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)

Adult A/J mice inoculated with 1 x 10(6) syngeneic C1300 neuroblastoma cells had a palpable tumor after 1 week, and the tumor grew uniformly. The hypertonic KCl extract of the tumor induced blastogenic response of syngeneic spleen cells from tumor-bearing mice, and tumor antigens were considered to be solubilized by KCl from tumor cells. Although a higher blastogenic response to insoluble tumor antigens coupled to Sepharose 4B beads could have been expected as demonstrated in this mixed lymphocyte-tumor cell reaction (MLTR) assays, the blastogenic activity, which was approximately equal to that of soluble tumor antigens, was less than one-third of that in MLTR. The initial information of blastogenic response was found to be transmitted to the responder cells with out the entrance of tumor antigens into the cells by the use of insoluble tumor antigens. Blastogenic responses to soluble tumor antigens and to irradiated tumor cells (MLTR) in spleen cells from tumor-bearing mice were serially assayed after tumor inoculation. The response to soluble tumor antigens reached a peak 2 weeks after inoculation but a progressive depression of the responses was observed after a marked tumor growth. Although the blastogenic activity of soluble tumor antigens was small, changes in consecutive response to soluble tumor antigens in tumor-bearing mice were well correlated with those in MLTR. The blastogenic responses to soluble tumor antigens and MLTR were considered to be the manifestation of tumor-specific cell-mediated immunity. Furthermore, the serial blastogenic responses to concanavalin-A and lipopolysaccharide were also coincident with those of tumor-specific immunity.
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PMID:Blastogenic response of spleen cells from C1300 neuroblastoma-bearing mice to tumor cells or soluble and insoluble tumor antigens. 15 10

The murine neuroblastoma appears to be a useful model for elucidating the mechanism of cellular differentiation. In tissue culture, MNB cells were induced to "irreversibly" differentiate into neuronal-like cells by DBcAMP alone or in combination with cAMP phosphodiesterase inhibitors: papaverine (Pap) and theophylline (Theo). Cells differentiated by DBcAMP, Pap, and Theo were no longer tumorgenic when reinoculated into animals of the host strain. In vivo, DBcAMP, Pap, and Theo caused a reduced tumor volume growth rate in animals with established tumors. Morphologically, this effect appears to be secondary to an arrest of cellular mitoses. Cells insensitive to these agents emerged after 3 to 4 days, and tumor growth accelerated to parallel the rate of the untreated tumors.
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PMID:Differentiation of mouse neuroblastoma cells in vitro and in vivo induced by cyclic adenosine monophosphate (cAMP). 18 80

The effect of papaverine on transplantable C1300 murine neuroblastoma model was evaluated. Subcutaneous inoculation of A/J mice with 10(6) C1300 cells resulted in predictable tumor growth and animal death in 36 +/- 5 days. In 33% of control animals, lung and liver metastases were observed. Subcutaneous injections of papaverine prior to tumor inoculation and during the tumor growth failed to show any detectable effect on local growth of the tumor. Benign transformation of the primary tumor was not observed. However, papaverine injection 21 days after tumor inoculation was associated with only 9% incidence of metastatic development. Papaverine treatment, when started one day prior to tumor inoculation or 10 days after tumor implant, resulted in complete prevention of all detectable metastatic growth, while having no apparent effect on local tumor growth. Further study of papaverine effect in the neuroblastoma murine model is indicated.
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PMID:A study of the effect of papaverine in neuroblastoma using the experimental C1300 murine system. 62 92

Frequently the first clinical sign of neuroblastoma is not caused by local or metastatic tumor growth but is a paraneoplastic symptom (PNS). Such PNS are fever, diarrhea, hypertension, weakness of muscles, Horner's syndrome and myoclonic encephalopathy. Certain PNS disappear with tumor removal, other do not. The clinical importance of PNS is the prognostic and especially diagnostic value. The pathogenetic relations between tumor and PNS as discussed in the literature are interesting but mostly speculative. Effects of Catecholamines and/or immunologic reactions are thought to be the most probable cause of PNS.--The article is based on current literature; in addition, two short case histories are presented.
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PMID:[Paraneoplastic symptoms of neuroblastoma (author's transl)]. 77 98

