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)

Spleen lymphoid cells from A/J mice recognize specific antigenic differences on the surface membranes of syngeneic C1300 neuroblastoma cells and incorporate 3H-thymidine into DNA in unidirectional mixed cell cultures in the absence of isologous serum. The response requires an optimal ratio of responder to stimulator cells, and is detectable after 24 h. It is specifically blocked by the presence of a papain-solubilized crude membrane extract from the same neuroblastoma cells, the extent of inhibition being dependent on the concentration of the extract and the time when it is added to the cultures. Spleen cells from mice bearing the neuroblastoma respond earlier and incorporate more 3H-thymidine than cells from unsensitized mice. The enhanced response of the primed spleen cells to the stimulator cells is similar to a secondary immune response and can be induced by soluble crude tumor extracts in the absence of stimulator cells.
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PMID:In vitro stimulation of mouse lymphoid cells by C1300 neuroblastoma cells or tumor membrane extracts. 6 46

Spleen cells from mice immunized with a cultured human neuroblastoma were hybridized with the mouse plasmacytoma P3X63Ag8. Hybrid myelomas were screened for production of antibodies that reacted with human neuroblastomas but not with cells from other tissues. One of these hybridoma antibodies reacted with an antigen present on the six human neuroblastomas tested, one of two retinoblastomas, a glioblastoma, and fetal brain, but did not react with other tumors or tissues including adult human brain.
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PMID:Hybrid myelomas producing antibodies against a human neuroblastoma antigen present on fetal brain. 42 40

Rarely retroperitoneal neuroblastoma is a well localized, encapsulated tumor, like it my appear somewhere else, as in the pelvic floor or mediastinum. Even with the same histological findings they are different from de point of view of invasion. Therefore the surgical approach should be different in each case. This is our main conclusion after de study performed in 48 cases operated upon in the last 8 years. We have tried three kinds of operations. 1. The so called curative, total resections. Performing a surgical ablation of the tumor and the organs macroscopically involved, either prior or after radiotherapy or quimiotherapy. At any risk, even of life in the early postoperative period. This kind of surgery has been undertaken in 34 cases with an early mortality of 9. The main aim of this technique is to divide the tumor in two across the supraaortic line well below the renal vessels and up to the diaphragm. In 18 cases the homolateral kidney was resected with the suprarrenal gland. Spleen and pancreas in 5 cases, colon in 4, and the inferior vena cava in 3. The survivors over 2 years are 19 cases. 2. Paliative resection, taking out the main tumor only, has been achieved in 4 cases, with the highest mortality because postoperative hemorrhage. We believed is a dangerous procedure. None of these children survived more than one year. 3. Biopsy and surgical macroscopic diagnosis of invasion plus placing clips at their margin has been carried out in 12 occasions. This had naturally the best early postoperative but not in the long run, none survived more than 2 years. A second look up with resection was undertaken in 3 cases with mortality of one. Most surgeons are puzzled when dealing with retroperitoneal neuroblastoma and some how disappointed before undertaking a long, difficult and highly risk operation, but in many instances still is about the only hope they may have.
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PMID:[Surgical approach of retroperitoneal neuroblastoma in infancy (author's transl)]. 101 79

BALB/c mice were immunized with an opioid receptor complex over the period of 1 year. Spleen cells from the mouse, whose serum inhibited opiate binding to rat neural membranes to the greatest extent, were fused with P3-X63-Ag8. 653.3 myeloma cells. By radioimmunoassay (RIA), 32 cell lines have been detected that secrete an antibody to a component of the isolated receptor complex. Antibodies from 2 of the cell lines have an effect on opiate binding to rat neural membranes. One antibody, OR-689.2.4 is an IgM cryoglobulin. This antibody partially inhibited the binding of 3H-dihydromorphine (3H-DHM), 3H-naloxone, 3H-ethylketocyclazocine (3H-EKC), and 3H-D-Ala2, D-Leu5 enkephalin (3H-DADLE) to rat neural membranes. The other antibody, OR-465.3, inhibited the binding of 3H-DHM and 3H-naloxone to rat neural membranes by a maximum of 70%. This antibody also inhibited the binding of 3H-DADLE to neural membranes but, did not affect the binding of this peptide to membranes from the neuroblastoma-glioma hybrid cell line, NG108-15. Work is ongoing to generate monoclonal antibodies specific for each subclass of opioid receptor.
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PMID:Generating monoclonal antibodies to the opioid receptor. 631 52

The hybridoma technique was used to generate monoclonal antibodies against a wide spectrum of melanoma-associated surface antigens. Mice were immunized against the human melanoma lines Mel A-375, SK Mel-25, and Mel S-5 (subclone of SK Mel-25), which differ with respect to a number of biological and biochemical properties. Spleen cells were fused with P3 X 63-AG8.653 myeloma cells. Twenty hybridomas producing antibodies that were negative on platelets, leukocytes, and monocytes but positive on melanoma cells were isolated and recloned. The specificity of antibodies was investigated on 30 human melanoma and nonmelanoma lines. Five groups of antibodies could be distinguished by their reactivity (1) with few melanoma lines and embryonic fibroblasts; (2) with melanoma, neuroblastoma, and teratoma; (3) with melanoma, neuroblastoma, glioblastoma, teratoma, and carcinoma; (4) with melanoma, teratoma, and carcinoma; and (5) with melanoma, neuroblastoma, teratoma, glioblastoma, carcinoma, embryonic fibroblasts, and B-lymphoblastoid cells. The antigen expression was qualitatively and quantitatively different from cell line to cell line. No evidence for melanoma-specific antigens was found. Eight antibodies were isolated detecting phenotypic differences on sublines of SK Mel-25.
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PMID:Detection of phenotypic differences on human malignant melanoma lines and their variant sublines with monoclonal antibodies. 655 61

