Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

10(7) mouse ascites tumor cells/ml incubated at 37 degrees C in 0.5 to 1.0 X 10(-4) M Janus green B or in 1.0 X 10(-4) M phenazine methosulphate are destroyed in 100 per cent oxygen atmosphere but remain transplantable in nitrogen atmosphere. The "sensitizing" effect of oxygen can be substituted by SH inhibitors (iodoacetic acid, iodoacetamide and their spinlabelled variants) as well as by some nitroxide free radicals. The "oxygen effect" is blocked by mercaptoethanole or cooling. Compared with the spectrum of native cells a more symmetrical singlet of larger amplitude, approximately g = 2 value, arose in the ESR spectrum of Janus green B treated cells. The "oxygen effect" observed in the presence of Janus green B differs in several ways from the oxygen effect of ionizing radiation and from the "photodynamic" effect.
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PMID:Study on the "toxic oxygen effect" of Janus green B in mouse ascites tumour cells. 7 98

Cellular injury was produced in Ehlrich ascites tumor cells by an inhibitor of the function of the cell membrane [10(-3M) parachloromercuribenzenesulfonic acid (PCMBS)] or by inhibitors of respiration (10(-4M) Antimycin A), glycolysis (10(-4M), iodoacetic acid, IAA), oxidative phosphorylation (10(-3M) 2,4 dinitrophenol, DNP) or by combinations of these in a medium with or without glucose. The contents of Na+, K+, Ca++, Mg++ and intracellular water in the treated cells and controls were correlated with the percentages of ultrastructural changes in the mitochondria of the cells. A moderate negative correlation (r = -0.66) was observed between K+ content of the cells and the condensation of mitochondria in selected experiments where mitochondrial swelling had not yet started. A moderate positive correlation (r = 0.44) was observed between mitochondrial condensation and Na+ content of the cells in the same experiments. K+ and Mg++ content of cells showed a moderate negative correlation (r = -0.58 and -0.65) with mitochondrial swelling in the material of all experiments and Ca++ content a moderate positive one (r = 0.58), but the Na+ content and intracellular water showed no correlation. The percentages of flocculent densities in mitochondria showed a moderate positive correlation (r = 0.43) with the Ca++ content of the cells and a moderate negative correlation (r = -0.61) with the magnesium content of the cells.
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PMID:Mitochondrial changes, ion and water shifts in the cellular injury of ehrlich ascites tumor cells. 17 Sep 4

The glycoprotein accounting for most of the nonadrenocorticotropic hormone (ACTH), non-beta-lipotropin (beta LPH) region of mouse tumor cell pro-ACTH/endorphin was purified from tumor cell culture medium and shown to contain 1/2 cystine residues. Preparations of the 16,000-dalton fragment-related material (referred to as 16K fragment) were heterogeneous with respect to size and charge. Despite this heterogeneity, a partial amino acid sequence for the NH2-terminal region of the molecule was determined by automated Edman degradationof the 16K fragment labeled by reduction and alkylation with [3H]iodoacetic acid or labeled biosynthetically with [3H]tryptophan. The sequence of 1/2 cystine and tryptophan residues in the mouse tumor 16K fragment can be aligned with one region of the amino acid sequence predicted from the cDNA for a bovine precursor to ACTH/beta LPH (Nakanishi, S., Inoue, A., Kita, T., Nakamura, M., Chang, A.C.Y., Cohen, S.N., and Numa, S. (1979) Nature 278, 423--427).
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PMID:Partial characterization of a glycoprotein comprising the NH2-terminal region of mouse tumor cell pro-adrenocorticotropic hormone/endorphin. 22 24

N-Ethyloxycarbonylaminomehyl-L-isoleucine (A-145), a novel antitumor amino acid derivative, is an anti-tumor agent effect in cases of Ehrlich ascites rather than against Sarcoma-180. The chemotherapeutic index of A-145 was 14.9 for Ehrlich ascites carcinoma and 4.2 for ascites Sarcoma-180. Experimental studies on ddy mice regarding the difference in susceptibility of these two tumor cell lines to A-145 gave the following results. In in vivo experiments, the uptake of 14C-A-145 by Ehrlich ascites carcinoma was greater than by Sarcoma-180, i. e. the uptake ratio of Ehrlich ascites carcinoma/Sarcoma-180 was 1.52 at 30 min and 2.7 at 24 hr after injection. In in vivo experiments, there was no remarkable difference between Ehrlich ascites carcinoma and Sarcoma 180 in the subcellular distribution of 14C-A-145, and the majority of the radioactivity taken up was distributed in nuclei and cytosol fractions. In in vitro experiments, the uptake of 14C-A-145 by both cell lines was found to be temperature sensitive, glucose dependent, and decreased on addition of KCN, 2, 4-dinitrophenol or iodoacetic acid. In in vitro experiments, competitive inhibition by L-isoleucine on 14C-A-145 uptake into tumor cells was observed in both cell lines, however, in vitro experiments, the inhibitory effect of A-145 on cell growth in cultured Sarcoma-180 was not reversed by L-isoleucine.
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PMID:[The difference of drug sensitivity of tumor cells on N-ethyloxycarbonylaminomethyl-L-isoleucine (A-145 (author's transl)]. 43 84

