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 fine needle aspiration (FNA) cytologic findings in 18 cases of metastatic neoplasms of the breast are reported. The cases were encountered in a combined series of 2,529 FNA breast biopsies, of which 666 were malignant; the metastatic neoplasms of the breast thus constituted 2.7% of all the malignant breast tumors. The series consists of 15 women and 3 men, with a mean age of 48 years (range of 11 to 73 years). Sixteen biopsies confirmed metastatic malignancy in patients with known extramammary primaries; the prebiopsy clinical diagnoses in six of the patients were benign breast lesions. In eight patients, the clinical differential diagnosis was either a benign or malignant primary breast lesion versus a metastatic malignancy. In two additional patients, the FNA biopsy identified metastatic neoplasms from unsuspected extramammary primaries. The metastatic neoplasms included three small-cell carcinomas of the lung, one squamous-cell carcinoma of the lung, two malignant melanomas, three ovarian malignancies, including a dysgerminoma, and one each of carcinoma of the fallopian tube, endometrial carcinoma, transitional-cell carcinoma of the urinary bladder, prostatic carcinoma, acute granulocytic leukemia, lymphoma, mycosis fungoides, hepatoma and neuroblastoma of the retroperitoneum. Recognition of unusual cytologic patterns raised the suspicion of, or confirmed the diagnosis of, malignancy in all cases, with no false-negative diagnoses. None of the cases were cytologically interpreted as a primary breast malignancy. Ancillary studies performed on the FNA material, including immunocytochemistry, contributed to a definitive diagnosis in three cases. FNA diagnosis of metastatic malignancy of the breast is essential in order to avoid unnecessary mastectomy and to ensure appropriate chemotherapy and/or irradiation treatment.
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PMID:Fine needle aspiration cytology of neoplasms metastatic to the breast. 347 62

Recombinant human tumor necrosis factor (rHu-TNF) was found to exhibit potent antitumor activities not only against murine tumors, i.e. Meth A sarcoma, B 16 melanoma, colon 26 adenocarcinoma, Lewis lung carcinoma and MH134 hepatoma, transplanted in syngeneic mice but also against human tumors, i.e. HMV-2 melanoma, PC-10 lung carcinoma and GOTO neuroblastoma, heterotransplanted in nude mice. rHu-TNF caused necrosis of all tumors tested and inhibited their growth in a dose dependent manner. Complete regression of tumors was observed in mice bearing Meth A, B16, colon 26, MH134, HMV-2 and PC-10 but not in mice bearing Lewis lung carcinoma and GOTO neuroblastoma. The prolongation of survival time was also observed in syngeneic mice transplanted with murine tumors except Lewis lung carcinoma. The antitumor effect of rHu-TNF was more evident when it was given intratumorally than when given intravenously. The feasibility of rHu-TNF as a drug for cancer therapy is discussed.
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PMID:Recombinant human tumor necrosis factor--II. Antitumor effect on murine and human tumors transplanted in mice. 352 34

Monoclonal antibodies that immunoprecipitate human monoamine oxidase (MAO) A or human MAO B, but not the corresponding mouse enzymes, were used to assay for the presence of immunoprecipitable MAO A or MAO B (presumably coded by the respective human genes) in mouse-human hybrid somatic cell lines containing small numbers of human chromosomes. The results were as follow: Extracts of a human lymphoblastoid x mouse hepatoma hybrid line that retained the human X chromosome contained immunoprecipitable MAO B, while a similar hybrid line that contained the same human chromosomes, except for the human X, did not. Extracts of a human fibroblast x mouse neuroblastoma hybrid cell line, whose human chromosomal material consisted solely of the X, contained both immunoprecipitable MAO A and MAO B. Extracts of a related hybrid line, whose human chromosomal material consisted solely of an autonomous fragment and a fragment translocated to a mouse chromosome, contained immunoprecipitable MAO A. However, the level of immunoprecipitable MAO B activity in extracts of this hybrid was low or undetectable. Among extracts of 33 human fibroblast x mouse hepatoma hybrids that had been selected for expression of the X-linked human enzyme HPRT, 60% contained immunoprecipitable MAO B. This figure was comparable to the 58% that expressed the X-linked human isozyme for glucose-6-phosphate dehydrogenase (G6PD). When 11 of these hybrid lines, which contained immunoprecipitable MAO B and human HPRT, were selected for loss of HPRT, all lost immunoprecipitable MAO B in addition to HPRT. These data demonstrate that genes controlling the expression of MAO A and MAO B, which can be immunoprecipitated with the human-specific monoclonal antibodies, are located on the human X chromosome. Properties of the immunological epitopes recognized by the monoclonal antibodies suggest that the X-linked genes detected in this study are probably structural genes for the enzymes.
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PMID:Assignment of genes for human monoamine oxidases A and B to the X chromosome. 354 Mar 17

