Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The surface membrane antigens of 7 neuroblastoma and 91 leukemia-lymphoma cell lines were studied with the use of a total of 36 murine monoclonal antibodies (MoAb) primarily developed against hematopoietic cells and 2 MoAb developed against human fetal brain. Five of the MoAb against hematopoietic cells (BA-1, BA-2, DU-ALL-1, J-5, and BA-3) consistently bound to common acute lymphoblastic leukemia cell lines, and 2 others (MCS-2 and OKM-1) reacted uniformly with acute myeloblastic-acute monoblastic leukemia cell lines. However, these 7 MoAb also reacted with 1-7 neuroblastoma cell lines. All the human neuroblastoma cell lines bound MoAb BA-2 and DU-ALL-1. Six of the 7 lines reacted with BA-1. Only 1 neuroblastoma cell line (SJ-N-CG) gave positive staining with J-5 and BA-3, and another line (SK-N-AS) bound MoAb MCS-2 and OKM-1. Anti-fetal brain MoAb (UJ-13A and UJ-127-11) were highly positive for all the neuroblastoma cell lines. By contrast, 4 of 43 leukemia-lymphoma cell lines tested bound these anti-fetal brain antibodies. Both B3/25 and OKT-9, anti-transferrin receptor antibodies, reacted with all of the hematopoietic and neuroblastoma cell lines. These results demonstrate that neuroblastoma and hematopoietic cell lines possess common antigenic determinants despite their different embryologic origins. The neuroblastoma cell lines may be classified into subgroups on the basis of phenotype profiles determined by the MoAb. MoAb may be useful in characterization and classification of neuroblastoma cells, as has already proved to be the case for cells of the hematopoietic lineages.
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PMID:Determination of cell surface membrane antigens common to both human neuroblastoma and leukemia-lymphoma cell lines by a panel of 38 monoclonal antibodies. 661 Jul 92

Apomorphine hydrochloride (APO) is known to be a dopamine receptor agonist, and has recently been found to be a novel drug for Alzheimer's disease (AD). We found that APO treatment ameliorated oxidative stress in an AD mouse model and specifically attenuated the hydrogen peroxide-induced p53-related apoptosis in the SH-SY5Y neuroblastoma cell line. To further understand the mechanism behind this action, we investigated the actions of APO on intracellular redox systems, such as the glutathione cycle and catalase. We studied the effects of specific inhibitors for glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (BCNU, MCS, and ATZ, respectively) on the effects of APO. Treatments with MCS or BCNU, but not ATZ, significantly attenuated the protective effects of APO. Interestingly, APO treatment elevated GPx activity, but did not increase the expression of the GPx1 protein. Although BCNU treatment attenuated APO effects, GR activity was not elevated by APO treatment. The same effects were observed in primary neuronal cultures. In addition, treatment with dopamine D1, D2, D3 and D4 receptor antagonists did not counteract the protective action of APO. Thus, APO may enhance GPx activity through dopamine receptor-independent pathways.
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PMID:Activation of glutathione peroxidase and inhibition of p53-related apoptosis by apomorphine. 2179 52