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 expression of common acute lymphoblastic leukemia antigen (CALLA) on a human neuroblastoma cell line, SJ-N-CG, was demonstrated by indirect membrane immunofluorescence, complement-dependent cytotoxicity, and quantitative absorption, using two monoclonal antibodies (J-5 and BA-3) directed against CALLA. Immunoprecipitation of solubilized 125I-labeled membrane proteins from SJ-N-CG cells with J-5 antibody revealed a protein with a molecular weight of 100,000 as determined on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Morphological differentiation of SJ-N-CG cells could be induced in the presence of 2.0 mM dibutyryl adenosine 3'-5'-cyclic monophosphoric acid for 10 days of culture. Changes in cell surface membrane antigens associated with morphological differentiation were studied by indirect immunofluorescence and complement-dependent cytotoxicity using a panel of seven monoclonal antibodies. Increases in the antigens recognized by BA-2 (detecting leukemia-associated antigen), anti-Thy-1, and antibody 390 (Thy-1 antigen) were found in "differentiated cells," while those detected by BA-1 (B-cell-associated antigen) and J-5 (CALLA) were unchanged. In contrast, the antitransferrin receptor defined by B3/25 was inhibited, and expression of B7/21-defined la-like antigen was not induced. Kinetic studies on antigenic alterations showed that the expression of BA-2-defined antigen rose on Day 2 and remained at the same level until Day 10. The expression of CALLA was not changed from Days 2 to 10. The augmentation of Thy-1 antigen was noted on Day 4 and reached the maximum on Day 10. These results show that dibutyryl adenosine 3'-5'-cyclic monophosphoric acid is capable of inducing phenotypic changes in SJ-N-CG cells. The changes of expression of some antigens on exposure of cells to dibutyryl adenosine 3'-5'-cyclic monophosphoric acid may enable us to have a greater understanding of the differentiation of neuroblastoma to a more mature ganglioneuroblastoma phenotype.
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PMID:Altered expression of cell surface membrane antigens in a common acute lymphoblastic leukemia-associated antigen-expressing neuroblastoma cell line (SJ-N-CG) with morphological differentiation. 298 Nov 59

Neuroblastoma (NB) arises from primitive sympathetic neuroblasts in the adrenal gland or the sympathetic ganglion. NB in situ, sometimes observed in the adrenal glands of autopsied infants, is considered to be a premalignant lesion that may develop into NB. Little is understood about the morphological and biochemical changes that accompany this malignant progression. In this study, a unique monoclonal antibody, KP-NAC8, raised against a human NB cell line is described. This binds to NB cells but not to fetal neuroblasts. The antibody recognizes a Mr 200,000 surface protein on NB cells. KP-NAC8 binds to 15 of 17 human NB cell lines and all 26 fresh NB samples either from tumor tissues or from marrow aspirates involved with tumor. The antibody was found to cross-react with some other tumor cell lines, namely, Ewing's sarcoma (1 of 2), melanoma (1 of 4), lung cancer (3 of 3), and leukemia (2 of 14) cell lines. However, KP-NAC8 did not bind to any rhabdomyosarcoma (0 of 4), Wilms' tumor (0 of 4), retinoblastoma (0 of 2), glioma (0 of 4), and gastric cancer (0 of 2) cell lines examined. Among fetal tissues, KP-NAC8 did not react with normal neuroblasts in the adrenal glands of 5 fetuses. In a further study, the membrane phenotype of fetal adrenal neuroblasts was analyzed by a panel of 12 monoclonal antibodies including KP-NAC8. A comparison of the binding of the same panel of antibodies to fresh NB revealed that antibodies UJ13A, UJ127:11, PI153/3, anti-Thy-1, A2B5, BA-1, BA-2, HSAN1.2, and Leu-7 bound to both fetal adrenal neuroblasts and NB cells. Monoclonal antibodies OKIa-1 and J5 did not bind to either tissues. The only antibody that could distinguish fetal adrenal neuroblasts from NB cells was KP-NAC8. KP-NAC8 may, therefore, define a differentiation-related antigen that may prove helpful in understanding the biological nature of NB and NB in situ.
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PMID:Cell surface membrane antigen present on neuroblastoma cells but not fetal neuroblasts recognized by a monoclonal antibody (KP-NAC8). 356 10

Tissue specimens of neural crest-derived structures like normal spinal and sympathetic ganglia and adrenals of adults, infants and fetuses were used as immunohistochemical test substrates for a panel of 10 monoclonal antibodies to neuroblastoma cells raised by immunization with a variety of immunogens (fetal brain, neuroblastoma cell lineages, chick retinal cells or purified Thy-1 antigen). Antigen expression varied among normal structures such as ganglion cells, satellite cells, various nerve fibres, and different cells in the adrenal cortex. This variability in immunoreactivity shown by different cell types and structures was comparable to that seen when the same panel of monoclonal antibodies was applied to neuroblastomas and to ganglioneuroblastomas of different degrees of maturation and differentiation. The neoplasms thus seemed to reflect the normal maturation in the neuroectodermally-derived structures. Also, the studies give indications as to the cell of origin of the undifferentiated neuroblastomas.
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PMID:Immunohistochemical performance testing of monoclonal antibodies to neuroblastoma cells on normal adrenals, spinal and sympathetic ganglia, and neural crest tumours. 359 74

