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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The modulation of clonal growth of cells of 15 human lung cancer lines was examined by coculture with different recombinant lymphokines, monokines, and several agents which induce differentiation in other malignant cell systems. Recombinant human tumor necrosis factor alpha (TNF) was inhibitory to all non-small cell lung cancer cell lines with a 50% effective dose of clonal inhibition (ED50) in the range of 30-2000 units/ml. Two representative squamous lines (SK-MES and P3) had 150 to 250 high affinity (Kd approximately equal to pM) cell surface TNF receptors. In contrast, clonal growth of small cell lung cancer lines was not inhibited by TNF, and two representative lines (H69c and R592) expressed negligible cell surface TNF receptors. Recombinant alpha, beta, and gamma interferons (4000 units/ml) each inhibited greater than or equal to 30% clonal growth of more than 50% of the non-small cell lung cancer lines. TNF (100-1000 units/ml) in combination with gamma-interferon was synergistic in the inhibition of clonal growth of these cells. Further studies showed that synergism of clonal inhibition occurred even when the cells were initially exposed to gamma-interferon, washed, and plated in soft agar with TNF. All-trans-retinoic acid (ED50, 5 X 10(-7)-10(-6) M), dimethyl sulfoxide (ED50, 1.2-1.6%), and 12-O-tetradecanoylphorbol-13-acetate (ED50, 5 X 10(-8)-10(-10) M) inhibited clonal proliferation of 7 of 9, 7 of 9, and 8 of 9 non-small cell lung cancer lines, respectively. In contrast, clonal proliferation of cells of small cell lung cancer lines was decreased only slightly at almost all concentrations of each of the agents. Interleukin-1 and -2 and granulocyte-monocyte colony-stimulating factor had no effect on the clonal growth of any of the lung cancer lines. Our results suggest that TNF in combination with gamma-interferon may be therapeutically active for some patients with non-small cell lung cancer, but small cell lung cancer probably will be unresponsive to all the agents that we examined.
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PMID:Effect of recombinant monokines, lymphokines, and other agents on clonal proliferation of human lung cancer cell lines. 303 6

The ability of IgG and IgE immune complexes and of phorbol myristate acetate (PMA), a soluble membrane activator, to stimulate hydrogen peroxide (H2O2) release and to induce oxygen radical-mediated cytotoxic activity by human peripheral blood (PBL) eosinophils and by PBL neutrophils was evaluated in normal volunteers and patients with hypereosinophilic malignant pleural effusions due to lung cancer. PMA stimulated a significant respiratory burst. Similar results were obtained with IgG IC stimulation, although the levels of H2O2 were lower. Agg IgE induced H2O2 release only by PBL and PE eosinophils and not by neutrophils. PMA stimulation resulted in detectable cytotoxic activity. IgG IC generated both PBL and PE eosinophil and PBL neutrophil cytotoxicity. Agg IgE induced significant cellular cytotoxicity in both PBL and PE eosinophils. This study suggests that eosinophil oxidative metabolic burst and cytotoxic activity stimulated by IgG and IgE immune complexes could represent a possible mechanism of parenchymal injury in eosinophilic disorders.
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PMID:Human peripheral blood and pleural fluid eosinophils can be induced by immune complexes to release IgG immune complexes and aggregated IgE. 318 Aug 52

Circulating immune complexes (CIC) levels were evaluated in two groups of cancerous patients to try to correlate CIC levels, tumor stage and chemotherapy received. There were 40 patients with Lung Cancer (LC) clinical stages III and IV; 60 patients with Breast Cancer (BC) stages II, III and IV and 38 normal controls. LC patients showed significant increase in CIC values before, during and after treatment as compared to controls, without any difference among groups under different treatment combinations and tumor stage. Stage II BC patients showed decreased CIC levels during treatment (p less than 0.01 vs initial value). This decrease was maintained after treatment (p less than 0.02). Stage III BC patients showed different behaviour according to treatment: those who only received chemotherapy (ADM + CTX) showed no significant differences during treatment, and those treated with ADM + CTX and megestol acetate (MA) displayed decreased CIC levels after treatment (p less than 0.05) reaching similar control values. Stage IV patients treated with ADM + CTX + MA returned to normal CIC values during treatment. These results proved that combined treatment of chemotherapy and hormone therapy diminished CIC levels in BC patients, while therapy given to LC patients did not present any modifications.
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PMID:Circulating immune complexes in breast and lung cancer, before and after chemotherapy. 360 38

