Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antibodies directed against the central nervous system were looked for by indirect immunohistochemistry in the sera of 8 patients with paraneoplastic neurological syndrome (group 1), 21 cancer patients without neurological signs, 23 patients with miscellaneous neurological diseases and 63 normal subjects (groups 2 to 4). Four patients in group 1 had very high titres of antibodies. In 2 patients with small-cell lung carcinoma associated with sensory neuropathy the antibody recognized the cytoplasm and nucleus of all neurons. A 37 Kd protein was recognized by Western blot. A woman with cancer of the ovary and cerebellar syndrome exhibited an antibody against Purkinje's cell cytoplasm with a band of about 50-55 Kd at Western blot. In a woman with chronic uveitis and cerebellar atrophy with disappearance of Purkinje's cells the antibody (in blood and CSF) recognized certain layers of the retina as well as glial cells and cells present in the subependymal areas of the brain. Two bands of 46 and 59 Kd were revealed by Western blot. Immunoglobulins were detected in the cytoplasm of white matter cells in the cerebellum and brain stem. Among the other groups, one patient with lung cancer had a moderate titre of neuronal antinuclear antibody. The Western blot test was negative. The relevance of these antibodies for the diagnosis and treatment is discussed.
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PMID:[Autoantibodies in paraneoplastic polioencephalomyelitis: 8 cases]. 129 56

Among 85 neuropathy patients admitted and studied in the Department of Neurology, University of Occupational and Environmental Health, Japan, from 1979 to 1990, four patients suffering from sensory ataxia are reported with special reference to their etiological and pathological conditions. All of them were classified as having immune-mediated neuropathy. The first patient, a 56-year-old woman, was diagnosed as having chronic progressive ataxic sensory neuropathy. Her symptoms became progressively worse over a nine-year period after onset, but no evidence of cancer has been revealed. The positive rheumatoid factor was the only other feature noted. The second patient, a 63-year-old woman, after extensive laboratory studies, including the biopsy of the lymph node at the bifurcation of the bronchus in search of the cancer, was diagnosed as having subacute sensory neuropathy with small cell carcinoma of the lung. Chemotherapy was completed without subsequent obvious clinical benefits. The clinical diagnosis was confirmed on autopsy 29 months after the onset. The symptoms of the first patient were indistinguishable from those of the second patient, especially in the early clinical stage. In both patients, the proprioceptive sensations were severely affected and the disturbance of the proprioceptive sensations seemed to be almost parallel with the ataxia signs. The main site of the lesion seemed to be the neuron in the dorsal root ganglion in the first patient, as well as in the second patient who showed a marked loss of neurons in the dorsal root ganglion considered to be the primary lesion on autopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sensory ataxia in peripheral neuropathies--etiological and pathological analysis of four cases]. 132 18

We report a patient with severe paraneoplastic encephalomyeloneuritis, occult small-cell carcinoma of the lung, and high titers of circulating antineuronal antibody who died shortly after developing limbic encephalitis. The antibody was of IgG class and reacted specifically with nuclei and cytoplasm of all neurons in the pattern typical for encephalomyelitis and subacute sensory neuropathy associated with small-cell carcinoma (type II, anti-Hu). At autopsy, perivascular inflammatory infiltrates were prominent. All samples of serum, CSF, and postmortem peritoneal and pleural fluid contained high titers of antibody. Direct immunofluorescence of frozen tissue revealed IgG bound to most remaining neurons in multiple brain regions in a pattern similar to indirect immunofluorescence of normal brain tissue. IgG was also bound to tumor. Attempts to elute antibody from tissue decreased background staining but did not remove neuronal immunofluorescence. These results indicate that antibody can access and bind specifically to neuronal antigens in the brain during the course of paraneoplastic disease.
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PMID:Localization of antibody in the central nervous system of a patient with paraneoplastic encephalomyeloneuritis. 165 26

Autoantibodies to neurons and to the cytoskeleton were demonstrated in the serum of a patient with small cell carcinoma of the lung (SCCL) and paraneoplastic sensory neuropathy. The serum reacted by immunofluorescence with the nuclei of neurons, and with cytochalasin B-sensitive "stress fibres" of cultured cells. The serum also reacted by immunofluorescence with the nuclei of some cultured cell lines. Immunoblotting experiments with brain tissue, with SCCL, HeLa and other cultured cells showed that the serum reacted with 1-4 bands of 35-39 kDa apparent m.w. Two dimensional immunoblotting showed that these molecules had a neutral pI. Antibodies, affinity-purified by elution from the 35-39 kDa bands, gave staining of the nuclei of neurons and of cultured cells and immunoblotted the same 35-39 kDa antigens. These observations show that the anti-neuronal autoantibody reacts not only with neurons and with SCCL but also with some cultured cell lines. Molecular mimicry has been invoked as the basis for the reactivity of this autoantibody with exposed epitopes on SCCL and on neurons.
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PMID:Autoantibodies to neurons and to the cytoskeleton in small cell carcinoma with paraneoplastic sensory neuropathy. 256 88

