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)

The presence of antibodies to the virus capsid antigen of the Epstein-Barr virus was established in the sera of children from different forms of neoplasms with the aid of the indirect method of immunofluorescence according to Henle. 69 sera were studied from children with Wilm's tumor, teratoblastoma, reticulosarcoma, neuroblastoma, sarcoma and also from children with benignant tumors. As control served sera from healthy children of corresponding age. As test cells synthesizing the virus capsid antigen the authors utilized a suspension culture of P3HR-I cells, being one of the clones of Burkitt's lymphoma. The performed investigations have shown that in no one group of children with tumor could there be discovered an increase in the content of antibodies to the Epstein-Barr virus in comparison to controls. It has also been revealed that the spread of the Epstein-Barr virus in different groups of patients and healthy children fluctuated between 83 and 100%.
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PMID:A study on the relation between the Epstein-Barr virus and some forms of malignant tumors in children. 18 36

Bone scintigraphy with 99mTc-polyphosphate or 99mTc-pyrophosphate was carried out in 54 children suspected of bone disease. Signs of skeletal metastases were recognized in 13 children by scintigraphy whereas X-ray examination showed lesions in only 10 of these. In 5 children with primary osteosarcoma, three cases of fibrous dysplasia, and 4 cases of osteomyelitis, the lesions were clearly demonstrated by scintigraphy. Abnormal accumulation of radioactivity in soft tissue lesions was observed in primary adrenal neuroblastoma, Hodgkin's granuloma, and metastatic Burkitt's lymphoma. Several cases are reported, and the value of bone scintigraphy in children is discussed.
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PMID:Bone scintigraphy in children. 18 23

The presence of antibody to virus capsid antigen (VCA) of Epstein-Barr virus (EBV) was determined in sera from children with various forms of neoplasia by the indirect immunofluorescence procedure of Henle. Eighty-one sera from children with Wilms tumor, teratoblastoma, reticulosarcoma, neuroblastoma, soft tissue sarcoma, as well as from children with benign tumors were examined. The controls included sera from normal children of the same ages. The test cells synthesizing VCA were suspension cultures of P3HR-1 cells which are one of the clones of Burkitt lymphoma. The studies showed no increase in the content of antibody to EBV in any of the groups of children with tumors as compared with the controls. It was also found that the percentage of EBV infection in various groups of sick and normal children varied from 82 to 100.
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PMID:[Antibodies to Epstein-Barr virus in the sera of children with different neoplasms]. 19 3

If the study of tumor immunology is to have a profound impact on clinical medicine, certain hypotheses must be proven to be valid. First and foremost, it must be demonstrated that malignant tissue possesses antigenic substances (probably protein moieties) that are unique to that particular malignant process. In addition, these antigenic substances must be very similar in histologically similar tumors. Second, the host defense mechanisms must be capable of reacting to these tumor-associated antigens. The reaction is, of course, necessary in order to develop both diagnostic and therapeutic routes of application. The reaction of the immunologic system to these tumor-associated antigens could be monitored as an early serodiagnostic tool for subclinical cancer, and the cytotoxic reaction holds great promise as an immunotherapeutic tool. The essence of tumor immunologic research can thus be stated in the form of the following questions: 1. Do histologically similar cancers from identical primary sites share common tumor-associated antigens? 2. Does the immunologic system react to these antigens? 3. Can this reaction be assayed on one hand for serodiagnosis and augmented on the other for immunotherapy? Specific antigens have been found in animal tumors and have been divided into two classes: the viral induced tumors, which share common antigens when caused by the same viral agent, and carcinogen-induced tumors, which appear to have unique antigenic determinants for each tumor. In recent years a great many human tumors have been found to have tumor-associated antigens; these include colonic carcinoma, neuroblastoma, melanoma, soft tissue and osteogenic sarcoma, bladder carcinoma and Burkitt's lymphoma. This report includes evidence for the existence of such antigens in adenocarcinoma of the ovary and squamous cell carcinoma of the cervix. The laboratory evidence that has been presented would suggest that there are both a cell-mediated response and humoral response to the antigenic determinants of these two gynecologic cancers. It would appear that the mediated (lymphocyte) effect is considerably more cytotoxic and definitive than the humoral factors measured. In addition, the allogenic experiments would suggest strongly that indeed (at least with regard to these two cancers) histologically similar cancers from the same organ share common antigenic determinants. The identification and isolation of these tumor-associated antigens appears complex. The complexity is increased when one studies patients afflicted with these cancers for plasma carcinoembryonic antigens. This antigen, which was thought to be specific for adenocarcinoma of the colon, is found in the blood of a significant number of patients with adenocarcinoma of the ovary and squamous cell carcinoma of the cervix.
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PMID:Tumor-associated antigens in gynecologic cancer. 76 38

