Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007095 (carcinoid)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diethylnitrosamine is known to cause squamous cell carcinoma and adenocarcinoma of the lung in Syrian golden hamsters. Sections of lungs obtained from hamsters treated with the systemic carcinogen diethylnitrosamine revealed a significant increase in the number of argyrophilic cells of neuroepithelial bodies. These affected cells also exhibited enhanced survival in vitro. After 7 days in culture, argyrophilia, dense-core vesicles, and corticotropin-like immunoreactivity were observed in many of the cells derived from the lungs of carcinogen-exposed hamsters by dissociation with pronase. In addition, nuclei of argyrophilic cells in neuroepithelial bodies of the exposed hamsters were labeled at 60 min following administration of [3H]thymidine. This suggests that the carcinogen stimulates the pulmonary neuroendocrine-like cells to divide. Normally, the component cells of neuroepithelial bodies may originate from nonargyrophilic precursor cells in the surrounding epithelium, as in control hamsters the argyrophilic cells of neuroepithelial bodies appeared labeled only at 8 days after the administration of thymidine. The relationship of the diethylnitrosamine-induced reactions to bronchial carcinoid tumors or small-cell carcinomas of the lung remains to be established.
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PMID:Effects of diethylnitrosamine on lung neuroendocrine cells. 618 6

Diethylnitrosamine is known to cause squamous cell carcinoma and adenocarcinoma of the lung in Syrian golden hamsters. Sections of lungs obtained from hamsters treated with the systemic carcinogen diethylnitrosamine showed a significant increase in the number of argyrophilic cells of neuroepithelial bodies. The hyperplastic response was retained at least 4 weeks after cessation of treatment. To examine whether these affected cells exhibited enhanced survival in vitro, lung cells were dissociated with Pronase and grown in culture. After 7 days, argyrophilia, dense-cored vesicles, and corticotropin-like immunoreactivity were observed in many of the cells derived from hamsters treated for 5 or 8 weeks. These findings suggest that the endocrine-like cells of neuroepithelial bodies are affected by diethylnitrosamine as evidenced by a numerical increase in vivo and by the properties exhibited by cells in vitro. The relationship of this diethylnitrosamine-induced reaction to bronchial carcinoid tumors or small-cell carcinoma of the lung remains to be established.
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PMID:Lung endocrine-like cells in hamsters treated with diethylnitrosamine: alterations in vivo and in cell culture. 694 63

This report is part of a comprehensive research programme to elucidate the role of physiological functions and pathways of pulmonary neuroendocrine cells in the cascade of events that lead to the development of neuroendocrine lung cancer. In this study, a well differentiated neuroendocrine cell line (NCI-H727) derived from a human lung carcinoid was used to investigate the ability of endogenous and tobacco-related amines to stimulate cell proliferation in neuroendocrine tumour cells. Cell line NCI-H727 was exposed in vitro to the endogenous amine serotonin and its precursor 5-hydroxytryptophan (5-HTP), to the tobacco-related amine nicotine, and the tobacco-related nitrosamines N-nitrosodiethylamine (DEN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The experiments were conducted in both 8% CO(2)-92% air and in 5% CO(2)-95% air. The effect on growth kinetics and ultrastructure of these conditions were studied. All amines had a dose-dependent stimulating effect on cell growth when tested in 8% CO(2)-92% air with nicotine exerting the strongest effect. No such effect was observed in 5% CO(2)-95% air and the control cells did not grow under these conditions. DEN, 5-HTP, serotonin and NNK all caused dedifferentiation of cytoplasmic organelles. Nicotine caused a change in size and ultrastructure of dense-cored granules suggestive of a change in the nature of stored neuroendocrine material.
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PMID:Effects of endogenous and tobacco-related amines and nitrosamines on cell growth and morphology of a cell line derived from a human neuroendocrine lung cancer. 2070 22