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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biosynthetically-radiolabeled MoAbs provide a tool to test whether structural modifications of the MoAbs influence the results of conventional immunoscintigraphy. When biosynthetically-labeled 75Se-MoAbs from the Mel-14 hybridoma were injected into mice with melanoma xenografts, the high tumor recovery supported the hypothesis of a structural advantage. The increased excretion of 75Se obtained by supplementing the diet of the mice with cold selenium did not reduce the tumor recovery, demonstrating an accumulation of the free radionuclide in normal tissue.
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PMID:Immunoscintigraphy with biosynthetically-labeled 75Se-antibodies--I. Biodistribution of 75Se-monoclonal antibodies and of free radionuclide. 239 Dec 44

In vitro E-rosette formation, lymphocyte mitogenesis, and natural killer (NK) cell activity of human blood lymphocytes were strongly inhibited by high concentrations (10(-4) M) of sodium selenite, sodium selenate, and selenium dioxide. Lower concentrations (10(-5) or 10(-7) M) also inhibited E-rosette formation and natural killer cell activity against K-562 tumor cells. Lymphocyte transformation induced by concanavalin A (con A) or pokeweed mitogen (PWM) was also inhibited by all selenium compounds tested, but only at the highest concentrations (10(-5) and 10(-4) M). There was depression of the total number of viable lymphocytes following incubation with selenium dioxide only at a high concentration (10(-4) M). Interferon production was enhanced at lower levels (10(-9) to 10(-6)M) of selenium dioxide while a higher concentration (10(-5) and 10(-4)M) appeared to inhibit its production. The mechanism of inhibition by selenium compounds (10(-4) M) is due, in part, to the decrease of viable lymphocytes. It is unclear how other and lower concentrations (10(-7) or 10(-9) M) of selenium compounds inhibit E-rosette formation, NK activity, or K-562 tumor cell growth.
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PMID:Effects of selenium in vitro on human T-lymphocyte functions and K-562 tumor cell growth. 241 67

Four different canine mammary tumor (CMT) cell lines and a nonneoplastic primary culture of mammary cells were examined for their in vitro responsiveness to selenium supplementation. These cell lines were found to vary in their metabolic response to increasing concentrations of selenium. Sensitivity to selenium, as sodium selenite, increased with increasing concentrations of this trace element in all of the neoplastic lines. These data also suggest that increasing the plating density of tumor cells further increases the sensitivity to selenium. A relatively selenium-sensitive cell line (CMT-13) and relatively insensitive cell line (CMT-11) were characterized on the basis of reduced growth resulting from selenium supplementation. Increasing the concentration of selenium to 0.75 microgram/ml depressed the growth of CMT-13 and CMT-11 cells by 75% and 11%, respectively, while no inhibition was observed in nonneoplastic cells. These cell lines also varied in their sensitivity to different forms of selenium. Selenodiglutathione was the most effective form of selenium examined that inhibited tumor cell growth. The sensitivity of the neoplastic lines was selenodiglutathione much greater than sodium selenite much greater than selenocystine greater than selenomethionine. None of the forms of selenium examined inhibited the growth of the nonneoplastic mammary cells in culture. Supplementation with sodium selenite (1 microgram Se per ml) for 60 min resulted in a dramatic depression in RNA biosynthesis in CMT-13, but not CMT-11 or nonneoplastic cells.
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PMID:Differential effects of selenium on normal and neoplastic canine mammary cells. 242 32

The role of nutrients in cancer causation has been a subject of considerable interest, research, and public discussion in recent years. Results from epidemiologic, clinical, and animal studies have suggested that: 1) a reduction in total calories decreases risk for a number of tumor types; 2) dietary protein is directly correlated with liver, prostate, and colon cancer, among others, with increasing dietary protein increasing the risk; 3) increased dietary fat is correlated with increased risk for breast cancer; the evidence for an effect of fat on colon cancer is equivocal in human and animal studies; 4) a deficiency of vitamin A may enhance lung and colon tumors in animal experiments but in human this is equivocal. Increasing vitamin A above normal levels, as an anticarcinogenic effect, has not been satisfactorily demonstrated in animal models. The synthetic retinoid, 13-cis retinoic acid, inhibits both colon and lung cancer in animal models; 5) zinc deficiency is associated with enhanced esophageal cancer in humans and markedly enhances animal tumors; selenium inhibits this form of neoplasia in animals, 6) diets low in lipotropes enhance liver cancer induced by a variety of hepatocarcinogens. Our data from studies in animal models agree in some cases with epidemiological observations, but disagree with others, particularly fat and colon cancer. Overall, some forms of cancer are enhanced by excessive calories, increased dietary protein and fat, and by deficiencies of vitamin A, selenium, zinc, and lipotropes. Decreasing total intake of calories, protein, and fat, and ensuring adequate dietary levels of vitamin A, selenium, zinc, and lipotropes decreases risk for some forms of cancer.
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PMID:The role of nutrients in cancer causation. 243 54

