Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cord factors are mycoloyl glycolipids in cell walls of bacteria belonging to Actinomycetales, such as Mycobacterium, Nocardia and Rhodococcus. They induce granuloma formation in the lung and interstitial pneumonitis, associated with production of macrophage-derived cytokines. We studied how cord factors induce biological activities in the cells. Cord factors isolated from M. tuberculosis, trehalose 6-monomycolate (mTMM) and trehalose 6,6'-dimycolate (mTDM), enhanced protein kinase C (PKC) activation in the presence of phosphatidylserine (PtdSer), diacylglycerol and Ca2+, and mTMM activated PKC alpha more strongly than PKC beta or gamma under the same assay conditions. Kinetic studies of mTMM in response to PKC activation revealed that mTMM increased the apparent affinity of PKC to Ca2+ in the presence of both PtdSer and diolein. Although this is similar to observations with unsaturated fatty acids, such as arachidonic acid, mTMM was synergistic with PtdSer for PKC activation, but arachidonic acid was not. mTMM was also different as regards PKC activation, as phorbol ester was. A single i.p. administration of mTMM to mouse induced tumor necrosis factor-alpha (TNF-alpha) in serum and in the lung, which is a unique target tissue of cord factors. Based on our recent finding that TNF-alpha is an endogenous tumor promoter, the correlation between lung cancer and pulmonary tuberculosis is discussed.
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PMID:Activation of protein kinase C by mycobacterial cord factor, trehalose 6-monomycolate, resulting in tumor necrosis factor-alpha release in mouse lung tissues. 755 98

Few studies have examined the relation between passive smoking and dietary intake in a large population. This report examines the nutrition and behavioral characteristics of 3,896 nonsmoking women from the first National Health and Nutrition Examination Survey (NHANES I) population in relation to exposure to environmental tobacco smoke. The data indicate that nonsmoking women who were exposed to husbands who smoked were more likely to be older, have lower education, live in the city, and have other health behaviors that could increase their risk of lung cancer compared with nonsmoking women with husbands who did not smoke. The nonexposed women were more likely to take vitamin supplements, to not drink alcohol, and to consume higher levels of dietary vitamin A, vitamin C, and calcium. The exposed and nonexposed women showed no difference in the levels of fatty acid intake nor in the levels of several other foods from the food frequency list after correction for age. Many of the differences that the authors observed between the women who were exposed and nonexposed to passive smoking could affect the risk of cancer. Therefore, they recommend that future studies of nonsmokers examine the influence of both passive smoking and diet on the risk of disease rather than examine the influence of a single factor.
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PMID:Characteristics of nonsmoking women in NHANES I and NHANES I epidemiologic follow-up study with exposure to spouses who smoke. 759 14

We have introduced a human gastrin-releasing peptide receptor expression vector into an immortalized human bronchial epithelial cell normally unresponsive to the ligand bombesin. Successfully transfected cells express specific binding sites at a density similar to that found at the surface of human lung cancer cells and show an elevation of intracellular calcium concentration in response to bombesin. We found that cellular strains expressing the receptor showed a growth stimulation in response to bombesin in proportion to cell surface receptor density. We conclude that expression of bombesin receptors contributes to the growth potential of human bronchial epithelial cells.
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PMID:Expression of the gastrin-releasing peptide receptor confers a growth response to bombesin in immortalized human bronchial epithelial cells. 772 52