The induction of ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase in mouse epidermis by various classes of tumor-promoting and nonpromoting compounds has been studied in order to determine the specificity of this response for tumor promotion. The effect of topical applications of a series of phorbol esters on these enzyme activities correlated well with their promoting abilities. Iodoacetic acid, anthralin, and Tween 60, all promoting compounds, also stimulated both of these enzyme activities after single and multiple applications. The hyperplastic agents acetic acid, cantharidin, and ethyl phenylpropriolate, however, had little effect on ornithine decarboxylase activity but a pronounced effect on epidermal S-adenosyl-L-methionine decarboxylase activity. The specificity of the ornithine decarboxylase response for tumor promotion was suggested by the results of the above experiments as well as the stimulatory effect of a completely carcinogenic dose of 7,12-dimethylbenz[a]anthracene; a lower initiating dose had no effect. In addition, epidermal tumors produced by a two-stage procedure showed consistently high levels of ornithine decarboxylase activity but variable levels of S-adenosyl-L-methionine decarboxylase activity.
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PMID:Induction of the polyamine-biosynthetic enzymes in mouse epidermis and their specificity for tumor promotion. 80 25

An undifferentiated human pancreatic carcinoma has been established in continuous culture and is grown in Dulbecco's modified. Eagle's medium fortified with 10% fetal calf serum and 2.5% horse serum. The established cell line (MIA PaCa-2) has a doubling time of 40 h. The cells are large with abundant cytoplasm, exhibit a high degree of aneuploidy and have a tendency to grow on top of other cells. MIA PaCa-2 grows in soft agar with a colony-forming efficiency of 19%. Both MIA PaCa-2 cells and a cell line from another pancreatic carcinoma obtained from National Cancer Institute (NCI) are sensitive to asparaginase, a property not shared by several other human tumor cell lines tested.
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PMID:Human pancreatic carcinoma (MIA PaCa-2) in continuous culture: sensitivity to asparaginase. 83 18

The presence and localization of neoantigens induced in cultured cells, infected or transformed with avian tumor viruses (ATV), were studied ultrastructurally on carbon platinum replicas of cell surfaces. The use of antibody, labeled with hemocyanin molecules, provided sensitive detection and analysis of cell surface antigen distribution. The subgroup-specific antigens of the viral envelope were found in considerable amount in the plasma membranes of ATV-infected chick embryo fibroblasts. The distribution of these antigens over the cell surface, evaluated on cells which were prefixed with glutaraldehyde, was found to be diffuse with a greater density on the cell processes in some cells. Reaction of antibody to viral envelope antigens with living ATV-infected cells resulted in a number of patterns of redistribution of membrane antigen-antibody complexes (AAC). Redistribution occurred in symmetrical or asymmetrical modes. The former consisted of randomly oriented aggregates (patches) of AAC over the cell surface. The latter included: (a) linear accumulation of AAC at cell margins; and (b) condensation of compexes into one or more centers of coalescence. These observations could be made on chick embryo cells infected (but not transformed) by avian leukosis virus, or on cells oncogenically transformed by avian sarcoma virus. The regions of coalescence were suggestive of the "capping" phenomenon seen in other systems, and their formation was temporally correlated with endocytosis of labeled AAC and the gradual loss of AAC from the surface. The effects of several biologically perturbing substances on the processes of redistribution were investigated in ALV-infected fibroblasts. Sodium azide, puromycin, actinomycin D, and colchicine had no effect on either form of asymmetrical redistribution. Cytochalasin B (CB) and iodoacetic acid (IAA) appeared to have some effect on the marginal redistribution, and to completely prevent the condensation into foci of coalescence (FC). When treated with these compounds, reacted with antibody at low temperature, washed free of unbound antibody, and warmed at 37 degrees C, cells rapidly cleared their surfaces of AAC. This was not accompanied by formation of FC or endocytosis. In some of these cells, a distribution was observed which suggested a possible centrifugal flow of antigenic sites-perhaps an alternate route for disposal of AAC. None of the drugs tested affected symmetrical redistribution. Repeated attempts at detection and topographical analysis of a tumor-specific antigen on the surface of Rous sarcoma virus-transformed chicken and rat cells have provided no evidence for antibody to such an antigen in the serum of immunized animals. Autochthonous, homologous, and heterologous immunizations of chickens and rats did not produce a detectable antibody response to a virus-specific tumor surface antigen. Preliminary results, however, suggest the expression of an individual-specific (unique) tumor antigen on the surface of Rous sarcoma cells.
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PMID:The expression and localization of surface neoantigens in transformed and untransformed cultured cells infected with avian tumor viruses. 125 61

