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

The effects of dieldrin and mirex on Ehrlich ascites tumor cells were assessed, using certain in vivo (in mice) and in vitro measurements. Mirex retarded the development of Ehrlich ascites tumor in vivo, but dieldrin did not. Effects of dieldrin on de nova RNA purine synthesis from formate in vivo were slight, while mirex inhibited the synthesis of both RNA purines. Dieldrin inhibited the in vitro incorporation if thymidine, uridine, and L-leucine into DNA, RNA, and protein, respectively, but mirex was virtually without effect.
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PMID:Some effects of dieldrin and mirex on Ehrlich ascites tumor cells in vivo and in vitro. 86 89

Ribose 1-phosphate concentrations have been measured in tumor cells incubated with purine and pyrimidine nucleosides and with glucose. Highest concentrations (0.15 to 0.2 mumol/ml of cells) were attained in cells incubated with inosine. Although uridine was cleaved at approximately the same rate as inosine, as judged by lactate accumulation, concentrations of ribose 1-phosphate that accumulated were only approximately 0.06 mumol/ml. Ribose 1-phosphate accumulation in tumor cells incubated with inosine was dependent on the phosphate concentration of the medium up to at least 25 mM. Ribose 1-phosphate formed from inosine was readily converted both to phosphoribosyl pyrophosphate and to lactate.
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PMID:Ribose 1-phosphate metabolism in Ehrlich ascites tumor cells in vitro. 92 6

Native small ribosomal subunits in cultured Ehrlich ascites tumor cells, analyzed by high-resolution CsCl isopycnic centrifugation, consist of at least five classes of particles. These particles with buoyant densities of 1.39, 1.42, 1.45, and 1.51 g/cm3 were designated as SI, SII, SIII, SIV and SV, respectively. They were different from the ribosome-derived 40-S subunits which have a density of 1.54 g/cm3. Native large ribosomal subunits consist of at least two classes of particles with densities of 1.57 g/cm3 (LI) and 1.59 g/cm3 (LII), respectively. The ribosome-derived 60-S subunits have the same buoyant density as LII particles. Labeling of Ehrlich ascites cells with radioactive uridine and a subsequent chase in the presence of RNA-synthesis inhibitors shows that radioactivity was incorporated first in precursor particles with a density of 1.48 g/cm3 and then subsequently appeared in SIII and SII particles. Met-tRNAf is found exclusively on native 40-S particles with densities of 1.42 and 1.49 g/cm3. This result has been observed in cells labeled with [35S] methionine in vivo as well as with tRNA charged in vitro. The possibility that SII particles contain 40-S initiation complexes is discussed.
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PMID:On the heterogeneity of native ribosomal subunits in Ehrlich-ascites-tumor cells cultured in vitro. 94 60

Ehrlich ascites tumor cells were labeled with [5,6-3H]uridine in vivo during the exponential growth phase of the tumor in the mouse. Hydroxyapatite column chromatography of the total cell nucleic acid revealed a level of activity in the DNA approaching 50% of the incorporated activity of the RNA after 24 hours. After perchloric acid hydrolysis, the constituent bases of the DNA, separated by paper chromatography, contained more than 90% of the tritium radioactivity in the cytosine and thymine, at a ratio of approximately 2:1. Prior to digestion of the polymer, the level of label in the DNA was not sensitive to RNase, alkaline, or heat denaturation. Equilibrium density gradient centrifugation produced a single peak, coincidental for radioactivity and optical density at 260 nm. Our results indicate that tumor cells under replicative stress incorporated more than one-third of the tritium radioactivity of uridine into the DNA, whereas those at a growth plateau had less than 10% of the label in the DNA. This exogenous uridine radioactivity observed in the DNA represented neither a DNA-RNA hybrid, RNA primer pieces in DNA synthesis, nor any other RNase-sensitive species, but was apparently the consequence of amination and methylation of the tritium-labeled uracil moiety to satisfy the metabolic needs of the replicating cells for cytosine and thymine bases.
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PMID:Incorporation of tritiated uridine into DNA of Ehrlich ascites tumor cells. 100 13

