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)

Understanding local pulmonary immunoregulatory mechanism(s) in patients with carcinoma of the lung is an important step towards the development of innovative methods of treatment. Prostaglandin E2 plays an integral role in immunoregulation. Therefore, we evaluated PGE2 concentrations in BALF from 18 patients with bronchogenic carcinoma, compared to that from six patients with pulmonary diseases other than carcinoma and ten normal smokers of similar age. The level of PGE2 in patients with lung carcinoma (158.1 +/- 88.7 pg/ml) was significantly (p less than 0.001) higher than the other two groups (16.2 +/- 6.9 and 4.4 +/- 3.4 pg/ml). Levels of PGE2 also varied among patients with carcinoma of different cell types. Patients with SQCA had significantly (p less than 0.001) higher levels of PGE2 (242.7 +/- 29.4 pg/ml) than patients with ADCA or SCCA (82.3 +/- 27.9 and 66.3 +/- 15.2 pg/ml, respectively). Furthermore, there was a marked difference in PGE2 concentration between carcinomatous lung and clinically noninvolved lung in patients with SQCA and ADCA. Further study is warranted to determine the interactions between PGE2 and other cytokines (interleukin-1, IL-2, and tumor necrosis factor), as well as the activity of cytolytic lymphocytes (LAK cells) in the lungs of patients with bronchogenic carcinoma.
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PMID:Elevated prostaglandin E2 levels in bronchoalveolar lavage fluid of patients with bronchogenic carcinoma. 217 96

An antimetastatic effect associated with macrophage activation by liposome-encapsulated glucosaminylmuramyldipeptide was found to enhance in malnourished mice with the Lewis lung carcinoma. These changes were not matched by further increase in the functional activity of macrophages. It has been suggested that enhancement of the antimetastatic effect in malnourished animals is due to the inhibition of neovascularization necessary for the beginning of metastatic exponential growth. The induction of neovascularization may be caused by the tumor necrosis factor, main product of activated macrophages.
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PMID:[The enhancement under the action of a limited diet of the antimetastatic effect due to macrophage activation in mice with Lewis carcinoma]. 222 68

The antitumor activity of recombinant human interleukin-1 alpha (rHIL-1 alpha), recombinant human tumor necrosis factor, and recombinant murine interferon-beta (rIFN-beta) was augmented by concomitant administration of recombinant human interleukin-2 (rHIL-2) in the treatment of adenocarcinoma 755. Especially when a divided dose (two doses/day) of rHIL-1 alpha or rIFN-beta was combined with a divided dose of rHIL-2, the antitumor effect was markedly potentiated. However, only a marginal effect was seen by combination of rHIL-1 alpha and/or rIFN-beta and rHIL-2 against Lewis lung carcinoma, a tumor that is resistant to cytokines.
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PMID:Effect of recombinant interleukin-1 alpha, recombinant interleukin-2, recombinant interferon-beta, and recombinant tumor necrosis factor on subcutaneously implanted adenocarcinoma 755 and Lewis lung carcinoma. 239 6

Treatment of C57BL/6 mice bearing Lewis lung carcinoma or of BALB/c mice bearing EMT6 sarcoma with tumor necrosis factor (TNF), lipopolysaccharides (LPS) or interferon caused necrosis of the solid tumors and regression. Toxicity was observed in tumor-bearing animals when TNF or LPS were used at effective antitumoral doses. Similar antitumoral effects could be achieved using less than 1 million macrophages from C57BL/6, lung of from BALB/c peritoneal cavity expanded in vitro, and spontaneously fully activated to cytotoxicity during culture. This effect, observed after transfer twice a week by intravenous or peritumoral route, was not dependent on histocompatibility. Additive effects were observed after combined treatment with activated macrophages and a low dose of LPS or TNF. The biodistribution of labelled LPS and of labelled cytotoxic macrophages was studied in tumor-bearing mice. Although, as expected, LPS was concentrated essentially in the liver, a slow accumulation in the center of the tumor was observed. Macrophages injected intravenously accumulated in the lung and were then redistributed towards liver, kidney and the tumor periphery. Macrophages injected locally remained essentially in the tumor periphery with a slow redistribution in the body. The complementary localization of LPS and of cytotoxic macrophages respectively in the center and periphery of solid tumors might explain their synergism.
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PMID:Antitumoral effects of lipopolysaccharides, tumor necrosis factor, interferon and activated macrophages: synergism and tissue distribution. 281