The presence of angiotensinogen messenger RNA (mRNA) was assessed in total RNA extracted from hepatoma, glioma, neuroblastoma, and glioma-neuroblastoma hybrid cell lines. Total RNA from 1 X 10(7) cells was extracted, transferred to a membrane, and hybridized with a 32P-labeled, full-length (1650-base pair) rat angiotensinogen complementary DNA (cDNA). Angiotensinogen RNA sequences could be definitively detected only in hepatoma cells. Steroids were used in an attempt to increase the angiotensinogen mRNA level. Dexamethasone (2 X 10(-6) M) or 17 beta-estradiol (1 X 10(-7) M) was added to the cultures 18 to 24 hours prior to harvest. Dexamethasone treatment of the hepatoma cells resulted in a large increase in angiotensinogen mRNA, whereas estradiol had no effect. Steroids failed to induce detectable levels of angiotensinogen mRNA in total RNA from the other cell lines. That the RNA was intact was ensured by hybridizing duplicate Northern blots to a 32P-labeled actin cDNA. Actin mRNA sequences were detected in all cell lines. Blot hybridization of poly(A)+RNA resulted in the visualization of a weak angiotensinogen mRNA signal for a glioma cell line and a glioma-neuroblastoma hybrid line. However, the ability to detect angiotensinogen mRNA in a cell may depend on the phenotype expressed, which can be governed by culture conditions.
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PMID:Presence of angiotensinogen messenger RNA in various cultured cell lines. 359 87

A conditioning treatment of 30 min at 42 degrees C or 43 degrees C, followed by a 4-h recovery period at 37 degrees C, induces thermotolerance state in the cytoskeleton of Reuber H35 hepatoma cells and N2A neuroblastoma cells. Evidence for the involvement of heat shock proteins in the development of thermotolerance in the cytoskeleton has been obtained from the following observations: only those conditioning treatments inducing the enhanced synthesis of heat shock proteins (HSPs) are able to induce the heat-resistant state of the cytoskeleton; prevention of HSP synthesis by actinomycin D or cycloheximide also prevents the acquisition of thermotolerance in the cytoskeleton; an alternative inducer of HSP synthesis, sodium arsenite, is also able to induce the cytoskeletal thermotolerance; the kinetics of development and disappearance of thermotolerance in the cytoskeleton is parallel to the kinetics of accumulation and decay of HSPs. The possible function of HSPs in the heat-resistant cytoskeleton of H35 hepatoma and N2A neuroblastoma cells is discussed.
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PMID:Stress-induced thermotolerance of the cytoskeleton of mouse neuroblastoma N2A cells and rat Reuber H35 hepatoma cells. 381 63

A 20 h pre-treatment of human cells from normal (foetal lung) or malignant origin (glioma, lines U118 MG and U251 MG and bladder carcinoma, line EJ) with dexamethasone failed to increase their radiation resistance in vitro despite a 2-fold increase in the GSH content of a glioma cell line, U251 MG, and a small but significant increase in the GSH content of EJ bladder carcinoma cells. In contrast, there was a correlation between an increase in radiation resistance and an elevated GSH content of rodent cells (Chinese hamster lung, line V-79-379A; ovary, line CHO; rat hepatoma, line HTC, and mouse neuroblastoma, line NB413A) after a similar pre-treatment. The results suggest that enhancement of radiation resistance cannot be directly ascribed to an elevated GSH content in steroid-treated cells. On the basis of these data it is unlikely that the efficacy of radiotherapy will be diminished amongst patients receiving concomitant treatment with dexamethasone. However, in vivo testing is required to confirm these findings.
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PMID:Studies on the relationship between the radiation resistance and glutathione content of human and rodent cells after treatment with dexamethasone in vitro. 387 26

The role of calmodulin (CaM) in cellular heat injury of neuroblastoma N2A and hepatoma H35 cells has been investigated, using specific calmodulin-inhibiting drugs (Trifluoperazine, Compound 48/80 and Calmidazolium). These CaM-specific drugs potentiate hyperthermia-induced cell killing, suggesting CaM to be involved in processes aimed on the repair of heat injury. The CaM inhibitors also prevent hyperthermia-induced cytoskeletal alterations in the cell types studied. The action of CaM inhibitors was dose dependent, and seems to be confined to the first period of the hyperthermic treatment. Neither production of heat shock proteins in heat-shocked cultures, nor the rate of protein synthesis in control cultures were affected by the CaM inhibitors. It was concluded that an inverse correlation exists between hyperthermic cell killing and cytoskeletal alterations. Activation of CaM is suggested to be a fundamental aspect of the cellular heat shock response.
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PMID:Calmodulin inhibitors potentiate hyperthermic cell killing. 391 13