During the development of leucosis a progressively retarded incorporation of 2-C14-thymidine and C14-uridine into DNA and RNA of a separate tumor cell and an active incorporation of 2-C14-thymidine into DNA of hepatic and splenic cells were observed. Repeated injections of NMU (20 mg/Kg X 5) in tumor-bearing animals result in a twice increase of life terms in mice and suppression of total tumor cells growth. The observed therapeutic effect is related with deep inhibition of DNA and RNA synthesis in leucosis L-1210 cells, while DNA synthesis in hepatic and splenic cells is only insignificantly suppressed (compared with the normal level typical for intact animals), but RNA synthesis in these organs is actually not involved.
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PMID:[Effect of N-nitroso-N-methylurea on DNA and RNA synthesis in cells of liver and spleen tumors in leucosis L-1210]. 101 95

Two cell lines derived from a primary MSV-M-induced tumor in a BALB/c mouse were studied. One line (MS-2) was subject only to continuous tissue culture transfer (tct). After 21 tct, MS-2 cells produced progressive tumors (MS-2 tumors) in syngeneic hosts. The second cell line (MS-2T) was established by cultivation of a MS-2 tumor. The ability to produce progressive tumors decreased with increased number of tct, in both cell lines. The virus content of MS-2 and MS-2T cells was very low, as shown by uridine incorporation and electron microscopy. Immmunofluorescence tests demonstrated that antigens different from the viral MSV-M antigens were present on the cell lines, and that antigenic changes occurred with increased number of tct. Serum of mice bearing progressive MS-2 tumors reacted with MS-2T cells when these cells produced progressive tumors and did not react with MS-2 cells when they produced regressing tumors. MS-2 cells producing regressing tumors reacted with serum from mice in which the MS-2 tumor had regressed and with serum from mice immunized with MS-2T cells at late tct when they were poorly oncogenic. The antigenic changes seemed, therefore, to parallel the decrease of malignancy. A chromosomal analysis carried out on MS-2 and MS-2T cells, when both produced progressive tumors, showed a modal number of 48 and 44, respectively. MS-2T cells showed a large acrocentric chromosome. In contrast, the MS-2 cells at late tct, when they gave regressing tumors, showed a modal number of 60 and a wide range of distribution of chromosome number.
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PMID:Biological properties of cell lines derived from Moloney virus-induced sarcoma. 102 48

Rates of incorporation of thymidine and uridine, but not leucine, decrease markedly in L1210 (V) cells within 1 hour of incubation in DULBECCO'S medium containing 10% serum. 2-Mercaptoethanol (2-ME) after a latent period of more than 5 hours causes an increase in nucleotide incorporation. Bovine serum albumin can substitute for serum in the medium, but a higher concentration of 2-ME is required for growth. After charcoal treatment of the albumin less 2-ME is required. These experiments suggest that inhibition of the tumor cells is caused by a serum factor whose effect is antagonized by the thiol.
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PMID:Studies of the mechanism of growth promotion of lymphoma cells by 2-mercaptoethanol in vitro. 105 63

Variations in DNA synthesis as measured by tritiated-thymidine autoradiography in mammary carcinoma before and during endocrine therapy were studied in patients treated for inoperable or locally recurrent mammary carcinoma. Tumor cells were collected by aspiration biopsy and immediately expelled into the incubating solution. Cell viability was assessed by staining unfixed cells with trypan blue and fixed cells with orecin. To assess viability tritiated-uridine incorporation was used in some experiments. The same cells were identified by each method. Bilateral oophorectomy was done in 4 patients. In the 1 case in which regression followed, a 5-fold decrease in DNA-synthesis was noted 1 week after oophorectomy but at 2 weeks no cells incoporated thymidine. In the 3 patients with tumor progression the fraction of labeled cells was unchanged. For antiestrogen therapy, Tamoxifen (Nolvadex) was used. Serial needle aspirates were collected from 38 patients who received 20 mg of Tamoxifen twice daily. Complete remission followed in 7, incomplete remission in 8, stationary disease in 7, and progression in 16. DNA synthesis fell to very low values after 1-3 weeks and remained low in the 7 cases with complete regression. Tumors showing partial regression showed diminished fractions of 5-phase cells (tritiated-thymidine-labeled cells) after 1-5 weeks. In 1 instance at 72 weeks the S-phase fraction of cells was higher than initial value. Tumor value remained stationary for 40 weeks and then increased. Antiestrogen therapy was stopped at 82 weeks. In those with progressive tumor growth there was high DNA synthesis. Between 20-30% of the cells were replicating DNA. None showed decrease in the fraction of S-phase cells, and 1 showed increase. For estrogen therapy, estradiol valepianate was given im every 2 weeks. Of the 3 patients who received estrogen therapy, 2 of the tumors responded and the DNA-synthesis rapidly decreased until none was measurable after 4 weeks. S-phase values prior to endocrine therapy showed no correlation with the therapeutic response. Tumors that responded showed a decrease in the proportion of S-phase cells during the first 3 weeks. In tumors responding to encocrine therapy the decrease in tritiated-thymidine incorporation was rapid and preceded reduction in tumor size. Data suggest that 2 aspirates should be studied before therapy and repeated after 2-4 weeks in order to include the minimal proportion of S-phase cells. The patients accepted the needle biopsies well. There were no growths of carcinoma at the puncture sites. About 5 weeks must elapse before tumor response can be assessed. Determining hormone receptors in surgically removed carcinoma specimens gives much more rapid indications as to possible response to endocrine therapy.
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PMID:3H-thymidine incorporation into mammary carcinoma cells obtained by needle aspiration before and during endocrine therapy. 106 73

