naloxone has been researched along with Carcinoma--Small-Cell* in 3 studies
3 other study(ies) available for naloxone and Carcinoma--Small-Cell
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Imaging delta- and mu-opioid receptors by PET in lung carcinoma patients.
In the present study, we measured the kinetics and distribution in vivo of the selective delta-opioid antagonist 11C-methylnaltrindole (11C-MeNTI) and the mu-opioid agonist 11C-carfentanil (11C-CFN) in patients with lung carcinoma using PET.. Paired measurements of 11C-MeNTI and 11C-CFN binding were performed in biopsy-proven small-cell (n = 2), squamous (n = 2), and adenocarcinoma (n = 3) lung cancer patients. Dynamic PET scans of increasing duration (0.5-8 min) were acquired over 90 min after an intravenous bolus injection of 370 MBq of tracer. Time-activity curves for tumor and normal lung parenchyma binding were generated using the region-of-interest (ROI) method. The mean activity at equilibrium was measured, and the specific-to-nonspecific binding ratio (tumor - lung)/lung was calculated. Four of 7 patients underwent an additional static 18F-FDG PET scan for clinical indications. Three of 7 patients underwent surgery, and stained sections of tumor were inspected for inflammation, necrosis, and scar tissue.. Increased binding of 11C-MeNTI and 11C-CFN was detected in all tumor types studied. 11C-MeNTI binding in tumor and healthy lung tissue was significantly more intense than that of 11C-CFN. The average specific-to-nonspecific binding ratio across cell types for 11C-MeNTI (4.32 +/- 1.31; mean +/- SEM) was greater than that of 11C-CFN (2.42 +/- 1.17) but lower than that of 18F-FDG (7.74 +/- 0.53). Intravenous naloxone produced 50% and 44% decreases in the specific-to-nonspecific binding ratios of 11C-MeNTI and 11C-CFN, respectively.. These data provide in vivo evidence for the presence of delta- and mu-opioid receptor types in the 3 major human lung carcinomas and suggest the suitability of 11C-MeNTI and 11C-CFN as investigational probes of lung carcinoma biology. Topics: Adenocarcinoma; Aged; Carcinoma, Non-Small-Cell Lung; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Coloring Agents; Female; Humans; Inflammation; Lung Neoplasms; Male; Middle Aged; Naloxone; Narcotic Antagonists; Necrosis; Radionuclide Imaging; Radiopharmaceuticals; Receptors, Opioid, delta; Receptors, Opioid, mu; Tissue Distribution | 2007 |
Activation of opioid receptors inhibits neuronal-like calcium channels, distal steps of secretion, and cell proliferation in human small cell lung carcinoma cells.
Topics: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Analgesics; Bucladesine; Calcium Channels; Carcinoma, Small Cell; Cell Division; Cyclic AMP; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalin, D-Penicillamine (2,5)-; Enkephalins; Humans; Kinetics; Lung Neoplasms; Naloxone; Neurons; Receptors, Opioid, delta; Serotonin; Thapsigargin; Time Factors; Tumor Cells, Cultured | 1998 |
Human small cell lung cancer cells express high affinity naloxone-insensitive [125I]-endorphin binding sites.
Previous reports have demonstrated that beta-endorphin stimulates the clonal growth of human small cell lung carcinoma (SCLC) cell lines. In this study, the human SCLC lines, NCI-H69, NCI-H345, and NCI-N417, were observed to be highly-enriched in saturable, high-affinity binding sites which are labeled by [125I]beta-endorphin. In contrast to conventional opioid receptors, [125I]beta-endorphin SCLC binding was insensitive to naloxone and other mu, delta, or kappa opioid ligands. Further analysis of the NCI-H69 cells demonstrated that specific (naloxone-insensitive) binding was dependent on receptor concentration, reversible, sensitive to sodium ion, but insensitive to the GTP analogue, Gpp(NH)p. These results suggest a role for naloxone-insensitive beta-endorphin in modulating SCLC metabolism. Topics: Animals; beta-Endorphin; Binding Sites; Binding, Competitive; Carcinoma, Small Cell; Cell Membrane; Humans; Iodine Radioisotopes; Lung Neoplasms; Naloxone; Prosencephalon; Rats; Receptors, Opioid; Sensitivity and Specificity; Tumor Cells, Cultured | 1995 |