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

Ouabain is a cardiac glycoside that blocks the sodium, potassium-pump (Na,K-Pump). When A549 human lung adenocarcinoma cells were treated with 10(-6) M ouabain for 4 hr starting 1 hr before irradiation, they were sensitized (enhancement ratio at 1% survival 1.46 +/- .07, N = 5). Ouabain affected radiation repair because it decreased the shoulder of the cell survival curve and it sensitized cells when added after radiation. CCL-210 normal human lung fibroblasts were not radiosensitized by ouabain concentrations from 10(-8) M to 10(-5) M. These results suggest that it may be possible to exploit differences in the Na,K-pumps of normal cells and tumor cells to improve the therapeutic index of radiation.
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PMID:Ouabain sensitizes tumor cells but not normal cells to radiation. 318 36

Definition of survival and measurement of colony size in soft agar assays is important in establishing in vitro radiation survival curves. Conventionally, survival is assessed according to colony-forming ability. The distinction between small colonies that are abortive and those that are viable often involves a difficult and arbitrary choice for the investigator. We have examined the effect of different minimum colony sizes (greater than or equal to 25, greater than or equal to 50, greater than or equal to 75, and greater than or equal to 100 cells) on ionizing radiation survival curves for cells from established murine (CCL 53.1) and human (M1RW5) melanoma cell lines as well as from short-term human melanoma cell strains (C8146A, C8146C, C8161, C83-2C, C82-7A1, and C8442) and patient biopsy (83-4). Single cell suspensions were plated in the upper layer of the agar bilayer and cells were irradiated by single dose X rays. Giant cells did not form in colonies containing 50 or more cells. D0 values were highest (D0 values, from 390 to 100 cGy) for cells forming smaller colonies (greater than or equal to 25 cells, greater than or equal to 4-5 doublings) and lowest (D0 values, from 190 to 50 cGy) for cells forming larger colonies (greater than or equal to 100 cells, greater than or equal to 6-7 doublings). Therefore, apparent radiosensitivity was dependent on colony size selected for analysis. Precise measurement of colony size was important in establishing radiation survival curves because errors in determining the colony size will alter apparent radiosensitivity of cells. These results should help define the biological meaning of tumor colony growth in semisolid medium, and alter the interpretation of survival curves which measure sensitivity to agents using this assay.
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PMID:Effect of tumor colony definition on ionizing radiation survival curves of melanoma-colony forming cells. 366 79

The cell surface glycopeptides from an epithelial cell line (CCL 239) derived from normal human colon were compared with those from three cell lines (HCT-8R, HCT-15, and CaCo-2) derived independently from human colonic adenocarcinomas. Cells were incubated with D-[2-3H]mannose or L-[5,6-3H]fucose for 24 h and treated with trypsin to release cell surface components which were then digested exhaustively with Pronase and fractionated on Bio-Gel P-6 before and after treatment with endo-beta-N-acetylglucosaminidase H. The most noticeable difference between the labeled glycopeptides from the tumor and CCL 239 cells was the presence in the former of an endo-beta-N-acetylglucosaminidase H-resistant high molecular weight glycopeptide fraction which was eluted in the void volume of Bio-Gel P-6. This fraction was obtained with both labeled mannose and fucose as precursors. However, acid hydrolysis of this fraction obtained after incubation with [2-3H]mannose revealed that as much as 60-90% of the radioactivity was recovered as fucose. Analysis of the total glycopeptides (cell surface and cell pellet) obtained after incubation with [2-3H]mannose showed that from 40-45% of the radioactivity in the tumor cells and less than 10% of the radioactivity in the CCL 239 cells was recovered as fucose. After incubation of the HCT-8R cells with D-[1,6-3H]glucosamine and L-[1-14C]fucose, strong acid hydrolysis of the labeled glycopeptide fraction excluded from Bio-Gel P-6 produced 3H-labeled N-acetylglucosamine and N-acetylgalactosamine. This high molecular weight glycopeptide fraction was susceptible to mild alkaline borohydride reduction, yielding a mixture of labeled oligosaccharides which contained N-acetylgalactosaminitol. Thus, the HCT-8R cells are expressing fucosylated mucin-type glycoproteins on their surface.
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PMID:Cell surface glycopeptides from human intestinal epithelial cell lines derived from normal colon and colon adenocarcinomas. 405 24

