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 large inbred family is described in which there were seven cases of Hodgkin's disease, three of lymphosarcoma, two of thymoma, two of common variable immunodeficiency, and single cases of retinoblastoma, neuroblastoma, and rhabdomyosarcoma. There have been no other lymphoma cases in the community during the past decade. Further study of this family may help to define the genetic basis for development of Hodgkin's disease and other disorders.
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PMID:Common variable immunodeficiency, Hodgkin's disease, and other malignancies in a Newfoundland family. 4 22

Thirty-two children with solid tumors (lymphangioma, fibrosarcoma, hepatocarcinoma, osteogenic sarcoma, rhabdomyosarcoma, lymphosarcoma, mesenchymoma, hepatoma, Ewing's sarcoma, reticulum cell sarcoma, neuroblastoma, Hodgkin's disease, and brain tumors) were studied for alterations in coagulation by means of platelet counts, platelet aggregation, thrombelastogram, procoagulant and antigenic factor VIII, fibrin split products, and antithrombin III level. Results indicated hypercoagulability as shown by abnormally short thrombelastograms and elevated factor VIII levels and platelet counts in approximately one-half of the group. With the exception of increased fibrin split products in a third of the patients, little laboratory or clinical evidence for disseminated intravascular coagulation was seen. Hypercoagulability, as noted in adult carcinoma patients, can also occur in childhood sarcoma patients.
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PMID:Hypercoagulability in childhood cancer. 120 73

Carminomycin is an original antitumor antibiotic from the anthracycline group isolated at the Institute of New Antibiotics (USSR) in 1973. Pharmacological investigation of carminomycin revealed its satisfactory absorption from the gastrointestinal tract which proved to be a distinguishing property of the antibiotic as compared to other anthracyclines such as adriamycin and rubomycin. The clinical trials of carminomycin showed that it was mainly active against soft tissue sarcoma and breast cancer, lymphosarcoma, neuroblastoma, Wilms' tumor and Ewing's sarcoma in children, as well as acute leukemia. Various regimens for the antibiotic administration were applied: short-term, single and long-term. Suppression of hemopoiesis was considered as a limiting toxic effect. By the data available carminomycin had lower cardiotoxicity as compared with rubomycin and adriamycin. Development of oral carminomycin is believed promising.
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PMID:[Experience with using carminomycin in oncological clinical practice]. 132 45

We have studied the cellular pharmacokinetics of carboplatin (CBDCA), as part of the evaluation of the antitumor activity of CBDCA in cancers limited to the peritoneal cavity in comparison with cisplatin (cDDP). The uptake of CBDCA into L1210 (lymphosarcoma), CC531 (colonic carcinoma), COV413.B (human ovarian carcinoma) and NB1 (human neuroblastoma) cells was 1.5 to 13 times lower than the uptake of cDDP. The uptake of CBDCA into human ovarian carcinoma cells, taken directly from patients, was also 8-20 times lower than cDDP. Platinum concentrations, expressed as a percentage of the total intracellular Pt concentration, were similar for CBDCA and cDDP in cytosol and nucleus/membrane fractions. A second major difference between the drugs was their binding to DNA. Less CBDCA-DNA than cDDP-DNA adducts were formed after incubation at equimolar amounts of drug with isolated salmon sperm DNA (5-25 times less). A 16-69 times higher concentration of CBDCA than cDDP was needed to induce similar changes in cell growth activity (50% [3H]thymidine inhibition) in CC531 and COV413.B cells, indicating that equitoxicity can only be achieved when tumor cells are exposed to higher concentrations of CBDCA than cDDP. Similar toxicity was achieved in CC531 cells after incubation with a 16-fold higher CBDCA dose than cDDP. Comparable intracellular platinum concentrations, however, were obtained with a 10-fold higher CBDCA dose, suggesting that cellular pharmacokinetics of the drugs are different. Regarding drug uptake and pharmacokinetics the mechanism of action of CBDCA differed from cDDP at a cellular level.
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PMID:Cellular pharmacokinetics of carboplatin and cisplatin in relation to their cytotoxic action. 185 50

The involvement of mitochondrial damage in the antiproliferative effects of m-iodobenzylguanidine [MIBG] and methylglyoxal bis (guanylhydrazone) [methylGAG] was studied in human neuroblastoma SK-N-SH, mouse neuroblastoma N1E115 and mouse lymphosarcoma S49 cells. Proliferation of SK-N-SH cells was insensitive to MIBG (100 microM gave 15% inhibition), but sensitive to methylGAG (IC50 = 50 microM). MIBG and methylGAG were approximately equitoxic to N1E115 cells (IC50 of 92 and 87 microM, respectively). S49 cells were most sensitive to both MIBG (IC50 = 11 microM) and methylGAG (IC50 = 5 microM). In isolated sonicated mitochondria, MIBG inhibited respiration a complex I of the respiratory chain (EC50 = 0.5 mM), whereas methylGAG was much less effective (EC50 greater than 15 mM). In intact cells, MIBG at 31 microM impaired mitochondrial respiration and stimulated the glycolytic flux. In contrast, equimolar concentrations of methylGAG had no effect on oxygen consumption, ATP content, glucose consumption and lactate production. MethylGAG significantly increased putrescine levels in N1E115 and S49 cells within 12 hr via inhibition of S-adenosylmethionine decarboxylase. No such effects were seen in SK-N-SH cells for up to 48 hr. Equimolar concentrations of MIBG had no effect on the putrescine levels in the various cell lines, suggesting that MIBG did not inhibit S-adenosylmethionine decarboxylase. It is concluded that the antiproliferative mechanisms of the guanidino compounds are essentially different. MIBG inhibited mitochondrial respiration at complex I with concomitant stimulation of the glycolytic flux but was essentially without effect on polyamine levels. On the other hand, cytotoxicity of methylGAG was not associated with mitochondrial dysfunction.
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PMID:Mitochondrial effects of the guanidino group-containing cytostatic drugs, m-iodobenzylguanidine and methylglyoxal bis (guanylhydrazone). 186 36

