which lasted 12 months. A patient with brain metastases of osteosarcoma has had complete response for greater than 2 years. Complete response was also observed in a patient with B-cell lymphoma. Toxicity consisted of mild to moderate nausea and vomiting, transient reversible myelosuppression, occasional elevation of serum BUN or creatinine, and transient neurotoxicity characterized by somnolence, confusion, weakness, tremor, hallucinations, or seizures. We conclude that ifosfamide is an important alkylating agent without apparent complete cross-resistance with cyclophosphamide, and as such should be further investigated for determination of its activity in patients with pediatric neoplasms and considered for incorporation into phase II-III trials for certain tumors.
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PMID:Phase II trial of ifosfamide in children with malignant solid tumors. 310 34

The derivation of an IgG1k monoclonal antibody (HSAN 1.2) recognizing a cell membrane determinant on human neuroblastoma cells is reported. The determinant was found on all 17 cultured human neuroblastoma cells that were tested, but the density of the antigen varied widely on different cell lines. The antibody also bound to fresh and cultured Wilm's tumor cells, retinoblastoma cells, and one of two Ewing's sarcoma cell lines tested, it did not bind to mouse neuroblastoma cells, normal fibroblasts, blood, or bone marrow. Tumor cells that did not stain with HSAN 1.2 included glioma, medulloblastoma, melanoma, rhabdomyosarcoma, mesenchymoma, leukemia, and lymphoma cells. The distribution of the HSAN 1.2 antigen in normal tissues was confined to brain and newborn kidney. As few as 0.1% tumor cells in bone marrow aspirates were detectable by fluorescein-conjugated HSAN 1.2 antibody and flow cytometry. This antibody should be useful for the discrimination of neuroblastoma from other pediatric malignancies, for the detection of tumor cells in metastatic sites such as bone marrow, and for selective removal of neuroblastoma cells from marrow harvested for autologous transplantation.
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PMID:Monoclonal antibody recognizing a human neuroblastoma-associated antigen. 332 7

The decline in childhood cancer mortality in Italy from 1955 to 1980 has been evaluated through (1) comparison of age-specific and age-standardized (0-14 years) rates for the periods 1955-1960 and 1979-1980 and (2) computation of expected numbers of deaths by application of the age-specific rates for the period 1955-1960 to the population structure of subsequent periods. Certified mortality fell by 35% for leukaemias, 90% for Hodgkin's disease, 30% for non-Hodgkin's lymphomas, 40% for bone sarcomas, 30% for kidney (Wilms') tumours, 65% for retinoblastoma. No clear trend was reported for other neoplasms, including neuroblastoma. About 300 cancer deaths per year were avoided in the period 1979-1980 compared with the expected number based on the 1955-1960 rates (170 for leukaemias alone). Although clearly encouraging, these trends are substantially less favourable than those from several other developed countries. It is therefore likely that several dozen other deaths from childhood cancer could be avoided each year through earlier (or more accurate) application of effective therapies, particularly for neoplasms requiring radiotherapy or surgical treatment.
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PMID:Decline of childhood cancer mortality in Italy, 1955-1980. 335 78


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