The total cellular content of the fluorescent mitochondrial-specific dye rhodamine 123 (Rh-123) was quantified by butanol extraction as a function of time of exposure and dose for a variety of cell lines. These results were compared with observations made by fluorescence microscopy on dye localization and mitochondrial morphology. There appeared to be two categories of cell types based on Rh-123 uptake: those which progressively accumulate the dye, such as Ehrlich ascites tumor cells, carcinoma-derived lines MCF-7, PaCa-2, EJ, HeLa, and normal fibroblast line CCL 64; and those which appear to equilibrate with the extracellular dye within 1 h of incubation in Rh-123 (1 microgram/ml) with a minimal level of uptake, such as the normal epithelial-derived lines CV-1 and MDCK and the transformed fibroblast line 64F3. Within the first category, the absolute value of uptake per cell correlated with the concentration of Rh-123 in the medium and with the period of exposure to the dye up to a point of apparent cellular saturation. The length of time required for apparent saturation depended on the cell type. In the second category equilibration was very early, and the total uptake was a function of the extracellular concentration of Rh-123. This probably does not represent a saturation level of dye content in the non-accumulating, low uptake cell lines. Fluorescence microscopy revealed that Rh-123 localization was initially mitochondrial-specific for all of the cell lines examined. Over time, alterations in mitochondrial morphology and cytoplasmic fluorescence were observed in the high uptake cell lines but not in the minimal uptake cell lines. Incubation of the high uptake HeLa cell line with the mitochondrial membrane potential inhibitor p-trifluoromethoxyphenylhydrazone substantially decreased Rh-123 uptake. These observations may indicate a transformation-related characteristic of carcinoma cell mitochondria. It may be possible to exploit the mechanism responsible for the progressive accumulation of Rh-123 by carcinoma-derived cell types for chemotherapeutic approaches to certain types of carcinomas.
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PMID:Increased rhodamine 123 uptake by carcinoma cells. 406 67

In the present report, we have studied the effects of butyrate and dimethyl sulfoxide (DMSO) on the characteristics of four human intestinal tumor cell lines in vitro; namely a duodenal adenocarcinoma HTB-40 and three adenocarcinomas of colon: HT-29, CCL-218, and CCL-222. In the presence of concentrations of 2 mM butyrate and 2% DMSO the growth of all these four cell lines was significantly inhibited. Both these agents lengthened the doubling time of these cell lines by about twofold. In addition, the morphology of the treated cells was altered. All four cell lines grow in semisolid agar and form characteristic colonies. Butyrate and DMSO inhibited the colony forming efficiency of these cell lines by 40-60%. Using flow cytometric analysis, the cells that were grown in the presence of butyrate and DMSO were analyzed for their lectin-binding properties. For this purpose the lectins used were concanavalin-A (Con-A), peanut agglutinin (PNA), wheat germ agglutinin (WGA), and succinylated wheat germ agglutinin (SWGA). All four cell lines showed an increase in lectin-binding cells. CCL-218, which showed no PNA binding when grown without these agents, acquired about 25% reactivity when grown in the presence of butyrate or DMSO. All these cell lines showed an increase in the percentage of positive cells for the lectin SWGA that unlike WGA does not bind to sialic acid on the cell surface, suggesting an increase in nonsialated residues on all the treated cells. These results indicate a differentiation inducing effect of butyrate and DMSO on these cell lines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differentiation inducing effects of butyrate and DMSO on human intestinal tumor cell lines in culture. 406 44

Methionine starvation causes changes in the protein pattern of HL-60 promyelocytic leukemia cells as observed by two-dimensional electrophoresis. One group of proteins is apparently modified, appearing in new positions. A further series of proteins, including several principal nuclear polypeptides, is substantially diminished. The morphology of a fraction of the cells in the culture changes concomitantly, with condensation and fragmentation of the nucleus and eventual remolding of the cell to a "grape-cluster" appearance. Similar effects are produced by a DNA methylation inhibitor, 5-azacytidine, but not by various other toxic agents tested. A defect in DNA methylation, either by depletion of S-adenosyl-L-methionine (the methyl donor) or by inactivation of the relevant enzyme, may be responsible. The T-lymphoblastoid line CCL-119 and the histiocytic lymphoma line U-937 also show these effects, but most fibroblast, epithelial, and lymphoblastoid lines do not. These changes can be largely prevented in each of the three susceptible lines by prior treatment with the tumor promoter, phorbol myristate acetate (PMA), an agent known to cause differentiation in at least two of the lines. The results thus suggest interesting relationships between methionine metabolism, protein and structural changes in the cell nucleus, and PMA-induced cell differentiation.
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PMID:Protein-pattern changes and morphological effects due to methionine starvation or treatment with 5-azacytidine of the phorbol-ester-sensitive cell lines HL-60, CCL-119, and U-937. 620 32

The cloning efficiencies of a murine melanoma cell line (S91 CCL 53.1) and a human melanoma cell strain (C8146c) were inhibited by dexamethasone (DEX), prostaglandin A1 (PGA1), and beta-all-trans-retinoic acid (RA) in a dose-dependent manner. Murine melanoma tumor colony-forming units (MTCFU) were inhibited more than 99% by DEX (1 X 10(-7) M) and RA (1 X 10(-7) M) with a concentration needed to produce a 50% reduction in colony formation for both hormones of 5 X 10(-9) M. Combinations of DEX and RA effected a synergistic inhibition on colony formation, which was reflected by a 11/2 log reduction in the hormone concentration needed to produce a greater than 99% inhibition of colony formation. When PGA1 was added to DEX and RA, a greater than additive reduction in colony formation was observed. Human MTCFU from cell strain C8146c were inhibited more than 85% at an RA concentration of 1 X 10(-7) M, but they were reduced only to 40% of control at a DEX concentration of 1 X 10(-6) M. DEX-RA produced an additive inhibition of colony formation. Addition of submaximal amounts of PGA1 to DEX-RA combinations or to either hormone alone resulted in synergistic reduction of human MTCFU. These results demonstrated that the proliferative potential of human and murine melanomas can be simultaneously regulated by DEX, PGA1, and RA.
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PMID:Dexamethasone, prostaglandin A, and retinoic acid modulation of murine and human melanoma cells grown in soft agar. 658 Apr 94

