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)

We have studied the uptake of 125I-labelled low-density lipoprotein (LDL) by seven experimental murine tumours in vivo. Four tumours (Lewis Lung carcinoma, B-16, MS-2 and Colon 26) showed a higher relative uptake of lipoprotein as compared to the liver, two (L-1210 and P-388) had a very low lipoprotein uptake, while lipoprotein uptake by tumour M5 was similar to that of the liver. The data was confirmed by tracing tissue uptake of lipoproteins using [14C]sucrose-labeled LDL. These in vivo findings correlated well with the in vitro specific binding of 125I-beta-VLDL to membranes prepared from tumours, thus suggesting that the expression of the LDL receptor in the tumours is related to the in vivo uptake of lipoprotein. Further analysis of the LDL receptor by ligand blotting showed that the tumor receptor has several of the liver LDL receptor characteristics (including apparent Mr, sensitivity to proteinases, and Ca2+ requirement of lipoprotein binding). In summary, our data show that experimental murine tumours express the LDL receptor and suggest that the high relative in vivo uptake of LDL is determined by the elevated LDL-receptor expression in the tumours.
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PMID:Assimilation of LDL by experimental tumours in mice. 250 Sep 72

The antitumor activity of calcium gluconate in combination with mitomycin C and 5-fluorouracil was examined against subcutaneously implanted Lewis lung carcinoma-bearing C57BL/6 mice. The mice were divided into four groups: group 1 received mitomycin C (2 mg/kg) and 5-fluorouracil (50 mg/kg) intraperitoneally once a week for four weeks beginning from the day after implantation of tumors, as well as calcium gluconate (155 mg/kg) twice a week for the same four weeks; group 2 received only mitomycin C and 5-fluorouracil; group 3 received only calcium gluconate; group 4 received a vehicle (physiological saline). Significantly enhanced inhibition of tumor growth was observed neither in a comparison between groups 3 and 4, nor in a comparison between groups 1 and 2 (expect on day 20 post implantation). Thus calcium gluconate given alone or in combination with antitumor agents hardly appeared to possess effective antitumor activity.
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PMID:Antitumor activity of calcium in combination with antitumor agents against Lewis lung carcinoma. 251 48

Severe hypercalcemia (serum calcium, 4.37-4.84 nmol/L) was found in a 70-yr-old man who had a small cell carcinoma of the lung with multiple metastases. The plasma immunoreactive PTH concentration was markedly elevated, as measured in three different PTH assays [N-terminal PTH, 4,650 ng/L (normal, 230-630); midregion PTH, 13,850 ng/L (normal, 180-560); C-terminal PTH, 9,900 ng/L (normal, less than 1,300)], but at autopsy the parathyroid glands were histologically normal. The PTH concentration of a liver metastasis was 503.5 ng/g wet wt (normal liver, less than 4.2-5.9), and the PTH in the tumor extract eluted at nearly the same position as synthetic human PTH-(1-84) on gel filtration chromatography. Northern blot analysis revealed PTH mRNA in the tumor as a single band of 0.9 kilobase. These results indicate that the ectopic PTH production by the lung cancer was the cause of hypercalcemia in this patient.
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PMID:Ectopic production of parathyroid hormone by small cell lung cancer in a patient with hypercalcemia. 254 Nov 61

We compared the effects of Lambert-Eaton myasthenic syndrome (LEMS) immunoglobulin G (IgG) obtained from patients with and without small-cell lung carcinoma (SCLC) on voltage-gated (K+-stimulated) 45Ca2+ flux in cell lines derived from a human SCLC (MAR10) and from a rat pheochromocytoma (PC12) and related these to electromyographic indexes of clinical severity. Control IgG was obtained from patients with other neurological disorders or healthy individuals. Inhibition of Ca2+ flux by LEMS IgG was time and dose dependent. The flux was significantly reduced in MAR10 cells grown in either SCLC-LEMS IgG (0.38 nmol/10(6) cells; p less than 0.001) or non-SCLC-LEMS IgG (0.35 nmol/10(6) cells; p less than 0.001), compared with that in MAR10 cells grown in control IgG (0.7 nmol/10(6) cells). Similar significant reductions were also observed in PC12 cells. The reduction in amplitude of the resting compound muscle action potential in the LEMS patients correlated positively (r = 0.70; p = 0.007) with the inhibition of Ca2+ flux in MAR10 cells by their IgG. These results strongly support the view that IgG autoantibodies that can inhibit Ca2+ flux in SCLC cells are responsible for the disorder of transmitter release at motor nerves in SCLC-associated LEMS.
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PMID:Lambert-Eaton myasthenic syndrome: immunoglobulin G inhibition of Ca2+ flux in tumor cells correlates with disease severity. 254 62