Thirteen cell lines of tissue culture originated from human malignant neoplasms were transplanted into cheek pouches of adult golden hamsters treated with anti-hamster thymocyte serum. In eleven cell lines, transplantation tests with 3.5 X 10(6) to 6.8 X 10(6) cells resulted in neoplastic growth within 4 weeks. In other two cell lines including one from neuroblastoma and another from Burkitt's lymphoma, the inoculum size had to be raised to 11.8 X 10(6) and 12.2 X 10(6) cells to get tumor growth, respectively. The histological appearance of those tumors was consistent with that of the individual primary neoplasms despite of their long in vitro histories. Anaplasia grading of the tumors appeared not to be correlated with the frequency of take.
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PMID:Heterotransplantation of cell lines derived from human malignant neoplasms into golden hamsters treated with antithymocyte serum. 108 79

The secretion of insulin-like growth-factor-binding proteins (IGFBPs) and expression of the genes encoding IGFBP-1, IGFBP-2 and IGFBP-3 have been studied in a panel of cell lines derived from breast carcinomas, Wilms' tumour, neuroblastoma, retinoblastoma, colon carcinoma, liver adenocarcinoma, Burkitt's lymphoma and a non-small-cell lung carcinoma. All cell lines, with the exception of the Burkitt's lymphoma cell line, secreted IGFBPs, as detected by affinity labelling. A 34-kDa BP was present in the conditioned media of all IGFBP-secreting cell lines, whereas BPs ranging from 18 kDa to 53 kDa were variably secreted. All IGFBP-secreting cell lines expressed the IGFBP-2 gene as determined by Northern blot analysis. The Wilms' tumour, the neuroblastoma and the retinoblastoma cell line expressed the IGFBP-2 gene only. All other cell lines, with the exception of the Burkitt's lymphoma, expressed the IGFBP-2 gene and, in addition, either the IGFBP-1 gene and/or the IGFBP-3 gene. IGFBP-1 gene expression could be detected by reverse transcriptase polymerase chain reaction only. IGFBP-3 gene expression was detected by Northern blot analysis, but transcripts were less abundant than IGFBP-2 mRNAs. These findings indicate that the expression of multiple BP genes and the secretion of BPs may be a common property of tumour cells.
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PMID:Insulin-like growth-factor-binding protein gene expression and protein production by human tumour cell lines. 137 87

We reviewed epidemiological data and outcome of 134 children with abdominal tumors (AT) among a total of 460 children with solid tumors (ST) seen between 1971-1989. There were no significant differences in ethnic distribution or sex ratio between children with AT and ST. The mean age was younger in those with AT than with ST (4.7 vs 7.2 years). The 3 major histologic AT types were Burkitt lymphoma, Wilms' tumor and neuroblastoma, with a relative increase after 1978 in those with abdominal Burkitt lymphoma. A comparison of our therapeutic results in AT treated before and after 1981 shows significant improvement in the actuarial survival at 5 years: 71.1% of those treated after 1981 were then alive with no evidence of disease, vs only 32.8% of those treated before 1981. Since 1981 the actuarial survival at 5 years in our children with Wilms' tumor and abdominal Burkitt lymphoma is about 80%.
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PMID:[Abdominal malignancies in childhood]. 165 40

