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

Polybrene, in conjunction with dimethyl sulfoxide (DMSO) shock has been shown to increase the frequency of DNA-mediated gene transfer to mammalian cells as compared with the frequency obtained with calcium phosphate transfection. We have successfully adapted this procedure for use with human epidermal keratinocytes. Non-tumorigenic human epidermal epithelial cells immortalized by SV40 tumor antigen were neoplastically transfected, using Polybrene at a concentration of 10 micrograms ml-1, followed by a 4 min shock, with 30% DMSO, with a plasmid carrying the activated H-ras gene from the EJ bladder carcinoma cell line. The transfected cells showed morphological alterations and induced carcinomas when transplanted into nude mice. They contained integrated copies of the transfected H-ras gene and expressed high levels of the p21 protein. Polybrene-induced DNA transfection, therefore, offers the opportunity to transfer genes effectively into human epidermal keratinocytes and should accelerate the study of the interaction between oncogenes and human epithelial cells. This study appears to represent the first neoplastic conversion of nontumorigenic, immortalized human epidermal keratinocytes by an activated human oncogene.
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PMID:Neoplastic transformation of human keratinocytes by polybrene-induced DNA-mediated transfer of an activated oncogene. 268 64

A novel culture method has been developed to study the interaction of epithelial cells in the absence of a solid substratum. Starting with either a single cell suspension or aggregates, cells were floated at the interface of air and liquid culture medium. Two epithelial cell lines have been studied in this system: Madin-Darby canine kidney cells (MDCK), and a rat bladder tumor cell line (NBT-II). Starting with a single cell suspension of MDCK, the floating cells coalesced in 24 h into sheets of cells. The cells were morphologically polarized with the apical surface facing the liquid medium. Domes were observed regularly in these sheets of cells. NBT-II cells migrated actively from aggregates at the air-liquid interface. In this floating culture, NBT-II cells produced extensive cell processes similar to those seen in cells grown on a solid surface. Because cells at the air-liquid interface lack a solid substratum for adhesion, cell membrane processes such as lamellapodia, retraction fibers, pseudopods, and long, intercellular connections can only exert a tension equal to or less than the surface tension of the liquid. Dimethyl sulfoxide 2% stimulated desmosome formation in floating NBT-II cells, resulting in a cribriform pattern in the sheet of cells. This method of interface can lead to new understanding of morphogenesis of epithelial cells, and the mechanism of cell motility and formation of cell processess.
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PMID:Epithelial cell interaction in air-liquid interface culture. 273

Dihematoporphyrin ether, also known as Photofrin-II (Pf-II) is currently used in the diagnosis and management of a variety of epithelial neoplasms, in a modality known as photodynamic therapy (PDT). A major drawback of these porphyrins for PDT is their ability to evoke prolonged cutaneous photosensitization. The mechanism of tumor ablation and cutaneous photosensitization by these photosensitizers is thought to relate to the generation of one or more reactive oxygen species such as superoxide anion, singlet oxygen and hydroxyl radical. However, the role of these oxygen species has not been established unequivocally. In this study, the mechanism of Pf-II-mediated cutaneous photosensitization was examined using murine ear swelling as a marker. The mice treated with Pf-II and light demonstrated two-fold enhancement of ear swelling whereas animals treated with the SOD mimic, beta-carotene and dimethyl sulfoxide (DMSO) had considerably less ear swelling (p less than 0.01). The observed protective effect was dependent on the dose of each quencher and followed the pattern SOD mimic DMSO beta-carotene. The histopathologic alterations caused by Pf-II photosensitization were significantly alleviated by pretreatment with SOD mimic whereas beta-carotene and (DMSO) were less effective. Inhibitors of superoxide dismutase (sodium diethyldithiocarbamate) and catalase (hydroxyl amine and 3, amino 1,2,4-triazole) augmented Pf-II-mediated cutaneous photosensitization. These data provide the first in vivo evidence for the involvement of superoxide anion in cutaneous porphyrin photosensitization.
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PMID:In situ evidence for the involvement of superoxide anions in cutaneous porphyrin photosensitization. 283 53

