Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histogenesis of alveolar soft part sarcoma (ASPS) has been investigated since its description. Twenty ASPS cases were analyzed for immunohistochemical content, with emphasis directed toward the paraganglial, Schwann cell, and muscle theories of histogenesis. In addition, the cases were examined for possible prognostic clinical features. The clinical characteristics of the patients were similar to those reported previously concerning average age (23 years); male:female ratio (1:1); and predominant primary site (lower extremity, nine cases). Despite a local recurrence rate of 20% and a metastatic rate of 68% (including four at presentation), the natural history was often indolent and relapse commonly occurred very late. The average follow-up period was 10.1 years. While the overall 5-year survival was 67%, only seven of 18 patients were alive without disease at last follow-up (1.7-32 years), and one patient died of tumor after a 28-year disease-free interval. Neither tumor size nor site appeared to affect prognosis. The tumors were analyzed immunohistochemically for neurofilament, S-100 protein, met-enkephalin, leu-enkephalin, acetylcholinesterase, alpha 1-antichymotrypsin, Factor VIII-related antigen, serotonin, lysozyme, neuron-specific enolase, myoglobin, cytokeratins, desmin, and vimentin. Except for weak vimentin immunoreactivity, no other antigenic expression was detected despite multiple repeated experiments with several antibodies. S-100 protein which is present in virtually all granular cell tumors was absent in the cases of ASPS. The lack of detectable expression of neurofilament, met-enkephalin and leu-enkephalin, and neuron-specific enolase is interpreted as evidence against the paraganglial theory of histogenesis. Similarly, the repeated absence of the muscle proteins, desmin and myoglobin, in contrast to a previous report, is interpreted as evidence against a myogenic origin.
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PMID:Alveolar soft part sarcoma. A clinicopathologic and immunohistochemical study. 243 29

In order to clarify the histogenesis of clear cell sarcoma of tendons and aponeuroses (CCS), two cases of human and one nude mouse-transplanted CCS line were studied using an ultrastructural and enzyme cytochemical approach. Most of the tumour cells obtained from the primary and transplanted CCS demonstrated melanosomes in various stages of development within the cytoplasm, whereas no melanosomes could be identified in the metastatic CCS. However, cholinesterase and tyrosinase activities could be demonstrated not only in the melanotic primary and transplanted CCS but also in the amelanotic metastatic CCS. The results therefore support the hypothesis that CCS is a soft tissue tumour derived from the neural crest.
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PMID:Neural crest origin of clear cell sarcoma of tendons and aponeuroses. Ultrastructural and enzyme cytochemical study of human and nude mouse-transplanted tumours. 249 78

We characterized retrovirus-induced changes in PC-12 cell function and neuronal differentiation. PC-12 cells were infected with a neurotropic retrovirus (temperature-sensitive Moloney murine leukemia virus, mutant BA-1). We isolated a cell clone from this infected culture that displayed altered response to nerve growth factor; increased choline acetyltransferase activity; and decreased basal and nerve growth factor-stimulated acetylcholinesterase activity. In addition, Kirsten murine sarcoma virus infection of and subsequent expression of the v-ras oncogene in PC-12 cells induced neurite extension, enhanced choline acetyltransferase activity, and limited the growth potential of the infected cells.
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PMID:Altered cellular functions in a PC-12 cell clone chronically infected with retrovirus. 302 28

Activity of hexokinase and acetylcholinesterase and pyridoxal co-enzyme content of brain subcellular fractions were studied in rats, bearing sarcoma 45, after local exposure of the tumor to 20 Gy X-radiation and microwave hyperthermia. The carbohydrate metabolism was sharply inhibited while the pyridoxal coenzyme content and acetylcholinesterase activity increased.
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PMID:[Brain metabolism of sarcoma 45-bearing rats undergoing radiation and the effect of hyperthermia on the tumor]. 339 38