Guanidinoacetate methyltransferase, the enzyme catalyzing the last step in creatine biosynthesis, has previously been considered to be restricted to a few tissues, but it has been found to occur in the cultured cells H4Az C2 rat hepatoma, N4TG1 mouse neuroblastoma, and IMR-90 human fetal lung fibroblast, as well as in skeletal and cardiac muscle of the rat. Activity was highest in the hepatoma, but tissues and cultured cells of nonhepatic origin had 5-20% of the activity of rat liver. Dialyzed 100,000g supernatants prepared from cultured cells or skeletal muscle tissue yielded values for apparent Km in the range of 1.2-3.4 microM for S-adenosylmethionine and 0.050-0.096 mM for guanidinoacetate. Intact monolayers of the three types of cultured cells converted labeled guanidinoacetate in the culture medium to creatine, which was identified by chromatographic behavior and by reaction with creatine kinase. The amounts of guanidinoacetate converted to creatine by fibroblasts and neuroblastoma cells during an 18-h period of incubation suggested that synthesis was proceeding at rates approaching Vmax, even in medium containing the relatively low physiological concentrations of guanidinoacetate. Fibroblast and neuroblastoma cell monolayers also have the capacity to take up creatine provided in the culture medium. The amounts of creatine taken up by monolayers of those cells were measured under the same conditions that were used for measurement of creatine synthesis. Comparison of the amounts of creatine synthesized with the amounts taken up showed that synthesis can make a significant contribution to intracellular pools of creatine plus phosphocreatine in fibroblasts and neuroblastoma cells.
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PMID:Guanidinoacetate methyltransferase activity in tissues and cultured cells. 397 May 26

Between 1919 and 1981, 16 children with primary cardiac tumors (8 rhabdomyomas, 5 fibromas, 2 myxomas, and 1 rhabdomyosarcoma) and 59 children with secondary tumors of the cardiovascular system were seen at The Hospital for Sick Children in Toronto. Distant metastases in 45 children of the latter group, in descending order of frequency, were from non-Hodgkin's lymphoma, neuroblastoma, soft tissue and bone sarcoma, Wilms' tumor, and hepatoma, and involved the myocardium and pericardium. In the remaining 14 children, tumor thrombi from Wilms' tumor (9 cases), adrenal (2 cases) and hepatocellular carcinoma (2 cases), and endodermal sinus tumor (1 case) extended directly into the great veins and/or cardiac chambers. Children with primary and secondary tumors often present with nonspecific clinical, plain radiographic, electrocardiographic, and M-mode echocardiographic findings. Early recognition, utilizing special diagnostic procedures such as two-dimensional echocardiography, computerized axial tomography, angiocardiography, and inferior venocavography, followed by elective surgical resection of tumor under cardiopulmonary bypass and/or radiation and chemotherapy, offers patients with cardiovascular tumors the best chance of cure.
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PMID:Primary and secondary tumors of childhood involving the heart, pericardium, and great vessels. A report of 75 cases and review of the literature. 401 74

The factor(s) present in extracts prepared from the brains of newborn A/J or C57B1/6 mice, which inhibits S20Y neuroblastoma cell growth in vitro, was partially characterized. Twice as much inhibitory activity was extracted per gram wet weight of brain than torso, and inhibitor recovery was greatest in extracts prepared from brains of mice 1 week or less in age. The inhibitory factor(s) was water-soluble and was stable to heating at 100 degrees C, to freezing, and to lyophilization. It was susceptible to the action of pronase. The factor(s) behaved like a molecule of molecular weight approximately 700 upon passage through ultrafiltration membranes. Growth of rat hepatoma (H4), murine melanoma (B16), and transformed murine fibroblasts (WT19 and B6-HCMV) was not significantly inhibited by brain extract. Growth of rat glioma cells (C6) was significantly reduced but to a lesser degree than that of murine neuroblastoma cells (S20Y and N115) and glioma cells (G26-20). These results suggest that the inhibitor expresses a cell specificity.
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PMID:Partial characterization of a brain extract factor(s) inhibitory to transformed neural cells. 405 87


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