The participation of lysosomal enzymes, hydroxyl radicals, and mitochondrial respiration in the cytocidal effect of TNF on tumor cells was investigated. The cytotoxicity of TNF on L-M cells was clearly reduced by lysosomotropic agents, DMSO (hydroxyl radical scavenger), NDGA (lipoxygenase inhibitor), and sodium azide (mitochondrial respiration inhibitor). The results suggest that lysosomal enzyme and hydroxyl radicals play an important triggering role in the destruction of tumor cells by TNF, and that the process of destruction might require ATP.
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PMID:Cytocidal mechanism of TNF: effects of lysosomal enzyme and hydroxyl radical inhibitors on cytotoxicity. 283 28

The tumorigenic activities of 6-nitrochrysene and its metabolites were evaluated in the newborn mouse model. Groups of mice were treated with the appropriate compounds in DMSO by i.p. injections on the 1st, 8th and 15th day of life. Seven hundred nmol/mouse of 6-nitrochrysene induced significant incidences and multiplicities of lung tumors in both sexes; only males were susceptible to liver tumor induction. At 100 nmol/mouse, 6-nitrochrysene had significant tumorigenicity in both lung and liver but was less active than at the higher dose. Administration of 100 nmol/mouse of 6-nitrochrysene, only on day 1, caused about the same tumor yield as was observed after treatment with 700 nmol/mouse given over 3 days. Among the metabolites of 6-nitrochrysene which were tested at 100 nmol/mouse, 6-nitrosochrysene and 6-aminochrysene were significantly less active in the lung and in the liver than 6-nitrochrysene. In the lung, trans-1,2-dihydro-1,2-dihydroxy-6-nitrochrysene and trans-1,2-dihydro-1,2-dihydroxy-6-aminochrysene had activities comparable to those observed in mice treated with equimolar doses of 6-nitrochrysene. In the liver, trans-1,2-dihydro-1,2-dihydroxy-6-nitrochrysene was more active than 6-nitrochrysene based on the number of tumors per mouse. These observations support our hypothesis that 6-nitrochrysene is metabolically activated by ring-oxidation to trans-1,2-dihydro-1,2-dihydroxy-6-nitrochrysene, followed by nitro-reduction to trans-1,2-dihydro-1,2-dihydroxy-6-aminochrysene and, finally, oxidation to a diol-epoxide.
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PMID:Comparative tumorigenicity of 6-nitrochrysene and its metabolites in newborn mice. 291 88

The addition of dimethyl sulfoxide (DMSO) to cultures of line 1 carcinoma cells can increase the surface expression of H-2K and H-2D antigens at least 100-fold from barely detectable initial levels, as determined by using specific monoclonal antibodies and flow cytometry. H-2 values stabilize approximately 1 wk after exposure to maximally inducing concentrations of DMSO (3% vol) at densities found on normal spleen cells. Increased expression of H-2 antigens is not the result of cell selection, it is specific in that expression of an unrelated surface protein decreases, and it is associated with increased synthesis of these antigens as measured by incorporation of [35S]methionine. Additional DMSO-induced changes in the growth, cycling, lectin binding, and antigenic properties of line 1 cells are consistent with increased cell maturation. All changes are reversed when DMSO is removed. This system may facilitate study of products associated with differentiation that influence tumor cell malignancy.
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PMID:Dimethyl sulfoxide induces expression of H-2 antigens on mouse lung carcinoma cells. 298 54

Retinoic acid induces the differentiation of NTERA-2 cl. D1 human embryonal carcinoma (EC) cells into neurons, cells permissive for the replication of human cytomegalovirus (HCMV), and other cell types that cannot as yet be classified but are distinguishable from the stem cells. We tested several additional agents for their ability to induce the differentiation of these EC cells. No differentiation was induced by butyrate, cyclic AMP, cytosine arabinoside, the tumor promoter 12-0-tetradecanoylphorbol 13-acetate (TPA), or the chemotherapeutic agent cis-diaminedichloroplatinum, although morphological changes were detected at the highest concentrations of these agents that permitted cell survival. However, retinal, retinol, 5-bromouracil 2'deoxyribose (BUdR), 5-iodouracil 2'deoxyribose (IUdR), hexamethylene bisacetamide (HMBA), dimethylacetamide (DMA), and dimethylsulfoxide (DMSO) all induced some neuronal differentiation, but to a lesser extent than retinoic acid. Also, BUdR, IUdR, HMBA, and DMA induced the appearance of many cells permissive for the replication of HCMV. Differentiation was, in all cases, accompanied by the loss of SSEA-3, a globoseries glycolipid antigen characteristically expressed by human EC cells. However, another glycolipid antigen, A2B5, which appears in 60%-80% of differentiated cells 7 days following retinoic acid induction, was detected in less than 20% of the cells induced by the other agents studied. This implies that the HCMV-permissive cells induced by retinoic acid are not identical to those induced by BUdR, IUdR, and DMA.
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PMID:Differentiation of TERA-2 human embryonal carcinoma cells into neurons and HCMV permissive cells. Induction by agents other than retinoic acid. 301 99