Eight species of novel recombinant tumor necrosis factor-S (rTNF-SAM group) were constructed in which N-terminal amino acid sequences were based on that of TNF-S from THP-1 cells with higher basicity than conventional rTNF-alpha. Two of this rTNF-SAM group, denoted as rTNF-SAM1 and rTNF-SAM2, showed more cytocidal activity on A549 lung carcinoma cells and G401 Wilm's tumor cells than did rTNF-alpha. In addition to these cell lines, rTNF-SAM1 revealed strong cytocidal activity on T24 bladder carcinoma cells, which are resistant to rTNF-alpha. Moreover, possible cachectin activity of rTNF-SAM2 seemed to be lower than that of conventional rTNF-alpha, suggesting that rTNF-SAM2 has less side effects. Actually, toxicity as expressed by LD50 value of rTNF-SAM2 as well as others of the rTNF-SAM group was significantly lower than that of conventional rTNF-alpha. Thus, newly constructed rTNF-SAM1 and rTNF-SAM2 should be more promising antitumor reagents for clinical use, since they were shown to be superior to conventional rTNF-alpha both in antitumor effect and in less side effects.
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PMID:Biological activities of novel recombinant tumor necrosis factor having N-terminal amino acid sequences derived from cytotoxic factors produced by THP-1 cells. 285 Oct 34

Local induction of a cytotoxic factor (CF), which was reported by us to be a tumor necrosis factor (TNF)-like molecule, in murine tumor tissues by i.v. administration of antitumor polysaccharides was studied. The CF was measured by cytolysis assay against L929 fibroblasts in vitro. The antitumor polysaccharides mannoglucan polyalcohol (MGA), lentinan, carboxymethyl-(1----3)-beta-D-linear glucan DP540 (CM-TAK) and yeast mannan induced the CF in MH134 hepatoma tissues inoculated intradermally, with MGA inducing the highest level of the CF. MGA induced the CF in MM46 mammary carcinoma, Ehrlich carcinoma, and MH134 hepatoma, the growth of which were all inhibited by MGA, but not in Lewis lung carcinoma and EL-4 lymphoma, which are therapeutically resistant to MGA. MGA induced the CF in solid MH134 hepatoma tissues inoculated subcutaneously or intramuscularly as well as intradermally, but not in ascitic fluids with intraperitoneal MH134 hepatoma on which MGA is ineffective. These findings suggest that CF induction is correlated with the antitumor activity of polysaccharides. CF induction in tumor tissues was detectable 6 h after i.d. inoculation of MH134 hepatoma. Even in nontumorous inflammatory skin tissues produced by injection of TAK, the CF was induced by MGA. Thus, the early inflammatory reaction with accumulation of host cells and MGA treatment act cooperatively in local induction of the CF.
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PMID:Local induction of a tumor necrosis factor (TNF)-like cytotoxic factor in murine tissues with tumorous and nontumorous inflammation after systemic administration of antitumor polysaccharides. 318 25

Recombinant human tumor necrosis factor (rHu-TNF) was found to exhibit potent antitumor activities not only against murine tumors, i.e. Meth A sarcoma, B 16 melanoma, colon 26 adenocarcinoma, Lewis lung carcinoma and MH134 hepatoma, transplanted in syngeneic mice but also against human tumors, i.e. HMV-2 melanoma, PC-10 lung carcinoma and GOTO neuroblastoma, heterotransplanted in nude mice. rHu-TNF caused necrosis of all tumors tested and inhibited their growth in a dose dependent manner. Complete regression of tumors was observed in mice bearing Meth A, B16, colon 26, MH134, HMV-2 and PC-10 but not in mice bearing Lewis lung carcinoma and GOTO neuroblastoma. The prolongation of survival time was also observed in syngeneic mice transplanted with murine tumors except Lewis lung carcinoma. The antitumor effect of rHu-TNF was more evident when it was given intratumorally than when given intravenously. The feasibility of rHu-TNF as a drug for cancer therapy is discussed.
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PMID:Recombinant human tumor necrosis factor--II. Antitumor effect on murine and human tumors transplanted in mice. 352 34

