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)

To provide guidelines for handling the very labile phorbol ester, RPA,2 its stability under various laboratory conditions was studied. RPA will remain undecomposed for 8 weeks if stock solutions are made in ethanol, ethyl acetate, or DMSO and stored in absolute darkness at -20 degrees C. When exposed to light RPA readily isomerizes to 13'-cis-RPA. Structure/activity investigations of irritant polyfunctional diterpene esters of phorbol, ingenol, and resiniferonol with saturated and unsaturated aliphatic or with aromatic acids indicate that their irritant activity is a necessary, yet insufficient prerequisite for initiation- (or tumor-) promoting activity (e.g., Refs. 3 and 4). For further testing of this hypothesis, the retinoic acid analogue of the mouse skin irritant and initiation-promoter TPA, i.e., RPA, was designed (7). In initiation/promotion experiments of skin of NMRI mice, it proved to be an irritant almost as active as TPA, but only marginally active as a promoter. In combination with TPA, it turned out to be a "second stage" promoter (PII-promoter) (1, 6) in our strain of mice (2, 7). RPA is a much more labile compound than TPA (5), especially in the solid form. If stored in solution, special precautions have to be taken to ascertain that the concentration or dose intended is represented by undecomposed RPA.
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PMID:Stability of the "second stage" promoter 12-O-retinoylphorbol-13-acetate. 398 82

NMR can discriminate between malignant and normal tissues. This study attempts to determine if NMR can discriminate between tumor clones of differing metastatic potential derived from the same parent tumor. Rat 13762NF mammary adenocarcinoma clones of either high (MTLn3), intermediate (MTC), or low (MTPa) metastatic potential were grown in roller-bottle tissue culture, harvested during exponential growth phase, centrifuged to form a 0.75-cm3 pellet, and analyzed in a Varian 360L spectrometer operating at 60.0 MHz. Dimethyl sulfoxide (10%) was used as an internal standard at 3.1 ppm downfield from tetramethyl silane (TMS). NMR spectra of replicate samples were analyzed and compared. The position of the water peak for MTLn3 (n = 7) was 5.14 +/- 0.0301 vs 5.07 +/- 0.0207 for MTC (n = 5) and 5.05 +/- 0.009 for MTPa (n = 5) (P less than or equal to 0.001). Integrated area of upfield peaks (where glycoproteins residues are expected to resonate) was 47.43 +/- 7.17 for MTLn3 (n = 6) and 40.95 +/- 5.48 for MTC (n = 4) vs 32.06 +/- 10.1 for MTPa (n = 5) (P less than or equal to 0.05). Previous work with these tumor clones suggests quantitative changes in surface glycoproteins are associated with differences in metastatic behavior. This study demonstrates differences in water peaks between cells of high, intermediate, and low metastatic potential and differences in the integrated area of upfield spectral peaks. How these observations relate to the biologic properties of the cells is uncertain. If they prove to have general validity, NMR could be used to profile biologic potential of human malignancies.
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PMID:Differences in NMR spectra between tumor clones of defined metastatic potential. 399 Feb 81

It has been shown that agents that are known to be scavengers of hydroxyl radicals may induce differentiation and inhibit growth of murine neuroblastoma cells in tissue culture. The present study tests dimethyl sulfoxide as a differentiation agent of the human neuroblastoma cell lines LA-N-1 and murine neuroblastoma NIE-115. Results indicate that DMSO induces morphologic and biochemical differentiation of neuroblastoma cells coupled to growth inhibition and inhibition of colony formation in semi liquid tissue culture systems. DMSO treatment in vitro had no effect on tumorigenicity of NIE-115 cells. In vivo DMSO treatment of athymic nude mice with transplanted LA-N-1 human neuroblastoma tumors has not affected tumor size or animal survival. No diminishing effect of natural killer cell activity could be attributed to DMSO treatment.
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PMID:Dimethyl sulfoxide-induced differentiation does not alter tumorigenicity of neuroblastoma cells. 399 89

Previous studies have demonstrated that retinoids possess antineoplastic properties against melanoma. The purpose of this study was to determine whether topically applied retinoic acid could prevent melanoma development in syngeneic mice after intracutaneous cell inoculation. Trans-retinoic acid in DMSO was applied daily for 28 days after melanoma implantation and tumor growth was quantitated by the uptake of [14C]thiouracil, a tracer compound specific for melanoma which is incorporated linearly according to the weight of the tumor. Marked reduction in tumor growth was noted at the highest concentration (0.1%) tested and lesser but significantly decreased tumor growth patterns were also realized at lower concentrations in a dose-dependent manner. Thus, topically applied retinoic acid is capable of inhibiting S91 melanoma growth in vivo.
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PMID:Effects of topical retinoic acid on intracutaneously implanted S91 melanoma in mice. 402 Jan 64