A case of hyperamylasemia with lung cancer is described. Macroamylasemia was excluded by a normal amylase/creatinine clearance ratio and by a sedimentation constant obtained by sucrose density gradient centrifugation. Positive immunofluorescent staining of tumor cells with a specific antibody against human salivary amylase and significant amylase activity in the primary tumor and metastases support the hypothesis of independent production of amylase by the lung tumor. Cellulose--acetate membrane electrophoresis demonstrated three bands of amylase activity. The major component corresponded to normal salivary amylase in electrophoretic mobility, isoelectric point and molecular size. The minor bands, one of which occupied about 10% of the total amylase activity in serum, urine and tissue homogenates, demonstrated a lower electrophoretic mobility and a more acidic isoelectric point. Gel filtration and electrophoresis disclosed that these minor bands were derived from an amylase isozyme with a larger molecular size than that of normal salivary amylase. The results suggest ectopic tumor production of heterogenous amylase isozymes, with the larger form being secreted into the circulation.
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PMID:Amylase-producing lung cancer: case report and review of the literature. 617 Apr 23

The serum factor responsible for the humoral leukocyte adherence inhibition (H-LAI) reaction in lung cancer patients has been purified. It is precipitable by ammonium sulfate between 30-70% saturation. On DEAE ion exchange chromatography activity is eluted in the 0.12-0.2 M acetate fraction. The serum factor has affinity for Con A. This gives evidence for a glycoprotein nature of the factor. Electrophoresis indicates an apparent mol. wt of 71,000 dalton. The data suggest that the protein can be separated into subunits of 43,000 and 28,000 dalton under reducing conditions. Isoelectric focusing gives a mean pI of 4.5. The applied fractionation procedure gave a 1120-fold purification relative to lung cancer serum. Antiserum against the purified factor has been produced in rabbits. The factor can be demonstrated in high concentrations in serum of lung cancer patients, but is also found in smaller quantities in sera of other types of cancer. Minor quantities are present in normal serum. The results suggest that quantitation of the H-LAI factor can be used in cancer diagnosis.
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PMID:Purification of a cancer-associated protein factor in serum of lung cancer patients. 654 Jan 82

In 52 patients with malignancies such as lung cancer, carcinoma of the stomach, and cancer of the colon (25, 18, and 9 cases, respectively) activity and intracellular localization of alpha-naphthyl acetate esterase has been evaluated by means of semiquantitative cytochemical method. Patients with advanced metastatic process occurring during clinical evolution of those malignancies showed decreased activity of above enzyme within the peripheral blood neutrophils and decreased numbers of enzyme-positive lymphocytes having intact enzyme-positive lysosomal granules. The authors discuss the significance of that observation in relation to the enzymatic alterations of cells during antitumor response of immune system.
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PMID:The neutrophil and lymphocyte nonspecific esterase in patients with malignancies. 654 73

Chemiluminescence, indomethacin-sensitive suppression, and adherent cell cytotoxicity were measured in peripheral blood mononuclear cells (PBMC) from normal subjects and solid tumor cancer patients. These functions were found to be differentially affected by malignant disease. In cancer patients with disseminated disease, indomethacin-sensitive suppression and chemiluminescence emission were increased to a level significantly higher than normal without a concurrent increase in adherent cell cytotoxic function. In cancer patients with at most minimum residual diseases, the levels of chemiluminescence, indomethacin-sensitive suppression, and adherent cell cytotoxicity found were comparable to those of the normal study population. In vitro stimulation of cells from patients with disseminated disease by phorbol myristic acetate (PMA) increased chemiluminescence overcame the suppressive effects of indomethacin-sensitive suppressor cells, and increased adherent cell cytotoxicity; in cells from patients with at most minimum residual disease, PMA increased chemiluminescence and cytotoxicity without influencing the activity of indomethacin-sensitive suppressor cells. Vaccination of lung cancer patients with Freund's complete adjuvant or Freund's complete adjuvant plus tumor antigen extracts led to increased levels of chemiluminescence and increased levels of adherent cell cytotoxicity without altering indomethacin-sensitive regulatory cell function.
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PMID:Chemiluminescence, suppression and cytotoxicity in peripheral blood mononuclear cells from solid tumor cancer patients. 696 31