Exposure of A/J animals bearing transplanted neuroblastoma (C1300) to a 12 Gauss, 60Hz magnetic field for 16 days, starting 3 days post transplant resulted in - (a) early slowing of tumor growth, (b) more free red blood cells in the tumor areas and (c) a tendency to focal tumor cell destruction suggesting that a small alternating magnetic field may affect transplanted tumor growth.
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PMID:Effects of alternating magnetic field (12 gauss) on transplanted neuroblastoma. 84 89

The transplantable C1300 murine neuroblastoma has been characterized biochemically and an in vivo model for the screening of new therapeutic approaches to the treatment of neuroblastoma developed. Subcutaneous inoculation of A/J mice with 10)6) C1300 cells results in predictable tumor growth and animal death in 25 +/- 4 days. Tumor growth is Gompertzian, correlates with increases in tumor RNA and DNA content and with the rate of tumor DNA synthesis as measured by [3H] thymidine incorporation. The model proposed is based on the degree to which various therapeutic options are able to inhibit tumor DNA synthesis, and these observations have been confirmed autoradiographically. A single course of either cyclophosphamide (25, 50, 100 or 200 mg/kg), BCNU (2, 7.5, 15, or 30 mg/kg) or cytosine arabinoside (15, 30, 60, 90 mg/kg) resulted in dose-related inhibition of tumor DNA synthesis. The maximum decline in DNA synthesis that was produced by the highest dose of each agent was by 81%, 77% and 68% of untreated tumor values respectively. Adriamycin, however, even at lethal levels (10 mg/kg), did not elicit significant inhibition of tumor DNA synthesis. Radiotherapy (200 R, 500 R or 1000 R) also produced graded inhibition of tumor DNA synthesis. This model is potentially useful for the preclinical screening of therapuetic options in the treatment of neuroblastoma. Thus, single agent therapy, combination chemotherapy and combined radiotherapy and chemotherapy may be rapidly evaluated for possible clinical use.
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PMID:Pharmacokinetic studies in the chemotherapy of neuroblastoma using the C1300 murine system. 101 81

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

Transplanted A-10 breast adenocarcinomas grew more slowly in young-adult male A/HeJ mice from which the submandibular glands had been extirpated than in sham-operated or unoperated control mice of the same strain. The mitotic index was lower in tumors from experimental animals than in those from controls. Vascularization about the tumor margins was also less prominent. The C1300 neuroblastoma grew more slowly in sialoadenectomized mice than in controls. Modulation of tumor growth by factors of salivary gland origin may have been responsible for these effects.
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PMID:Tumor growth: suppression in mice by submanidibular gland extirpation. 120 48

Pretreatment of syngeneic strain A mice with aldehyde-fixed neuroblastoma cells (clone NB6R) almost completely protected the mice against challenge with viable NB6R cells. In contrast, tumor growth was enhanced in mice treated with fixed cells after challenge with viable cells.
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PMID:Modification of growth of neuroblastoma cells in syngeneic mice by aldehyde-treated neuroblastoma cells. 126 64

Stage IV-S neuroblastoma, characterized by a primary tumor plus disseminated tumors in liver, skin and bone marrow, has a favorable clinical prognosis when compared to metastatic Stage IV neuroblastoma. This favorable outcome also characterized mice receiving tumor transplants to these "IV-S" sites. We report the testing of the hypothesis that enhanced anti-tumor immunity in "IV-S" site neuroblastoma recipients explains this improved survival. A million murine C1300 neuroblastoma cells were inoculated into 256 A/J mice to either "IV-S" sites of skin, liver, peritoneal cavity, or to the disseminated stage "IV" sites of subcutaneous tissue, muscle, kidney and lung. After 21 and 28 days of tumor growth, spleen cells from tumor bearing mice were harvested and analyzed by a 51 Cr release lymphocytotoxicity assay. Cytotoxic T cell activity was consistently higher at day 28 than day 21. In the liver and in the peritoneal cavity, cytotoxic T cell activity was higher than in other organs, and at day 28 these values were significantly higher than Stage "IV" sites. On the other hand, skin is not a immunologically privileged site in vivo study.
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PMID:Influence of primary tumor site on host anti-tumor immunity. 129 50


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