The purpose of this study was to determine whether the energy metabolism of an experimental rodent sarcoma was selectively depressed by the combination of inhibition of glycolysis and respiration. In vivo phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor the response of tumor or brain high-energy phosphate compounds to insulin hypoglycemia, rhodamine 123, or both agents in fasting rats with subcutaneous methylcholanthrene-induced sarcomas. Insulin or rhodamine 123 alone produced a similar 50% to 60% reduction in tumor adenosine triphosphate (ATP) concentration compared with controls injected with saline solution (p less than 0.05, one-way analysis of variance [ANOVA]). The combination of insulin plus rhodamine 123 resulted in a 90% reduction of tumor ATP concentration, which was significantly different from the effect of either agent alone (p less than 0.05, one-way ANOVA). Brain phosphocreatine and ATP concentrations were unchanged by these agents. Administration of dimethyl sulfoxide (DMSO)/glycerol, the vehicle for rhodamine, produced a 35% reduction of tumor ATP, which was similar to the effect of insulin alone but significantly different from rhodamine. The combination of DMSO/glycerol plus insulin hypoglycemia resulted in a 70% reduction in tumor ATP, which was significantly elevated compared with the combination of rhodamine plus insulin. Glucose deprivation induced by insulin, and combined with the inhibition of oxidative phosphorylation, produces an additive depression of tumor energetics. The drug vehicle DMSO/glycerol significantly depresses tumor energy metabolism, presumably because of its DMSO component, which may explain the previously reported antineoplastic efficacy of this solvent. Combinations of inhibitors directed at different points of tumor metabolism produced an enhanced depression of tumor energetics, whereas host tissue was protected.
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PMID:Inhibition of tumor high-energy phosphate metabolism by insulin combined with rhodamine 123. 304 41

Treatment of B16-F10 melanoma cells with dimethylsulfoxide (DMSO) or butyric acid (BA) inhibits cell growth and delays tumor appearance in syngeneic mice. Both agents induce morphological changes in these cells. Treatment of melanoma cells with DMSO results in a marked increase in tyrosinase activity and melanin content. BA, on the other hand, does not increase melanin content and decreases tyrosinase activity. The data show that there are marked differences in the effect of DMSO and BA on melanin biosynthesis, whereas both agents inhibit cell growth and cause a delay in tumor appearance. These findings indicate that decreased proliferation of melanoma cells and induction of melanin biosynthesis are not necessarily associated phenomena.
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PMID:Growth inhibition of murine melanoma by butyric acid and dimethylsulfoxide. 307 93

The role of dimethyl sulfoxide [(DMSO) CAS: 67-68-5] in experimental tumorigenesis was investigated because of conflicting reports in the literature ranging from inhibition to no effect to enhancement. With the use of numbers of skin tumors produced on the back of the mouse following topical applications of carcinogenic agents as the variable and with acetone serving as the control solvent, the following results were obtained: When DMSO was the solvent for benzo[a]pyrene (CAS: 50-32-8) in the single-stage model (C3H mice), tumor numbers doubled. When DMSO was the solvent for 7,12-dimethylbenz[a]anthracene (CAS: 57-97-6) serving as initiator in the two-stage model (CD-1 mice), tumor numbers were unaffected. In the two-stage model, when DMSO was the solvent for the potent promoter phorbol-12-myristate-13-acetate [(PMA) CAS: 16561-29-8] or was applied to skin at the initiation site (the back) before PMA, tumor numbers were reduced to one-third of control. However, when DMSO was applied before PMA to the abdomen, a site remote from initiation, tumor numbers doubled. Enhancement of PMA appears to be unique. Recognition that diverse effects can occur depending on the method of application of DMSO may help to decipher the conflicting literature on its relation to tumorigenesis, could be of value in probing the mechanism of tumor promotion, and might signal further caution in its clinical use.
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PMID:Inhibition and enhancement of skin tumors in mice by dimethyl sulfoxide depending on method of application. 309 44


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