Morphometric studies at autopsy of a patient with sensory neuropathy associated with small-cell lung carcinoma showed preferential loss of large-diameter sensory nerve cell bodies (fifth lumbar dorsal root ganglion), marked decrease of large myelinated fibers in the dorsal root and sural nerve, and almost total loss of myelinated fibers in the fasciculus gracilis.
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PMID:Preferential loss of large lumbar primary sensory neurons in carcinomatous sensory neuropathy. 301 84

62-year old man who had small cell lung carcinoma (SCLC) with subacute sensory neuropathy had an antibody (IgM) recognizing the antigen on peripheral nerves. The antibody in the serum recognized cell surface antigen on small cell carcinoma cell lines and also reacted with peripheral nerves simultaneously, but not with central nervous system. Two months before admission, he felt difficulty in walking because of paresthesias in the extremities. He was found to have a tumor shadow in chest X-ray, and was diagnosed as SCLC by biopsy of right supraclavicular lymph node. Western blot analysis demonstrated that auto-antibody (IgM) in the serum recognizing the antigen on the neuronal axon with single band at 29 kD. Pathogenesis of carcinomatous neuropathy is still unexplained, but the findings presented here have given rise to the possibility that anti-SCLC antibody may cross-react with neuronal antigen, primarily resulting in neuronal disorder.
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PMID:[Antibodies of IgM type against small cell lung carcinoma and 29 kD neuronal antigen of rat in a patient with paraneoplastic sensory neuropathy]. 755 60

A new human small cell lung carcinoma (SCLC) cell line, designated MT-428, was derived from a patient who showed neurological paraneoplastic syndrome (combined with subacute cerebellar degeneration and peripheral sensory neuropathy) and was established in tissue culture. This cell line exhibited small cell (variant type) morphology as observed by phase contrast and electron microscopy. The MT-428 cells had a doubling time of 72 hours. Chromosomal analysis showed complicated rearrangements at short and long chromosomes with a modal number of 68. Several tumor markers, NSE, TPA and CPK-BB, were detected in culture medium. This cell line had a cloning efficiency of 1.3% in 0.8% methylcellulose. Finally, it should be noticed that autoantibody against MT-428 cell was demonstrated in serum of the patient. We concluded that the MT-428 cell line may provide a suitable model for studies of neurological paraneoplastic syndrome.
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PMID:[Establishment and characterization of a human small cell lung carcinoma cell line (MT-428) derived from the patient who showed neurological paraneoplastic syndrome]. 802 19

We followed 21 patients with sensory neuronopathy without evidence of cancer for up to 23 years. All were seronegative for type 1 antineuronal nuclear antibodies (ANNA-1, also called "anti-Hu"). We additionally studied 67 seropositive patients with sensory neuropathy or a related neurologic syndrome. Ninety-one percent of the seropositive patients had a small-cell lung carcinoma. One, with a normal chest x-ray, had been followed for 7 years for sensory neuronopathy of indeterminate cause before serologic testing for ANNA-1 led to the discovery of the tumor by CT. We conclude that ANNA-1 seropositivity in a patient with sensory neuronopathy is strong evidence for an underlying small-cell lung cancer.
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PMID:Seronegativity for type 1 antineuronal nuclear antibodies ('anti-Hu') in subacute sensory neuronopathy patients without cancer. 793 70

The authors describe the clinical and biological data of seven patients with anti-Hu antibodies. Six of them displayed a small cell lung carcinoma (SCLC), but no cancer was detected in the 7th patient in spite of an extensive workup. The clinical heterogeneity of the anti-Hu syndrome is emphasized. The major symptoms were linked to a severe sensory neuropathy in three cases, to cerebellitis in two cases, to dysautonomia in one case, and to gastro-intestinal pseudo-obstruction in one case. One patient also displayed EMG abnormalities characteristic of the Lambert-Eaton myasthenic syndrome. Two patients developed opsoclonus or ocular flutter associated with severe confusion in the late stage of their disease. In four patients, the neurological signs and symptoms preceded the discovery of the SCLC, and in two cases the initial detection of anti-Hu antibodies prompted the successful search for this tumor. Immunopathological events injuring the peripheral and central nervous system are briefly discussed.
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PMID:The anti-Hu syndrome: a clinical and immunological study of 7 cases. 871 83

A patient with diffuse intestinal pseudo-obstruction consisting of gastric paresis and impaired small and large bowel motility, mononeuropathy multiplex, and sensory neuropathy/neuronopathy was found to have small-cell carcinoma of the lung. The clinical symptoms were thought to be consistent with paraneoplastic neuropathy, and high antineuronal and anti-calcium channel antibodies led to the diagnosis of small-cell carcinoma of the lung. Identification of paraneoplastic neuropathy is important, because early treatment may halt the progression of the underlying carcinoma.
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PMID:Paraneoplastic intestinal pseudo-obstruction, mononeuritis multiplex, and sensory neuropathy/neuronopathy. 883 9


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