Sodium channels of human small-cell lung cancer (SCLC) cells were examined with whole-cell and single-channel patch clamp methods. In the tumor cells from SCLC cell line NCI-H146, the majority of the voltage-gated Na+ channels are only weakly tetrodotoxin (TTX)-sensitive (Kd = 215 nM). With the membrane potential maintained at -60 to -80 mV, these cells produced all-or-nothing action potentials in response to depolarizing current injection (> 20 pA). Similar all-or-nothing spikes were also observed with anodal break excitation. Removal of external Ca2+ did not affect the action potential production, whereas 5 microM TTX or substitution of Na+ with choline abolished it. Action potentials elicited in the Ca(2+)-free condition were reversibly blocked by 4 mM MnCl2 due to the Mn(2+)-induced inhibition of voltage-dependent sodium currents (INa). Therefore, Na+ channels, not Ca2+ channels, underlie the excitability of SCLC cells. Whole-cell INa was maximal with step-depolarizing stimulations to 0 mV, and reversed at +45.2 mV, in accord with the predicted Nernst equilibrium potential for a Na(+)-selective channel. INa evoked by depolarizing test potentials (-60 to +40 mV) exhibited a transient time course and activation/inactivation kinetics typical of neuronal excitable membranes; the plot of the Hodgkin-Huxley parameters, m infinity and h infinity, also revealed biophysical similarity between SCLC and neuronal Na+ channels. The single channel current amplitude, as measured with the inside-out patch configuration, was 1.0 pA at -20 mV with a slope conductance of 12.1 pS. The autoantibodies implicated in the Lambert-Eaton myasthenic syndrome (LES), which are known to inhibit ICa and INa in bovine adrenal chromaffin cells, also significantly inhibited INa in SCLC cells. These results indicate that (i) action potentials in human SCLC cells result from the regenerative increase in voltage-gated Na+ channel conductance; (ii) fundamental characteristics of SCLC Na+ channels are the same as the classical sodium channels found in a variety of excitable cells; and (iii) in some LES patients, SCLC Na+ channels are an additional target of the pathological IgG present in the patients' sera.
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PMID:Voltage-dependent sodium channels in human small-cell lung cancer cells: role in action potentials and inhibition by Lambert-Eaton syndrome IgG. 773 Oct 34

Parameters of lipid peroxidation and the levels of calcium ions in blood plasma and exhaled air condensate (EAC) were studied in 47 patients with lung cancer. The changes in EAC turned out to be more specific than those of blood plasma. The level of lipoperoxidation in condensate in cancer patients was lower than in healthy subjects. However, calcium cations concentrations in both blood and EAC were relatively higher, the latter difference being significant. The investigation pointed to a greater diagnostic value of EAC measurements, as compared with blood plasma, in lung cancer patients.
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PMID:[Diagnostic value of investigating exhaled air condensate in lung cancer]. 778 37

We assessed factors which affect cisplatin concentrations in human surgical tumour specimens. Cisplatin 10 mg m-2 was given i.v. to 45 consenting patients undergoing surgical resection of neoplasms, and platinum was assayed in resected tumour and in deproteinated plasma by flameless atomic absorption spectrophotometry. By multiple stepwise regression analysis of normalised data, patient characteristics that emerged as being most closely associated (P < 0.05) with tumour platinum concentrations (after correcting for associations with other variables) were tumour 'source' [primary brain lymphomas, medulloblastomas and meningiomas ('type LMM') > 'others' > lung cancer > head/neck cancer > gliomas) or tumour 'type' (LMM > brain metastases > extracerebral tumours > gliomas), serum calcium and chloride (positive correlations) and bilirubin (negative). Tumour location (intracranial vs extracranial) did not correlate with platinum concentrations. If values for a single outlier were omitted, high-grade gliomas had significantly higher platinum concentrations (P < 0.003) than low-grade gliomas. For intracranial tumours, the computerised tomographic scan feature that correlated most closely with platinum concentrations in multivariate analysis was the darkness of peritumoral oedema. Tumour source or type is a much more important correlate of human tumour cisplatin concentrations than is intracranial vs extracranial location. Serum calcium, chloride and bilirubin levels may affect tumour cisplatin uptake or retention. CT scan characteristics may help predict cisplatin concentrations in intracranial tumours.
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PMID:Factors affecting platinum concentrations in human surgical tumour specimens after cisplatin. 788 Jul 44