IgM antibodies to gangliosides, sialic acid-containing glycosphingolipids, have been shown to mediate anti-tumor effects in cancer patients with melanoma and neuroblastoma and to correlate with survival. Mechanisms by which the antibodies induce tumor suppression, however, have not been systematically studied. To investigate this point, we produced and characterized C57BL/6 mice transgenic for IgM antibody to ganglioside GD2. The transgenic (TG) mice showed high IgM, but not IgG antibody titers against GD2 in their sera. No significant clinical symptoms were observed. When EL4 cells, syngeneic T lymphoma that express ganglioside GD2, were injected into TG mice, prolonged survival was observed. Complement-dependent cytotoxicity (CDC) of EL4 cells was mediated with TG mice sera. Neither antibody-dependent cellular cytotoxicity with their sera nor cytotoxic T lymphocyte activity to EL4 cells was shown in TG mice. Spleen lymphocytes from TG mice had increased numbers of natural killer (NK) cells, but not T cells, B cells, or macrophages compared with wild-type mice. Depletion of NK cells with anti-asialo GM1 rabbit serum reduced or abrogated the observed anti-tumor effects, suggesting that NK cells play a major role in tumor eradication or suppression. NK cell activity in TG mice was much higher than wild-type mice. Moreover, TG mice showed prolonged survival after injection with syngeneic B16 melanoma cells, which express GM3, but not GD2 or GD3. Taking these results together, our studies demonstrate that the TG mice have significant anti-tumor characteristics, probably due to CDC and NK cell expansion and activation with anti-ganglioside GD2 antibody.
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PMID:Expansion of natural killer cells in mice transgenic for IgM antibody to ganglioside GD2: demonstration of prolonged survival after challenge with syngeneic tumor cells. 1285 87

IL-21 is a member of the IL-2 cytokine family, produced by CD4+ T cells. We previously showed that immunotherapy (IT) with IL-21-transduced neuroblastoma cells (Neuro2a/IL-21) cured 33% of syngeneic mice bearing systemic NB. Here, we studied whether the removal of Treg cells could potentiate the therapeutic efficacy of Neuro2a/IL-21 vaccine. The administration of anti-CD25 mAb, which targets Treg cells, slightly potentiated the effect of vaccine IT (50% cure rate), but anti-CD4 mAb had a more potent effect leading to 80% cure rate. Anti-CD25 mAb, indeed, only partially depleted CD4+CD25+FoxP3+ Treg cells, whereas anti-CD4 mAb was more effective in this respect, leading to 90% depletion of Treg cells. In mice receiving vaccine+anti-CD4 mAb, which developed systemic immunity to NB, CD4+ T cells counts completely recovered in 90 days. Depletion of CD8+ T cells abrogated the effect of the combined IT, indicating a predominant role of these cells in driving the immune response. In addition, CD8+ T cells from cured mice coinjected with Neuro2a/parental cells (pc) in NOD-SCID mice completely inhibited tumor growth. Spleen cells from mice receiving Neuro2a/IL-21 vaccination showed increased expression of IFN-alpha2, -beta1 and -gamma mRNA. Moreover, mice receiving vaccine therapy alone or vaccine+anti-CD4 mAb showed increased IFN-gamma serum levels and IFN-gamma-producing CD8+ T cells were found in spleen cells. In conclusion, anti-CD4 mAb potentiated IL-21-based IT by removing Treg cells and/or their precursors and other potentially immune-suppressive CD4+ cell subsets, thus allowing the development of an IL-21-driven CD8+ T cell response, which mediates NB rejection.
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PMID:Transient depletion of CD4(+) T cells augments IL-21-based immunotherapy of disseminated neuroblastoma in syngeneic mice. 2003 20

We designed multimodal tumor vaccine that consists of irradiated tumor cells infected with the oncolytic IL-12-expressing HSV-1 virus, M002. This vaccine was tested against the syngeneic neuroblastoma mouse model Neuro 2a injected into the right caudate nucleus of the immunocompetent A/J mice. Mice were vaccinated via intramuscular injection of multimodal vaccine or uninfected irradiated tumor cells at seven and 14 days after tumor establishment. While there was no survival difference between groups vaccinated with cell-based vaccine applied following tumor injection, a premunition prime/boost vaccination strategy produced a significant survival advantage in both groups and sustained immune response to an intracranial rechallenge of the same tumor. The syngeneic but unrelated H6 hepatocellular tumor cell line grew unrestricted in vaccinated mice, indicative of vaccine-mediated specific immunity to Neuro 2a tumors. Longitudinal analyses of tumor-infiltrating lymphocytes revealed a primary adaptive T cell response involving both CD4+ and CD8+ T cell subsets. Spleen cell mononuclear preparations from vaccinated mice were significantly more cytotoxic to Neuro 2a tumor cells than spleen cells from control mice as demonstrated in a four-hour in vitro cytotoxicity assay. These results strongly suggest that an irradiated whole cell tumor vaccine incorporating IL-12-expressing M002 HSV can produce a durable, specific immunization in a murine model of intracranial tumor.
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PMID:Effect of HSV-IL12 Loaded Tumor Cell-Based Vaccination in a Mouse Model of High-Grade Neuroblastoma. 2761 Mar 92