The behavior of some normal and tumor cell lines was studied after treatment with retinol. Human amnion CCL-25 cells, human embryonic intestine CCL-6 cells, human colon adenocarcinoma LOVO cells, and mouse hepatoma BW-1 cells were used. Acute and chronic toxicity of vitamin A was evaluated. The effect of retinol on cell proliferation was monitored with regard to the cell growth rate and the number of cells at saturation density. The influence of the metabolic status of the cell was studied with respect to its susceptibility to antiproliferative effect of retinol. Major effects on growth inhibition could be observed with BW-1 and CCL-6 cells, especially when they were seeded at low density.
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PMID:Growth modification of normal and tumor cell lines with retinol. 666 40

Karyotypes of nine human colorectal cell lines deposited with the ATCC were studied by trypsin-Giemsa banding. CCL 229,230,231 and 235 (Modal chromosome number, Sm, was 49, 68, 47, and 40, respectively) belong in the stable type that is characterized by karyotypes consisting mostly of normal chromosomes and stable markers. CCL 228, 234, and 238 (Sm=55,79, and 70 respectively) belong in the unstable type that has karyotypes consisting of numerous markers in addition to normal chromosomes and stable markers. The remaining intermediate type (CCL 233 and 237, Sm = 60 and 64, respectively) has karyotypic characteristics between the above two types usually with two or less unstable markers per cell. The stable markers (together with normal chromosomes) are constitutive components of a cell genome and are common to most cells within the same cultured population. Unstable markers, which generally constitute only a small portion of the total chromosome complement are the likely cause of karyotypic variations between cells and often are produced by balanced inter- or intrachromosome changes, or both. Consequently, total chromosome length per cell genome is remarkably consistent within a cell population, and karyotypes between cells, such as from four stable lines, are profoundly stable and mostly identical. Chromosome deletions and interhomologue exchanges (including isochromosomes) had the highest incidences among both stable and unstable markers. The complex markers occurred relatively infrequently. There were neither common markers nor unique chromosome breakages common to all of these established cell lines. However, chromosomes No. 7 and 1 had the highest incidence (15 and 12, respectively) of structural modifications resulting in the formation of stable markers (82 total exchanges in nine cell lines), and chromosomes No. 7 and 2 were involved at high incidence (21 and 15, respectively) in the formation of both stable and unstable markers (181 total exchanges). Moreover, No. 7 is overrepresented in eight of nine lines. The significance of chromosome changes involving No. 7 in this as well as other tumor pathotypes is briefly discussed.
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PMID:Karyotype consistency in human colorectal carcinoma cell lines established in vitro. 710 89

The glycoprotein hormone alpha subunit secreted by HeLa cells was retained by concanavalin A:Sepharose and by ricin:agarose, indicating, that the tumor protein has carbohydrate side chains containing both mannose and galactose residues. Lectin chromatography of the intracellular hormone suggests it is probably a precursor to the secreted protein, it was bound by concanavalin A but not by ricin, suggesting the presence of a high mannose core oligosaccharide but the absence of terminal sugar residues. The glycosylation inhibitors tunicamycin and 2-deoxy-D-glucose caused a reduction in alpha subunit secretion comparable to their reduction of general protein synthesis but considerably less than their inhibition of protein glycosylation. Various HeLa lines secreted alpha subunit at widely different rates, with HeLa CCL 2.2 having the highest rate of production, HeLa CCL 2.1 having the lowest, and HeLa CCL 2 being intermediate. Dose-response curves for alpha subunit from the different HeLa lines and from tunicamycin- and deoxyglucose-treated cells were sufficiently parallel to indicate similar immunological characteristics. The incorporation of radiolabeled glucosamine and N-acetylmannosamine into secreted proteins varied among the cell lines examined and was generally comparable to their hormone production rates. Concanavalin A:Sepharose chromatography of the alpha subunit secreted by HeLa CCL 2.2 and CCL 2.1 indicated that both proteins possess oligosaccharide side chains containing mannose while chromatography of these proteins on ricin:agarose suggested that less of the alpha subunit from CCL 2.1 contains galactose than that from CCL 2.2.
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PMID:Glycosylation of the chorionic gonadotropin alpha subunit synthesized by HeLa cells. 724 66


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