The lung contents of six workers who had been occupationally exposed to chrysotile asbestos were examined. Five were lung cancer cases from Quebec, Canada. The sixth, an American worker who had developed pleural mesothelioma, was particularly interesting, with the lung content strikingly distinct from the Canadian cases; chrysotile, the predominant fiber in his lung, was present at a concentration 300 times that of the average total fiber content in the Canadian cases. The fiber length distribution of the chrysotile recovered from the U.S. mesothelioma case was indistinguishable from that of chrysotile specimens known to produce mesotheliomas in rats. It was also found that the characteristics of the calcium-magnesium-iron silicate fibers present in all six cases were not readily comparable to tremolite asbestos specimens known to induce mesotheliomas in animals.
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PMID:Lung content analysis of cases occupationally exposed to chrysotile asbestos. 788 42

The effects of corticotropin-releasing factor (CRF) on human lung cancer cell lines was investigated. Corticotropin-releasing factor increased the cAMP levels in a dose-dependent manner; CRF (100 nM) elevated the cAMP levels approximately eleven-fold using NCI-H345 cells and increased the gastrin-releasing peptide (GRP) secretion rate by approximately 70%. Similarly, sauvagine, a structural analogue of CRF, elevated the cAMP levels with a half-maximal effective dose (ED50) of 20 nM. The increase in cAMP caused by CRF and sauvagine was reversed by alpha-helical CRF(9-41). Corticotropin-releasing factor had no effect on cytosolic calcium but stimulated [3H]arachidonic acid release from NCI-H1299 cells with an ED50 of 30 nM. The increase in [3H]arachidonic acid release caused by 100 nM CRF was significantly reversed by 1 or 10 microM alpha-helical CRF(9-41). Also, CRF stimulated the clonal growth of NCI-H345 and H720 cells and the growth increase caused by CRF was reversed by alpha-helical CRF(9-41). These data suggest that CRF may be a regulatory peptide in lung cancer.
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PMID:Corticotropin-releasing factor stimulates cyclic AMP, arachidonic acid release, and growth of lung cancer cells. 800 32

Lambert-Eaton myasthenic syndrome is a rare autoimmune neuromuscular and autonomic disease that produces fluctuating muscle weakness, hyporeflexia, and autonomic dysfunction, and often is associated with small-cell lung cancer. The pathophysiology is understood quite well; antibodies to voltage-gated calcium channels in motor and autonomic nerve terminals disrupt calcium influx and reduce acetylcholine release. The diagnosis may be suspected clinically, but must be confirmed with electrophysiologic testing. Initial and then periodic screening for malignancy is essential. Tumors other than small-cell lung cancer occasionally are found. Effective tumor treatment may induce remission. Active disease may respond to agents that enhance neuromuscular transmission or to immunosuppression. Combined therapy frequently is needed and control is often marginal despite this. It is expected that availability of 3,4-DAP will improve significantly the response to treatment in most patients.
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PMID:Diagnosis and treatment of Lambert-Eaton myasthenic syndrome. 804 48

We detected low level expression of the gastrin-releasing peptide and neuromedin-B receptor mRNAs in cultures of human bronchial epithelium from 4 of 6 individuals. Bombesin receptor subtype-3 mRNA was undetectable in these cells. An elevation of intracellular calcium concentration was observed in response to bradykinin (6 of 6) and neurotensin (1 of 5) but not to bombesin (0 of 6), vasopressin (0 of 6), or cholecystokinin (0 of 3). In contrast, such responses are frequently noted in lung cancer cell lines. Bombesin did not stimulate the in vitro growth of an immortalized human bronchial epithelium cell line expressing low levels of bombesin receptor mRNAs. We conclude that bombesin receptors are expressed at low levels in human bronchial epithelium cells which may acquire greater responsiveness to multiple neuropeptides in the course of multistep carcinogenesis.
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PMID:Receptor subtype expression and responsiveness to bombesin in cultured human bronchial epithelial cells. 813 67


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