The possibility to reveal the following types of neuroblastoma is described: with c-ALL-antigen; with Thy-1-antigen (ICO-10); with granulocytic antigen (ICO-G2); with B-cell antigen (IPO-10). Immunocompetent cells in the tumour may be studied with the use of monoclonal antibodies ICO-1, ICO-11, ICO-GM-1, OKT3, IPO-3.
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PMID:[Study of neuroblastomas in children using a complex of monoclonal antibodies]. 367 27

The accurate diagnosis of malignant tumor type is essential to enable the correct therapeutic regimen to be followed and to predict a patient's prognosis. However, the differential diagnosis of "small-round-cell" tumors, represented by neuroblastoma, rhabdomyosarcoma, lymphoma/leukemia and Ewing's sarcoma, can occasionally be difficult by conventional morphological and biochemical methods. If tumor membrane markers were available, these could provide rapid and accurate diagnostic aids. In the present work, a panel of 9 monoclonal antibodies raised against hematopoietic cells (BA-1, BA-2, J-5 and B7/21), brain cells (UJ-13A, UJ-127-11 and anti-Thy-1), and neuroblastoma cells (HSAN1.2 and PI153/3) was used to analyze the membrane phenotypes of 12 neuroblastoma, 4 rhabdomyosarcoma and 3 Ewing's sarcoma cell lines and cells of 3 fresh bone marrow tumors. BA-1, UJ-127-11 and PI153/3 antibodies may be useful for the differential diagnosis of neuroblastoma from rhabdomyosarcoma and Ewing's sarcoma.
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PMID:Possible differential diagnosis of neuroblastoma from rhabdomyosarcoma and Ewing's sarcoma by using a panel of monoclonal antibodies. 392 4

The Thy-1 antigen is a cell surface glycoprotein found in neural tissue of all mammalian species so far studied. The distribution and amount of this antigen has been measured on 4 human neuronal and 2 neuroglial cell lines and on fresh tumour cells of neuronal origin. In 3 out of 4 neuronal lines (LAN-1, TR14, CHP 212) more than 90% of cells were Thy-1+, however, LAN-1 cells showed only weak immunofluorescence and bore on average 2.4 times fewer molecules of Thy-1 per cell than those of either TR14 or CHP 212. The mean number of Thy-1 molecules per TR14 cell was shown to be approximately 2.25 x 10(5). In contrast, only 66% of cells in the fourth neuronal line (CHP 100) were Thy-1+, although these showed strong immunofluorescence. Both glial cell lines, UCH-203 and H314/123, showed strong Thy-1 immunofluorescence on more than 90% of cells. Similarly, with fresh neuronal tumour cells, although approximately 80% of tumours were Thy-1+ (essentially 100% of cells in these being positive) there were considerable differences in the intensity of labelling by immunofluorescence between different tumours. Such heterogeneity in cell lines and malignancy may reflect normal in vivo variation. Different phenotypes might therefore represent separate neural cell lineages, or simply differences in maturational status within a lineage. The very low frequency of Thy-1+ cells in normal bone marrow (less than 0.1% of nucleated cells) indicates that anti-Thy-1 antibodies may be valuable in both the diagnosis and subsequent treatment of neuroblastoma.
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PMID:Human Thy-1: expression on the cell surface of neuronal and glial cells. 612 10

Antibodies to the differentation antigen Thy-1 were linked via a dextran-hydrazide bridge to adriamycin. These monoclonal antibodies, which were previously prepared against first-trimester human fetal cells, reacted with several human brain tissue tumors such as neuroblastoma, glioma, and leiomyosarcoma through a common differentiation antigen, Thy-1. The conjugates were tested in vitro for their cytotoxic effects on a neuroblastoma cell line LA-N-I. The conjugate maintained its full drug and antibody activities. Moreover, the specific conjugate exhibited a higher efficacy in inhibition of RNA synthesis and was more cytotoxic than the nonspecific Ig-drug conjugate. Fluorescent microscopy showed that the specific conjugate was able to penetrate the cell membrane. Both the specific antibody and the drug were also observed to accumulate in the cell nucleus. Flow microfluorometric analysis of cellular DNA traverse showed that the specific antibody-drug conjugate caused a higher accumulation of neuroblastoma cells in stage G2 of the cell cycle than did the free drug, perhaps indicating a more efficient prevention of the progression of cells through mitosis.
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PMID:A conjugate of adriamycin and monoclonal antibodies to Thy-1 antigen inhibits human neuroblastoma cells in vitro. 614 73