Lewis lung carcinoma and EMT6 sarcoma growing as solid tumors in mice caused a gradual increase in the susceptibility of the animals to lethal toxicity of endotoxins (lipopolysaccharides [LPS]). By day 15 following inoculation of the tumors, the 50% lethal dose of LPS, which in normal mice was approximately 400 micrograms, decreased to 2 micrograms for the sarcoma-bearing mice and 0.1 microgram for the carcinoma-bearing mice. This sensitization to endotoxin was paralleled by a high sensitization to tumor necrosis factor (TNF). Human recombinant TNF given to normal mice was lethal at about 500 micrograms. It was lethal for 50% of the animals bearing EMT6 or Lewis lung carcinoma tumors in amounts of 4 and 0.01 micrograms, respectively, on day 15 following tumor inoculation. The sensitization of tumor-bearing animals to LPS and TNF was paralleled by marked granulocytosis.
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PMID:Growing tumors induce hypersensitivity to endotoxin and tumor necrosis factor. 362 99

The antitumor activity of partially purified rabbit tumor necrosis factor (TNF) in combination with lentinan or chemotherapeutic agents was tested. Partially purified TNF was obtained from TNF-containing rabbit sera by salt precipitation and ion-exchange chromatography. Its specific activity, determined in vitro as its cytotoxic activity against L929 cells in the presence of actinomycin D, was 10(5) U/mg protein or about 30-fold that of the crude rabbit sera. The growths of MH134 hepatoma in C3H/He mice and Lewis lung carcinoma in C57BL/6 mice were partially inhibited by intratumoral administration of a suboptimal dose of the TNF preparation. Additional treatment with lentinan, actinomycin D, mitomycin C or adriamycin significantly increased the antitumor activity. In particular, combination therapy with TNF and lentinan was very effective against MH134 hepatoma without having detectable side-effects, showing that lentinan expanded the therapeutical potential of TNF. These results are discussed in relation to our previous results on combination antitumor therapy.
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PMID:Combination antitumor therapy with rabbit tumor necrosis factor and chemo- and immuno-therapeutic agents against murine tumors. 392 60

Gene therapy with cytokine cDNA will provide a new tool for cancer treatment. We have already reported that immunization with interleukin-2 (IL2) cDNA transfected Lewis lung carcinoma (LLC) cells induced anti-tumor immunity, which, however, was not strong enough to eradicate an established tumor. In an attempt to develop more effective gene therapy methods, we have used tumor cells co-transfected with IL-2 and tumor necrosis factor (TNF) cDNAs. These cDNAs were introduced into pBMG-Neo and pcDV-X819 vectors, respectively, and then co-transfected into LLC cells. The co-transfectants were selected by incubating them in a medium containing G418 followed by the limiting dilution method twice to obtain IL2 and TNF cDNA co-transfected LLC (LLC-TNF-IL2) cells. When 5 x 10(5)/ml LLC-TNF-IL2 cells were incubated for 48 h, they secreted 7.56 U/ml TNF and 527.0 U/ml IL2 into the culture supernatant. When C57BL/6 mice were transplanted with 1 x 10(6) LLC-TNF-IL2 cells, all the tumors were rejected. The growth of transplanted LLC, but not B16F10 melanoma cells, was retarded in mice inoculated with LLC-TNF-IL2 on their contralateral sides, which suggests specific immunity was induced. The immunization effect by the co-transfectant was superior to that of the IL2- and TNF-transfectants alone.
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PMID:Gene therapy for Lewis lung carcinoma with tumor necrosis factor and interleukin 2 cDNAs co-transfected subline. 758 91


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