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)

Serum autoantibodies found by radioimmunoassay in 27 of 52 patients with the Lambert-Eaton myasthenic syndrome (LES) bound specifically to a soluble omega-conotoxin binding component of a voltage-gated Ca2+ channel (VGCC) complex extracted from small cell lung carcinoma (SCC). These antibodies were not found in 43 control patients with other neurologic diseases, including myasthenia gravis, peripheral neuropathies, and amyotrophic lateral sclerosis, or in 9 patients with endocrine autoimmunity, but they were found in 2 of 21 control patients with SCC without a history of LES, 1 of whom had severe autonomic neuropathy. Seropositivity was more frequent in patients with LES who had evidence of a primary lung cancer (76%) than in those with other neoplasms or without evidence of cancer (30%). Antigens extracted from SCC tumor lines derived from patients with and without LES and from a human neuroblastoma line yielded results that were highly correlated. A control extract of colonic carcinoma (derived from a patient with LES) yielded negative results. The data implicate a tumor-associated VGCC as the autoimmunizing stimulus in a subset of patients with LES and provide the first direct evidence that the VGCC complex in SCC is a target for some LES antibodies. The serologic test described should be a useful aid in diagnosing LES.
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PMID:Autoantibodies bind solubilized calcium channel-omega-conotoxin complexes from small cell lung carcinoma: a diagnostic aid for Lambert-Eaton myasthenic syndrome. 255 95

Type 1 diabetes is an autoimmune disease resulting in destruction of pancreatic beta cells. Many of the pancreatic beta cell autoantigens are also neuronal cell components. Using adrenergic neuroblastoma cells, we have previously demonstrated that humoral mechanisms may contribute to the development of diabetic neuropathy in Type 1 patients. We hypothesize that the toxic factor in Type 1 diabetic serum is an immunoglobulin. When neuroblastoma cells were exposed to immunoglobulins precipitated from serum of Type 1 diabetes patients with neuropathy, cell growth was significantly inhibited by day 5 (3.8 +/- 2.4 x 10(5) cells) compared to cells cultured with immunoglobulins from control (8.2 +/- 2.3 x 10(5) cells) or Type 2 diabetic serum (7.0 +/- 3.0 x 10(5) cells). The inhibitory effect (3.2 +/- 0.9 x 10(5) cells) could be removed from Type 1 diabetic serum by affinity precipitation with protein A-agarose (8.0 +/- 0.8 x 10(5) cells). Mild heat denaturing of the serum reversed the inhibitory effect (3.8 +/- 0.9 vs 1.4 +/- 1.4 x 10(5) cells), indicating a requirement for complement. Immunofluorescent labelling with anti-IgG secondary antibody of cells exposed to Type 1 diabetic serum indicated recognition of a membrane-bound antigen. The studies in this report support the hypothesis that autoimmune neuronal destruction may contribute to the development of diabetic autonomic neuropathy in patients with Type 1 diabetes.
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PMID:The neuronal toxic factor in serum of type 1 diabetic patients is a complement-fixing autoantibody. 764 98

The pathogenesis of diabetic neuropathy is incompletely understood. The possibility that humoral neurotoxic factors contribute as a cause of diabetic neuropathy was tested by application of serum from patients with Type 1 and Type 2 diabetes to mouse neuroblastoma cells, which have the characteristics of adrenergic neurons in culture. Serum from patients with Type 1 diabetes and somatic neuropathy significantly inhibited both proliferation and differentiation of neuroblastoma cells, while serum from patients with Type 1 diabetes but no symptoms of neuropathy and patients with Type 2 diabetes and neuropathy had no effect on proliferation, and serum from Type 2 patients only marginally inhibited differentiation. The effects of Type 1 diabetic serum could be reversed by pre-absorption of the serum to neuroblastoma cells, and were independent of glucose levels. Immunoglobulins precipitated from the sera mimicked the effects of whole sera. These results suggest that Type 1 diabetes mellitus causes a change in serum composition, possibly related to autoimmunity, that is capable of contributing to adrenergic autonomic neuropathy in diabetic patients.
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PMID:The toxic effects of serum from patients with type 1 diabetes mellitus on mouse neuroblastoma cells: a new mechanism for development of diabetic autonomic neuropathy. 830 88

Recent studies have linked autoimmunity to nervous tissue structures and diabetic autonomic neuropathy. To evaluate prospectively the early stage of type 1 diabetes and the natural history of this association, we monitored the autonomic function and the presence of autoantibodies (Ab) to sympathetic and parasympathetic nervous structures in a cohort of 92 diabetic adolescent patients, recruited and followed-up after 40+/-3 months. The presence of circulating Ab and their ability to activate complement was also assessed using a human adrenergic neuroblastoma cell line, and the effect of patients' sera on these cells was evaluated by different methods assessing cytotoxic effects and apoptosis. Thirty-nine percent of the Ab-positive patients had one abnormal test (p=0.07 vs. Ab-negative patients). Serum from four patients positive for anti-cervical ganglia Ab showed positive staining of neuroblastoma cells and displayed ability to activate complement. Serum from two adolescent patients with anti-cervical ganglia and anti-neuroblastoma cells Ab, induced cytotoxic effects and damaged the plasma membrane of the neuroblastoma cells. Moreover, sera from two adult patients with overt autonomic neuropathy, used as positive controls, induced apoptosis of these cells, assessed by TUNEL. Our data indicate that symptomatic autonomic neuropathy is not characteristic of young diabetic patients, but that autoantibodies to autonomic structures are present and persist in the first 20 years of disease, possibly associated with subtle autonomic dysfunction and cytotoxic effect on sympathetic cells.
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PMID:Autonomic function and autoantibodies to autonomic nervous tissues at follow-up in a cohort of young patients with type 1 diabetes. Effects of serum from diabetic patients on human adrenergic cells. 1279 22

We have developed and validated an assay to detect serum antibodies specific for the ganglionic AChR. The assay uses ganglionic AChR solubilized from membranes of the human neuroblastoma cell line (IMR-32) as antigen. The ganglionic AChR is radiolabeled by complexing with 125I-epibatidine. Among patients with acquired dysautonomia, seropositivity is highly associated with the diagnosis of idiopathic or paraneoplastic autonomic neuropathy and can distinguish these disorders from other forms of autonomic dysfunction. Ganglionic AChR binding antibodies are detectable in 50% of patients with subacute autoimmune autonomic neuropathy (AAN). These patients often have a high antibody value (>0.2 nmol/L). Lower values (0.05-0.20 nmol/L) are found in approximately 10% of patients with limited AAN.
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PMID:Neuronal ganglionic acetylcholine receptor autoimmunity. 1459 78