L1 is a transmembranal homophilic cell adhesion molecule of the immunoglobulin superfamily expressed by neural and lymphoid cells. The heat-stable antigen (HSA, murine CD24) nectadrin is a highly and heterogeneously glycosylated glycophosphatidylinositol-linked differentiation antigen of haematopoietic and neural cells. L1 and nectadrin have been shown to mediate cell adhesion and intracellular Ca2+ signals in neurons and B lymphoblasts, respectively. Here we show that nectadrin is co-expressed with L1 in murine cerebellar granule cell neurons and neuroblastoma N2A cells. Purified nectadrin bound to L1 with an apparent binding ratio of five nectadrin molecules to one L1 molecule at saturation. Binding between nectadrin and purified N-CAM was not observed. In co-capping experiments nectadrin co-redistributed with L1 and N-CAM. Since in these cells N-CAM and L1 cohere by cis-binding nectadrin appears to join the L1-N-CAM complex through binding to L1. Antibodies to each L1 and nectadrin evoked small increases in the intracellular Ca2+ concentration. However, when both antibodies were added together or in tandem to the cells, a strong intracellular Ca2+ signal was measured that was at least 6- and 10-fold stronger than the signal separately induced by L1 and nectadrin antibodies respectively. Such a cooperative effect was not observed in B lymphoblasts, using the same antibodies, or in neurons, using a combination of L1 and Thy-1 antibodies. Both the weak Ca2+ signal mediated by L1 alone and the enhanced signal jointly triggered by antibodies to L1 and nectadrin were inhibited by phorbol 12-myristate 13-acetate and were not significantly affected by Ni2+ and Cd2+ cations, suggesting that they are related to one another and involve recruitment of intracellular Ca2+. Nectadrin therefore appears to join a functional complex of neuronal adhesion molecules and to potentiate the signal transduction pathway of L1, possibly in response to neuron-neuron contact formation.
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PMID:Evidence for cis interaction and cooperative signalling by the heat-stable antigen nectadrin (murine CD24) and the cell adhesion molecule L1 in neurons. 761 34

It is understood that neuroblastoma (NB) in the liver of patients with clinical stage IV-S disease may disappear, but the mechanism of such regression is unclear. A genetic hypothesis has previously been suggested, although heretofore an immunologic explanation had not been reported. Using C1300 NB in AJ mice, we developed a model of liver metastatic disease by directly injecting tumor cells into a subcutaneously translocated spleen. Intrasplenic inoculation of 2 x 10(6) C1300 NB cells produced liver subcapsular foci of NB in 100% of animals, whose mean survival period was 18 days. Three days after tumor inoculation, interleukin-2 (IL-2) (2,400 U/d) was continuously infused for 14 days via a miniosmotic pump, and daily survival was followed. Animals were sampled serially by histological and immunohistochemical staining. Animal survival was significantly prolonged (P < .05) in the IL-2 group when compared with that of saline controls, but importantly, 50% of the mice were cured. Histological examination showed early infiltration of mononuclear cells, predominantly lymphocytes, around liver metastatic foci; and phenotypic analysis of these cells showed them to be Thy-1.2-positive and asialo GM1-positive, suggesting they are of natural killer (NK) and lymphokine-activated killer (LAK) origin. Most importantly, in cured animals the histological analysis of the liver demonstrated reversion to a scar-free anatomy, akin to that seen in stage IV-S NB survival. These data suggest that immune-mediated regression of NB in the liver is possible; whether the result of therapy or spontaneous, the liver histology reverts to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immune-mediated regression of 'metastatic' neuroblastoma in the liver. 817 85

Osteogenic protein-1 (OP-1) is a member of the TGF-beta superfamily that is expressed in the nervous system. We recently showed that human recombinant osteogenic protein-1 (hOP-1) strongly promotes the aggregation of dividing neuroblastoma x glioma hybrid NG108-15 cells, in part by inducing the major isoforms of the neural cell adhesion molecule (N-CAM) (Perides, G., Safran, R. M., Rueger, D. C., and Charness, M. E. (1992) Proc. Natl. Acad. Sci. U. S. A. 89, 10326-10330). Here we show that hOP-1 induces L1 expression approximately 6-fold in NG108-15 cells without changing the levels of N-cadherin, neurofilament 200, Thy-1, tau, and G alpha s. OP-1 induction of L1 and N-CAM was unassociated with changes in cell proliferation and was not reproduced by cellular differentiation. The increased adhesiveness of hOP-1-treated NG108-15 cells could be inhibited in part by Fab fragments of an anti-L1 polyclonal antiserum. L1 and N-CAM expression first increased 12-18 h after hOP-1 treatment, reached a maximum after 2-3 days, persisted for up to 5 days, and returned to control levels 3 days after hOP-1 withdrawal. The increases in L1 and N-CAM protein levels were preceded or accompanied by large increases in the abundance of L1 and all detectable N-CAM mRNAs. Actinomycin D prevented the induction by hOP-1 of L1 and N-CAM mRNAs, suggesting that hOP-1 regulates immunoglobulin CAM gene transcription. OP-1 is the first described growth factor that regulates both N-CAM and L1 gene expression.
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PMID:Osteogenic protein-1 regulates L1 and neural cell adhesion molecule gene expression in neural cells. 822 84


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