This paper reviews recent advances in the methods for assessing the quality of life of patients with lung cancer and recent applications of quality-of-life measures in lung cancer clinical trials. In terms of methodology, there exist today a number of self-report quality-of-life questionnaires that are valid, reliable, and sufficiently brief to be of practical use in clinical research settings. Application of these measures in lung cancer clinical trials has contributed to the evaluation of: 1) long-versus short-duration chemotherapy, four- versus two-drug combinations, intensive versus standard chemotherapy, and continuous versus bolus injection chemotherapy in the treatment of small cell lung cancer; 2) high versus low radiation doses in the treatment of non-small cell lung cancer; 3) megestrol acetate and hydrazine sulfate as supportive treatment for small cell lung cancer and non-small cell lung cancer patients receiving chemotherapy; 4) granulocyte colony-stimulating factor in small cell lung cancer patients receiving dose-intensified chemotherapy; and 5) the rehabilitation needs of lung cancer survivors. Future efforts should be directed toward achieving higher levels of compliance with clinical trial-based quality-of-life studies, and the development of techniques for integrating quality of life and clinical outcomes for purposes of cost-effectiveness evaluations.
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PMID:Quality-of-life and cost-effectiveness assessment in lung cancer. 775 77

As a part of a series of investigations on the functions of TIS21 and TIS1 genes, we measured in vivo 12-O-tetradecanoylphorbol-13-acetate (TPA) inducibility of primary response genes (TIS21, TIS8 and TIS1) in the Balb/c mice and the changes of TIS gene expression in thymic carcinoma tissues and A549 and NCIH69 human lung cancer cell lines. In vivo induction of the TIS genes (TIS21, -8 and -1) by intraperitoneal injection of TPA was dramatic only at the needle contact site, i.e. in the abdominal muscle, not in the thigh muscle. Expression of TIS21 and TIS1 in the Balb/c mice thymus, lung, stomach and spleen was very strong (Lim IK et al. 1994a), regardless of TPA injection. Thymic carcinoma tissues developed in SV40-T-antigen-containing transgenic mice did not express TIS21 and TIS1, and expressed TIS8 weakly. Interestingly, induction of TIS21 expression was obliterated in the human lung cancer cells; A549 cells completely lost the ability to express TIS21 after a combined treatment of TPA and cycloheximide. We also measured the induction of TIS genes by TPA and/or cycloheximide in Raw264.7 mouse macrophage cells and U937 human histiocytic lymphoma cells. However, the induction profile was quite different; repressed and deregulated expression in the U937 cells as compared to rapid and transient induction of TIS genes in the Raw264.7 cells. These data may suggest a repressed expression of TIS21 and TIS1 in the cancer tissues and cells derived from the organs that constitutively express TIS21 in mice and in human cancer cells.
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PMID:Differential expression of TIS21 and TIS1 genes in the various organs of Balb/c mice, thymic carcinoma tissues and human cancer cell lines. 776 65

This study examined the role of marijuana smoking in the pathogenesis of human lung cancer by measuring DNA damage in alveolar macrophages (AM). The alkaline unwinding method was used to determine DNA single-strand breaks in AM lavaged from non-smokers [NS] and smokers of marijuana [MS], tobacco [TS] or cocaine [CS], either alone or in combination. DNA damage was related to superoxide anion (O2-) production by AM stimulated with phorbol myristate acetate (PMA) and to nitric oxide content of smoke using cellular nitrite (NO2-) concentrations. The percentage of double-stranded DNA present after alkaline unwinding was higher in AM of NS (41 +/- 5% [11]) and CS (41 +/- 4% [9]) versus that of MS (31 +/- 4% [8]), TS (35 +/- 3% [11]), MTS (26 +/- 4% [3]), and CTS (27 +/- 5%* [10]), mean +/- SEM [n], * = p < 0.1 vs. NS). PMA stimulated O2- production by AM from NS and CS was lower than that of other smokers, but the differences were not significant. O2- release, however, had an inverse correlation with DNA single-strand breaks (r = -0.38, p = 0.009). Nitrite content of AM from NS and CS was less than that of other smokers' cells (p < 0.1 for TS & CTS vs. NS), but DNA damage had no relationship to NO2- concentration. We conclude that AM recovered from MS, either alone or in combination with tobacco smoking, show a trend towards DNA damage. Studies utilizing a larger population should verify our findings and further define its relationship to enhanced oxidant production by macrophages.
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PMID:Effects of smoking marijuana, tobacco or cocaine alone or in combination on DNA damage in human alveolar macrophages. 777 50


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