For an immunohistochemical analysis of cellular function of tumors, as related to acetylcholine, the antibody to choline acetyltransferase from bovine brain was obtained in guinea pigs. The specificity of the antibody was immunohistochemically studied in the cervical spinal cord of the mouse. And the findings coincided well with the biochemically and histochemically data on the distribution of choline acetyltransferase or acetylcholinesterase in the spinal cord. The choline acetyltransferase activity in the tumor cells at 6-10 days after subculture was 2.26 nmol/1 x 10(5) cells/hr in glioblastoma, 1.77 nmol/1 x 10(5) cells/hr in C-1300 and 1.45 nmol/1 x 10(5) cells/hr in sarcoma and the difference was statistical. In the immunohistochemical cell staining of these tumors, the rate of fluorescence-positive cells was 82.0% in glioblastoma, 37.3% in C-1300 and 4.2% in sarcoma. These findings coincide well with data on the enzymatic activity. The antibody is applicable not only in the field of the immunohistochemistry, but also for a mechanical analysis of cells at the single cell level, as demonstrated by Fluorescence Activated Cell Sorter (FACS).
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PMID:[Immunohistochemical analysis of tumor cells using choline acetyltransferase (author's transl)]. 703 12

Frontotemporal lobar degeneration (FTLD) describes a spectrum of clinically, pathologically and genetically heterogeneous neurodegenerative disorders of unknown aetiology. FTLD spectrum disorders collectively represent a leading cause of early-onset dementia, with most cases presenting between 45 and 64 years of age. FTLD is characterized by progressive changes in behaviour, executive dysfunction and/or language impairment and can be differentiated clinically into three frontotemporal dementia (FTD) syndromes as follows: (i) behavioural variant (bvFTD); (ii) semantic dementia (SD); and (iii) progressive nonfluent aphasia (PNFA). Additionally, there is a significant clinical, pathological and genetic overlap between FTD and motor neuron disease/amyotrophic lateral sclerosis (FTD-ALS) and the atypical parkinsonian syndromes, progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS). bvFTD is characterized by progressive behavioural impairment and a decline in executive function with frontal lobe-predominant atrophy, SD by a loss of object knowledge with prominent anomia and asymmetrical atrophy of the anterior temporal lobes and PNFA by expressive or motor speech deficits with predominantly left peri-sylvian atrophy. Recent advances in molecular biology and immunohistochemical staining techniques have further classified the FTLD spectrum disorders based upon the predominant neuropathological protein into three main categories: (i) microtubule-associated protein tau (FTLD-TAU); (ii) TAR DNA-binding protein-43 (FTLD-TDP); and (iii) fused in sarcoma protein (FTLD-FUS). Up to 40% of FTD patients report a family history of neurodegenerative illness, and one-third to one-half of familial cases of FTD follow an autosomal dominant inheritance pattern. Mutations in MAPT, PGRN, TARDBP, VCP and CHMP2B have been described, along with a recently identified C9ORF72 hexanucleotide repeat expansion. To date, there are no US FDA-approved treatments or disease-modifying therapies for FTD. Pharmacological strategies have focused on neurotransmitter replacement and modulation for the treatment of behavioural, motor and cognitive symptoms of FTD, and include selective serotonin reuptake inhibitors (SSRIs), atypical antipsychotics, acetylcholinesterase inhibitors and glutamate NMDA receptor antagonists. At present, adequate management of FTD symptoms involves a combination of pharmacological therapy with behavioural, physical and environmental modification techniques.
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PMID:Frontotemporal lobar degeneration: epidemiology, pathology, diagnosis and management. 2295 Apr 90

Frontotemporal dementia (FTD) is the clinical manifestation of progressive nerve cell loss in the frontal and anterior temporal lobes. It represents the second most frequent form of early-onset dementia. The two major types of FTD are determined by the localisation of the underlying pathology. The behaviour variant is characterised by disinhibition, socially inappropriate manners, loss of empathy, blunting of affect and hyperorality. Key features of the language variant are either non-fluent effortful speech and grammatical errors or impaired word finding and loss of meaning of words and objects. Histopathological changes are characterised by the abnormal processing of proteins including microtubule associated protein Tau, transactive response DNA-binding protein, and tumour-associated protein fused in sarcoma. The familial forms of FTD are caused by mutations in 5 genes. The diagnosis of FTD rests on careful history and psychiatric, neuropsychological and neurological examination supported by laboratory assessments and brain imaging. The management requires an interdisciplinary approach involving the carer and using non-pharmacological approaches in the first line. Current antidementia drugs, including cholinesterase inhibitors and memantine, have no consistent positive effects in FTD. Behavioural symptoms may respond favourably to selective serotonergic antidepressants. Antipsychotic agents should be used with caution regarding motor, cardiovascular and mortality risks.
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PMID:What is frontotemporal dementia? 2505 37