Rhodium(II) acetate, propionate, and butyrate showed a considerable variation in their antitumor activity against Ehrlich ascites tumor cells in mice, with the butyrate complex being the most active. The three complexes markedly inhibited DNA synthesis of Ehrlich ascites tumor cells in vivo. Rhodium (II) butyrate was the most potent inhibitor followed by the propionate complex. One hour after administration, rhodium(II) propionate and butyrate induce more uridine-5-3H incorporation into RNA than is seen in the controls. Equilibrium dialysis studied showed that rhodium(II) acetate-1-14C binds to single stranded DNA, poly-A, ribonuclease A, and bovine serum albumin but not to highly polymerized native calf thymus DNA, poly-G, or poly-C. In these cases binding occurred at the two axial positions of rhodium(II) acetate to a nitrogen donor in the ligands. The formation constants of the rhodium(II) acetate and propionate complexes with 5'-adenosine monophosphate were determined. The rhodium(II) propionate complex was more stable. Sedimentation and viscosity measurements of poly-A and poly-A/rhodium(II) acetate complexes indicate a high degree of intramolecular crosslinking in the rhodium(II) acetate/poly-A complex. The rhodium(II) carboxylate complexes were also found to be potent inhibitors of purified DNA polymerase I and RNA polymerase from Escherichia coli.
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PMID:Interaction of Rhodium(II) carboxylates with molecules of biologic importance. 110 39

Events preceeding the cortisol inhibition of uridine utilization by corticoid-sensitive P1798 lymphocytes have been investigated. When tumor cells were incubated with 1 muM cortisol for 15 min and then washed free of steroid and reincubated in the absence of hormone, the expected decrease of uridine uptake failed to appear 1.5 hr later. In contrast, the removal of cortisol after 30 or 60 min did not prevent subsequent development of the steroid effect. Addition of actinomycin D with cortisol, or 15 min after hormone treatment was started, blocked steroid action. However, when actinomycin D was added 30 or 60 min after the initial exposure to cortisol, hormone-induced depression of uridine uptake was no longer prevented. To study the role of protein synthesis, cycloheximide was added to the tumor cell suspensions at various times after cortisol treatment was started. Cortisol suppression of uridine utilization was blocked when cycloheximide was added with the hormone or 30 min after the start of hormone treatment. Cycloheximide added together with cortisol and washed out with the steroid after 30 min did not prevent subsequent appearance of decreased nucleoside uptake. Hydroxyurea, an inhibitor of DNA synthesis, did not prevent cortisol action, even when present throughout a 2 hr exposure to the steroid. Hormone removal or actinomycin D addition after 1.5 to 2 hr (when uridine uptake was already inhibited about 25%) did not prevent intensification of the steroid effect during a subsequent 1.5- to 2-hr incubation period, while addition of cycloheximide at this time completely prevented its progression. These results suggest aht: (a) cortisol inhibition of uridine uptake by P1798 lymphocytes involves an early irreversible step and appears to require continuing RNA but not protein synthesis during the first 15 to 30 min of hormone action; (b) protein synthesis but not RNA synthesis is required between 30 and 60 min; and (c) continuing protein synthesis but not RNA synthesis or hormone presence is necessary for the preestablished cortisol effect to progress.
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PMID:Sequential irreversible, actinomycin D-sensitive, and cycloheximide-sensitive steps prior to cortisol inhibition of uridine utilization by P1798 tumor lymphocytes. 114 29


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