m-Iodobenzylguanidine (MIBG) is a functional analogue of the neurotransmitter norepinephrine. Radio-iodinated 131I-MIBG is used clinically as a tumor-targeted radiopharmaceutical agent in the diagnosis and treatment of adrenergic tumors. Native MIBG has previously been demonstrated to be cytotoxic in cultured cells and to produce anti-tumor responses in animals when non-toxic schedules are used. In this study the effect of MIBG was investigated on isolated rat liver mitochondria and on various tumor cell lines (human neuroblastoma SK-N-SH, mouse neuroblastoma N1E115 and mouse lymphosarcoma S49). Results revealed that MIBG inhibits respiration of isolated liver mitochondria at complex I of the respiratory chain, without affecting F1 ATP-ase. In cell lines, impairment of the mitochondrial respiration was evident from reduced oxygen consumption and decreased intracellular ATP levels. In response to this effect, the glycolytic flux was stimulated as shown by increased glucose consumption and lactic acid production. Cytotoxicity of MIBG was proportional to drug-induced alterations in glucose metabolism.
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PMID:Impaired mitochondrial respiration and stimulated glycolysis by m-iodobenzylguanidine (MIBG). 238 75

At least 22 members of a large kindred have a bleeding tendency resulting from an autosomal dominant disorder of platelet production and function. Phenotypic manifestations include mild to moderate thrombocytopenia, bleeding time prolongation, and abnormal platelet aggregation. Platelet survival time is normal. The platelet disorder in this family appears to differ from known hereditary thrombocytopenic or thrombocytopathic syndromes and may represent a new genetic disease. Six family members reportedly developed hematologic neoplasms: acute monocytic leukemia nine years after treatment for congenital neuroblastoma; lymphosarcoma at age 10 years; myeloid leukemia at age 23 years; acute myelocytic leukemia at age 62 years; leukemia of unknown type at age 48 years; and lymphocytic lymphoma at age 52 years.
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PMID:Studies of a familial platelet disorder. 385 65

The objective of this investigation was to characterize non-cloned neuroblastoma cells immunohistochemically. In this study, the cholinergic cells in three mouse tumors were identified by using a choline acetyltransferase (CAT) antibody. Different cholinergic cell distribution patterns were found in the three tumors by using a fluorescence-activated cell sorter (FACS). An antibody to CAT was prepared by immunization of guinea pigs with CAT-antigen from bovine brain. The specificity of the antibody obtained was examined with mouse cervical spinal cord. Identification of the cholinergic cells was performed in three types of non-cloned tumor culture cells, neuroblastoma C-1300 in A/J mice, glioblastoma 203GL in C57BL6 mice and lymphosarcoma 6C3HED in CBA mice. The CAT content and distribution were determined by radiochemical assay, immunohistochemical staining, and individual cell counting with a FACS. The results of radiochemical assay and immunohistochemical staining were in agreement with the CAT distribution pattern determined by cell counting with FACS IV.
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PMID:Immunohistochemical identification of cholinergic cells in non-cloned tumor cells. 635 20

Review of the pathology of benign and malignant tumors of the adrenal gland. Generally, all neoplasms of the adrenal gland may show endocrine activity with respective clinical syndromes. Such syndromes may give first clues for the important differential diagnosis between hyperplasia and neoplasia. There is no correlation between morphology and function of the various tumors. Cancers of the adrenal cortex are extremely rare. They occur at any age. At infancy, neoplasms of the adrenal cortex are almost always hormonally active and malignant. Adenomas and carcinomas of the adrenal cortex are discussed with special reference to the difficulty of differential diagnosis. The prognosis of carcinomas of the adrenal cortex is poor. The five years' survival rate amounts to 10--25%. The dignity of phaeochromocytoma can hardly be established by morphology alone. Most of them are benign. Metastases of these tumors are the only certain criterion of malignancy. Neuroblastoma metastasizes very early and--in case of bone marrow involvement--must be separated from lymphosarcoma, Ewing's sarcoma, and from undifferentiated leukemias. Cysts of the adrenal gland are very rare but they are important in the differential diagnosis of adrenal masses. Finally, tumors like myelolipoma are briefly discussed.
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PMID:[Pathologic anatomy of adrenal tumors]. 741 71

More aggressiveness in treatment of childhood malignancies has had an evident impact on survival and rate of cure but, it has also allowed us to discover long-term effects of these treatments, and second malignant tumors of them. Between 1970 and 1993, 472 cases of malignant tumors in childhood were diagnosed in our department. Six of them (1.27%) developed a second tumor (five malignant and one benign). Relationship between first and second tumors are: seven years old boy, cervical lymphosarcoma-thyroid carcinoma; eleven years old boy, osteogenic sarcoma-vesical carcinoma: two years and six months old boy, cerebellar astrocytoma-soft tissue osteogenic sarcoma; five years old girl. Wilm's tumor-scapular osteogenic chondroma; one year and a half old girl, abdominal neuroblastoma-granulocytic sarcoma (chloroma); twelve years old boy. Hodgkin's disease-acute myeloblastic leukemia. All of them were clearly related to concogenic effect of radiation or chemotherapy.
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PMID:[Second tumors in childhood]. 776 70


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