The substrate specificity determinants of protein kinase C are probed using synthetic peptides encompassing the major phosphorylation site serine 115 in bovine MBP. The results indicate that basic residues arginine 107 and 113 N-terminal to the phosphorylation site are essential for the substrate activity of the peptides. Substitutions of these basic residues by alanine cause a marked decrease in their substrate activity and the resulting peptide analogs become specific and rather potent inhibitors of protein kinase C. Leukemic cells are particularly abundant in protein kinase C and its substrate proteins, and the enzyme system has been shown to play a key role in cell growth. The agents that stimulate protein kinase C include tumor promoting phorbol esters (such as TPA) and mezerein, and the putative second messenger diacylglycerol. Many antineoplastic agents, on the other hand, inhibit the enzyme which include adriamycin, tamoxifen, alkyl-lysophospholipid, selenium, retinal and lipoidal amine CP-46, 665-1. Immunocytochemical studies of protein kinase C in leukemic cells indicate that it is localized in the plasma membrane, cytoplasm, nucleus and Golgi apparatus, and the subcellular distribution of the enzyme might be related to the phases of the cell cycle. TPA induces translocation of the enzyme to plasma membrane, suggesting an additional mode of action for the tumor promotor.
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PMID:Phospholipid/calcium-dependent protein kinase (protein kinase C) system: a major site of bioregulation. 243 6

Sodium selenite was administered to the rats bearing subcutaneously transplanted adenocarcinoma. The following determinations were carried out in serum: gamma-glutamyl transferase, aminotransferases, alkaline phosphatase and its placental isoform, haptoglobin, protein- and lipid-bound sialic acid. Changes observed in catalytic activities and concentrations of the examined parameters could be ascribed rather to the presence of the tumor than to the effect of the selenium treatment.
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PMID:Enzymes and acute phase reactants in serum of selenium treated rats bearing adenocarcinoma. 245 7

In attempts to simulate the effects of diet on human breast cancer development groups of female C3H mice infected with mammary tumor virus (MMTV-) were maintained on diets formulated to resemble the typical American, Bulgarian, and Japanese human diets. The incidence of mammary tumors was the highest (84%) in group of mice receiving the simulated meat- and fat-rich American diet, which was also low in selenium (Se content: 0.15 ppm). The appearance of mammary tumors was delayed in the mice maintained on the simulated Bulgarian diet, and the final tumor incidence (27%) paralleled the correspondingly lower Bulgarian breast cancer incidence. The simulated Bulgarian diet contained more Se (0.25 ppm), and was lower in fat, meat, and sugar and higher in complex carbohydrates (cereals) than the simulated American diet. In the mice fed the simulated Japanese diet, the appearance of mammary tumors was also delayed, and the tumor incidence was diminished to 47%. In this diet, fish meal was a major source of Se, which is known to have low bioavailability. Additional supplementation of the Japanese-type diet with bioavailable Se (1 ppm) lowered the tumor incidence to 10%. Based on these studies, recommendations are made for breast cancer risk reduction by dietary means.
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PMID:Effect of simulated American, Bulgarian, and Japanese human diets and of selenium supplementation on the incidence of virally induced mammary tumors in female mice. 248 97

Selenium is a trace element that is essential to the human diet. Deficiency states have been described in both animals and humans. In addition, selenium compounds have demonstrated toxicity in humans, as well as in human tissues in culture. As early as 1956, one form of selenium was used as an antineoplastic agent in humans with some demonstrated activity. Recently, evidence in both tumor-bearing animals and human tumor cells in culture have confirmed an antitumor effect of potential clinical benefit. The mechanism of this cytoxic effect appears, at least in part, to relate to the property of some forms of selenium to oxidize critical sulfhydral groups in the cell. Evidence for this, and the resulting implications for the use of selenium in anticancer treatment, is presented in this manuscript.
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PMID:Selenium. Preclinical studies of anticancer therapeutic potential. 248 19

In cultures of rat tongue epithelial cells, cell proliferation following incubation with different doses of the potent tumor promoter TPA has been studied by using a stathmokinetic method counting colchicine arrested metaphases. It was demonstrated that 24 h incubation with concentrations higher than 5 ng TPA/mL medium caused inhibition, whereas below 5 ng TPA/mL medium caused stimulation of the mitotic activity reaching a maximum around 30 h from the start of the incubation period. Based on the evidence of the anticarcinogenic effect of selenium in several animal models, experiments have been performed elucidating the influence of an atoxic dose (1/1.000.000M) of selenite on the observed TPA-induced cell proliferation. Our results indicate that addition to the culture medium of an atoxic dose of selenite, not affecting the mitotic activity of control cultures, inhibits the TPA-induced stimulation of cell proliferation.
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PMID:Antagonistic effect of selenite on tumor promoter induced cell proliferation in cultures of rat tongue epithelium. 248 23

Aberrant differentiation is a frequent hallmark of tumors, suggesting that modulators for differentiation and proliferation play a role in multistage carcinogenesis and that their use can also be exploited in cancer chemoprevention and therapy. We have demonstrated that selenium (Se) may be a modulator for the differentiation and proliferation of tumor cells. Evidence has been obtained that Se exerts the following effects: reversing changes of biochemical phenotypes toward normal levels, including reduction of cGMP level and cAMP-dependent protein kinase isozyme type I; increase in cAMP level and cAMP-dependent protein kinase isozyme type II, and altering membrane properties. Furthermore, we have obtained support for this hypothesis utilizing experiments on cultured human liver cell lines. It is demonstrated that Se can lead to the following changes: a. reduction of mitotic index; b. increase in the adhesiveness of cells; c. decrease in confluent saturation density and induction of an early contact inhibition; and d. decrease in tumorigenicity. For the purpose of comparison, the effects of Se on the normal counterparts was also studied. Contrary to what was observed above, there was no significant change in both biochemical and cellular aspects of normal cells treated analogously.
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PMID:Biochemical and cellular aspects of the anticancer activity of selenium. 248 22


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