Using a database comprising 13,266 cytogenetically abnormal neoplasms, the geographic heterogeneity of neoplasia-associated chromosomal abnormalities was investigated by comparing the frequencies of characteristic aberrations in consecutive series of patients with the same diagnosis. Significant frequency differences between geographic areas were found for the aberrations +8, i(17q), +19, and an additional Ph1 chromosome in chronic myeloid leukemia (CML); -5, 5q-, and +8 in acute nonlymphocytic leukemia (ANLL); t(8;21) in ANLL-M2; t(15;17) in ANLL-M3; 5q- and -7 in myelodysplastic syndromes (MDS); t(9;22) and +21 in acute lymphocytic leukemia (ALL); t(14;18) in follicular lymphoma; -8 and -22/22q- in meningioma; and structural abnormalities of 12q in pleomorphic adenoma of the salivary glands (PAS). No geographic incidence variation was detected for -7 and +21 in ANLL; +8 in MDS; 6q- and +8 in ALL; +12 in chronic lymphocytic leukemia; 6q- in non-Hodgkin's lymphoma (NHL); t(8;14) in Burkitt's lymphoma; t(11;22) in Ewing's sarcoma; i(12p) in germ cell tumors; 1p- in neuroblastoma; structural abnormalities of 3q, 8q, and 9p in PAS; or 3p- in renal cell carcinoma. Intraregional frequency similarities between cytogenetically identical abnormalities in related tumor types were also analyzed. No significant correlations were found regarding the incidence of 5q- in ANLL and MDS, 6q- in ALL and NHL, -7 in ANLL and MDS, +8 in ANLL and CML, +8 in ANLL and MDS, +8 in ALL and ANLL, or +21 in ALL and ANLL. The findings indicate that some geographic heterogeneity of tumor-associated aberrations exists both in hematologic neoplasms and in solid tumors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Geographic heterogeneity of neoplasia-associated chromosome aberrations. 195 98

The immunomagnetic depletion method for removing tumor cells from bone marrow, previously refined using a Burkitt lymphoma model, was tested with neuroblastoma cells. The efficiency of depletion was quantified by immunofluorescence with a detection limit of 3.3 log of cell depletion corresponding to the elimination of 99.84% of an initial tumor cell content of 10%. A panel of five monoclonal antibodies (UJ13A; UJ127.11; UJ181.4; alpha-Thy1; H11) purged 2.8 log of SKNBE and LAN-1 cells, while two of these antibodies as single agents allowed only for a 1.7 log (UJ13A) and a 1.7 to 2.0 log (alpha-Thy1) depletion. This underlines the advantage of an antibody panel for neuroblastoma purging. The new antibody S-L 11.14, an IgG2a against small cell lung cancer which recognizes 90% of neuroblastoma cells purged 2.8 log.
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PMID:[Evaluation of a modified immunomagnetic procedure for the purging of neuroblastoma cells from bone marrow]. 219 50

Experience with high-dose cytosine arabinoside (HDAC) in pediatric solid tumors is limited. Sixteen children with solid tumors resistant to conventional therapies were registered in a pilot Pediatric Oncology Group (POG) study that required the administration of HDAC at 3 g/m2 every 12 hours for four doses. There were four cases of rhabdomyosarcoma, two cases of fibrosarcoma, four cases of neuroblastoma, and one case each of germ cell tumor, Wilm's tumor, retinoblastoma, hepatocellular carcinoma, Ewing's sarcoma, and Burkitt's lymphoma. All eligible patients had advanced diseases and had previously received extensive chemotherapy. Thirteen patients received one course of HDAC and three patients received two courses of HDAC. Due to prior treatments, patients had less than normal marrow reserves. Short-term toxicity included nausea, vomiting, suppression of hemopoiesis, drug fever, and increased blood urea nitrogen (BUN), creatinine, and liver enzymes. All evaluable patients recovered from their toxicities. There were no drug-related deaths. None of the patients had neurologic problems, including the only patient with prior irradiation to the skull. With the above schedule, HDAC appears to have manageable toxicity.
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PMID:Toxicity of high-dose cytosine arabinoside in the treatment of advanced childhood tumors resistant to conventional therapy. A Pediatric Oncology Group study. 222 60


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