Oat cells (of the small cell carcinoma of the lung) have been reported to generate calcium action potentials. The calcium channels have further been suggested to play a crucial role in the relation between oat cell carcinoma and the often associated myasthenic syndrome. We have examined cultured human oat cells (U-1690) under voltage-clamp conditions, using the patch-clamp technique. We found, contrary to previous reports, that the action potential was caused by sodium and potassium currents. No calcium current was detected under these conditions, which indicates that calcium channels, if present, are very rare. The findings restrict, but do not rule out, the hypothesis that calcium plays a key role in the carcinoma/myasthenic syndrome relation.
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PMID:Action potentials of cultured human oat cells: whole-cell measurements with the patch-clamp technique. 254 79

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

The effect of prospidin on Lewis lung carcinoma spreading under hyper- and hypocalcemia was studied. At early stages, increased extracellular calcium level was associated with inhibition of tumor dissemination to the lungs; however, later, colony growth was stimulated. Extracellular calcium level was shown to modulate the antitumor and antimetastatic effect of prospidin.
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PMID:[Effects of prospidin on the development of pulmonary metastases of Lewis tumors in rats in regard to changes in the level of extracellular calcium]. 264 Dec 10

Calcium levels were determined in sera of patients suffering from various lung diseases. Healthy volunteers served as controls. Significant differences were found between the serum calcium levels of patients with active lung tuberculosis and those of controls (P less than 0.01). After treatment, serum calcium levels decrease to normal values in these patients. It was also found that there were significant differences in serum calcium levels of patients with primary lung carcinoma (P less than 0.01) and of patients with metastatic lung carcinoma as compared to controls (P less than 0.01). On the other hand, normal serum calcium levels were found in patients with pulmonary diseases with or without an infection. In conclusion, it seems likely that a combination of mechanisms plays a role in the pathogenesis of hypercalcaemia in pulmonary tuberculosis and primary and metastatic lung carcinoma.
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PMID:Serum calcium levels in various lung diseases. 276 Jan 22

The human small cell lung carcinoma (SCLC) cell line NCI-H345 constitutively produces gastrin-releasing peptide (GRP), a peptide homologous to the mitogen bombesin. In addition, NCI-H345 cells express bombesin receptors and respond to bombesin with rapid activation of phospholipase C and mobilization of intracellular Ca2+. Treatment of NCI-H345 cells with a novel potent bombesin receptor antagonist [Leu13-psi-CH2NH-Leu14]bombesin blocked the increase in phosphatidylinositol turnover and cytoplasmic free Ca2+ ([Ca2+]i) stimulated by bombesin. Furthermore [Leu13-psi-CH2NH-Leu14]bombesin inhibited NCI-H345 colony formation in defined semisolid medium in the absence of exogenous GRP. The rapid, hormone-induced accumulation of inositol(1,4,5)trisphosphate was markedly more sensitive to antagonist inhibition than the hormone-induced Ca2+ transient, the sustained accumulation of inositol monophosphates, or colony formation in soft agarose. These data demonstrated inhibition of transmembrane signals associated with autocrine growth control in SCLC by a novel peptide receptor antagonist.
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PMID:A novel bombesin receptor antagonist inhibits autocrine signals in a small cell lung carcinoma cell line. 284 33

Serum was obtained from 7 patients with the Lambert-Eaton myasthenic syndrome (LES), 3 patients with small-cell carcinoma of the lung (SCCL), and 9 healthy control subjects. Serum samples were applied in vitro to the rat neuromuscular junction (for 1-3 h for control LES sera; 4 h for SCCL sera), following which the pre- and postjunctional physiological effects of serum factors were studied in the presence of 10 mM [Mg2+]o. All sera produced a marked reduction in the frequency of spontaneous miniature end-plate potentials (MEPPs), while causing slight to moderate changes in MEPP amplitude. There were no consistent changes in the quantum content of the impulse-evoked end-plate potentials, though the serum from one LES patient significantly and reversibly inhibited the evoked quantal release. No significant effect was found when a human intercostal muscle was exposed to serum from another LES patient for 2 h. Therefore, when applied in vitro on a short-term basis, the putative LES autoantibodies do not consistently react with voltage-dependent calcium channels in the motor nerve terminal and thus fail to reproduce the physiologic abnormality of the syndrome. We suggest that the pathogenic IgG molecules may require more than 3h of incubation in order to gain access to, and inhibit the function of, the prejunctional Ca2+ channels.
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PMID:Lambert-Eaton myasthenic syndrome: the lack of short-term in vitro effects of serum factors on neuromuscular transmission. 284 93


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