A model for metastatic skin cancer using intradermal injection of Walker 256 carcinosarcoma has been developed in the rat. Using this model, antitumor activity of topically applied doxorubicin and diaziquone in Vanicream, Plastibase, and dimethyl sulfoxide (DMSO) as vehicles was compared with intraperitoneal injection of the drugs at the same doses beginning 4 days after injection of tumor cells. Doxorubicin applied topically at 0.5 mg/day for 4 days in Vanicream or Plastibase exhibited no antitumor activity, while i.p. administered doxorubicin at 0.5 mg/day for 4 days inhibited tumor growth at day 20 by 66%. Diaziquone applied topically at 0.1 mg/day for 4 days in Vanicream, Plastibase, or DMSO inhibited tumor growth at day 20 by 66, 86, and 43%, respectively, and cured animals of the skin tumor at a dose of 0.5 mg/day. Diaziquone administered i.p. at 0.5 mg/day for 4 days was lethal to rats, and at 0.1 mg/day it produced 93% inhibition of tumor growth at day 20. Diaziquone applied topically at 0.1 mg/day for 4 days in Plastibase cured rats of advanced tumor when treatment was begun 12 days after injection of tumor cells. The area under the plasma radioactivity time curve over 5 h for a single 0.64-mg dose of topically applied [ring-14C]diaziquone in DMSO was 0.01% that of the same dose of [ring-14C]diaziquone administered i.p. in non-tumored rats. The decrease in WBC count following topical application of diaziquone at a dose of 0.1 mg/day for 4 days, compared to the same dose of diaziquone administered i.p., was 62% in Vanicream, 81% in Plastibase and 33% in DMSO. Topical diaziquone was non-toxic to normal skin in the rat and in the domestic pig. It is concluded that topical application of diaziquone offers a therapeutic advantage over systemic treatment for metastatic cancer of the skin.
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PMID:Topical chemotherapy of intradermal Walker 256 carcinosarcoma with diaziquone and doxorubicin in the rat. 405 22

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

A variety of agents can induce mammalian tumor cell lines to acquire characteristics of the normal cell counterpart. Dimethylsulfoxide (DMSO) has been an effective differentiating agent in many tumor cell lines. In the present study a Dunning rat prostate tumor subline, MAT LyLu, available as an in vitro continuous cell culture was treated with 2.25% DMSO (vol/vol). Treated MAT LyLu cells had a decreased growth rate, saturation density, and clonogenicity, an increased doubling time, and alterations in enzyme activity and tumorigenicity when compared to untreated MAT LyLu cells. The cell viability of treated cells at the saturation density was greater than 90%. MAT LyLu cells treated with DMSO and then removed from DMSO (posttreated) when compared to untreated cells had similar growth rates, doubling times, clonogenicities, enzyme activities, and tumorigenicities. Posttreated MAT LyLu cells had a different growth pattern than untreated MAT LyLu cells. Posttreated cell viability at saturation density was greater than 90%. This investigation demonstrated that a rat prostate adenocarcinoma grown in medium containing 2.25% DMSO acquired characteristics consistent with differentiated prostate cells. Posttreated MAT LyLu cells were similar in many characteristics to untreated cells but were not identical. The alterations noted were not cytotoxic and were not completely reversible. The results of this study correlated with the observations of other investigators who have studied mammalian tumor cell lines exposed to DMSO.
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PMID:Dimethylsulfoxide-induced changes in a rat prostate adenocarcinoma. 408 48

Dimethyl sulfoxide added to cultures first treated with 5-iododeoxyuridine increased C-type virus production approximately tenfold in a human rhabdomyosarcoma cell line. 5-Iododeoxyuridine followed by dimethyl sulfoxide also activated a similar C-type virus in a metastatic tumor from a bronchial node taken from a 52-year-old male.
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PMID:Activation of viruses in human tumors by 5-iododeoxyuridine and dimethyl sulfoxide. 500 40

The murine BW 1 and rat 32III 6/d tumor cell lines, derived from a spontaneous mouse hepatoma and a carcinogen-induced rat hepatocellular carcinoma, were used to investigate the effect of dimethylsulfoxide (DMSO) on liver cells in vitro. After a 4-day exposure to DMSO in final concentrations of 0.5 and 1.0%, BW 1 cell-associated albumin increased by 41.6 and 94.2%; extracellular albumin levels in these same cultures rose by 131.4 and 214.2%. Exposure of 32III 6/d cells to 2% DMSO produced increases in cell-associated and extra-cellular albumin concentrations of 67.8 and 188.7%, respectively. The lack of inducible gamma-glutamyl transpeptidase in BW 1 cells and its decrease in 32III 6/d cultures following DMSO treatment suggests that the DMSO-mediated enhancement of albumin production is not reflective of a random increase in the expression of cellular genes.
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PMID:Enhanced albumin production by malignantly transformed hepatocytes during in vitro exposure to dimethylsulfoxide. 610 31

The effects of the differentiation-inducing agent dimethylsulfoxide (DMSO) on the growth properties and protein synthetic capacity of BW77-1 mouse hepatoma cells were compared at various media concentrations of the polar solvent. DMSO produced a dose-dependent reduction in final population density, reduced or eliminated cell piling and stimulated synthesis of albumin. The rising albumin content reflected dose-related DMSO-induced increases in total cellular protein and in the albumin contribution to total cellular protein. In order to determine whether viral gene expression was associated with DMSO-induced stimulation of albumin synthesis, BW77-1 cultures were examined for the production of ecotropic and xenotropic type C virus. The BW77-1 hepatic tumor cell line was determined to be a nonproducer of type C virus by assays designed to measure extracellular reverse transcriptase, viral env gene product and infectivity on mouse and mink indicator cells. Type C virus could not be induced in BW77-1 cultures by treatment with DMSO under conditions which lead to a reduced proliferative capacity and enhanced expression liver-specific genes.
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PMID:Dimethylsulfoxide-induced alterations in the growth properties and protein composition of in vitro-propagated murine hepatoma cells. 617 24


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