Nude mice bearing xenografts of MIA PaCa-2 human pancreatic cancer cell line were treated for 4 weeks with AN-51, a somatostatin octapeptide analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121) containing methotrexate attached to the alpha-amino group of D-Phe in position 1. Control groups of mice received saline, RC-121 or methotrexate. Drugs were given in equimolar doses by daily s.c. injections. After 7 days of treatment with 25 micrograms/day of AN-51, tumor growth was completely inhibited although the treatment had to be suspended because of toxic side effects, especially on the gastrointestinal tract, accompanied by major weight loss of the animals. Mice were allowed to recover for 1 week and treatment was continued with 12.5 micrograms/day AN-51. After 2 weeks of additional therapy, tumor volume, percentage change in tumor volume, and tumor weights were significantly decreased, compared with controls, only in the group treated with AN-51. Methotrexate and RC-121 also inhibited tumor growth, but their effects were not statistically significant. AN-51 retained its hormonal activity and decreased serum growth hormone levels in mice. Binding affinity of AN-51 for somatostatin receptors on MIA PaCa-2 cells was found to be 2.5-times lower than that of parent compound RC-121. This is the first report on inhibition of human pancreatic cancer growth in vivo by somatostatin analogs carrying cytotoxic radicals.
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PMID:Cytotoxic analog of somatostatin containing methotrexate inhibits growth of MIA PaCa-2 human pancreatic cancer xenografts in nude mice. 131 46

Human lymphokine-activated killer (LAK) cells expressed a membrane-associated lymphotoxin-related molecule (mLT) which was detected by flow cytometric analysis with anti-lymphotoxin antibody. Upon removal of exogenous interleukin-2 from LAK cell culture medium and another 24 h cultivation, the expression of mLT was decreased. Corresponding to the decrease of mLT expression, the killing activity of LAK cells towards L929 cells was remarkably reduced and killing of MIA PaCa-2 and U937 cells was moderately reduced, whereas killing of Daudi and K562 cells was fully restored. The supernatant of mLT-expressing LAK cells had no cytotoxic activity towards L929 cells in the absence of actinomycin D. Moreover, not only the killing of L929 cells but also that of human tumor cell lines (MIA PaCa-2, U937) by mLT-expressing LAK cells was partially inhibited in the presence of anti-lymphotoxin antibody. These results suggest an involvement of mLT in the killing of some tumor target cells by LAK cells.
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PMID:Correlation between killing activity towards the murine L929 cell line and expression of membrane-associated lymphotoxin-related molecule of human lymphokine-activated killer cells. 163 9

We have evaluated in a homologous system the mechanisms of platelet activation by cells isolated from fresh human tumor tissues and the role of thromboxane B2 (TxB2) generation in this process. Thirty-eight of the 46 tumor tissues considered showed a high platelet-aggregating activity, with no particular distribution in any specific tumor type. Apyrase caused a nonsignificant reduction in the aggregation response, hirudin did not change it, while iodoacetic acid or p-hydroxymercuriphenylsulfonate, specific cysteine proteinase inhibitors, significantly reduced the platelet-aggregating capacity of these tumor cells. In 9 colon carcinomas and in 8 breast carcinomas the levels of TxB2 produced by platelets after addition of tumor cells were measured: tumor cell-induced platelet aggregation was accompanied by a significant production of the metabolite; indobufen, a cyclooxygenase inhibitor, significantly reduced aggregation and particularly TxB2 production, while the drug had no effect on both parameters if preincubated with tumor cells only. These data suggest that cells isolated from different human tumor tissues activate platelets through the activity of tumor-associated cysteine proteinase(s); platelet aggregation by tumor cells is largely dependent on arachidonic acid metabolism in platelets, while such metabolism in tumor cells does not play a significant role.
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PMID:Thromboxane production by platelets during tumor cell-induced platelet activation. 191 83


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