UMLS:C1261473 - FACTA Search

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Query: UMLS:C1261473 (sarcoma)
25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of parenteral nutrition in tumour patients is to offer an alternative nutritional support to the patient without accelerating the growth of the tumour. For this purpose we fed a total of 100 rats, divided into five groups of 20 animals each (10 with and 10 without tumours), for a total period of 15 days with various nutritional regimes. Group 1 received glucose, group 2 long-chain triglycerides, group 3 medium-chain triglycerides (MCT), group 4 omega-3 fatty acids, and group 5 an oral diet. On the 10th day the Yoshida sarcoma in its ascites form was implanted into the tumour-bearing rats. In animals receiving MCT or omega-3 fatty acids tumour growth was considerably smaller than in the other groups (group 1 vs. groups 3 and 4; p < 0.05). Unfavourable effects of the administration of these fatty acids on the general condition of the animals were not observed [muscle nitrogen content (mg/kg body weight): MCT = 82.3, omega-3 fatty acids = 65.25]. The impulse cytophotometric measurements did not demonstrate any influence on the pattern of cell division (p > 0.05). We think that modulation of the immune system by feeding with MCT or omega-3 fatty acids was responsible for the reduced tumour growth in relation to the other groups. The extrapolation of these results to the clinical situation, however, may not be possible.
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PMID:Influence of various fatty acids on tumour growth in total parenteral nutrition. 783 86

Recent evidence supports the critical and proximate role of IL-12 in regulating both T and NK cell function during inflammation. In these studies, we evaluated the in vivo antitumor activity of murine IL-12 in murine adenocarcinoma and sarcoma models using both systemic and peritumoral administration. Antitumor effects were consistently demonstrated both in models of microdisease, in which IL-12 treatment was initiated soon after tumor inoculation (1 to 5 days), and in animals bearing large established tumors (7 to 14 days). Treatment with IL-12 markedly prolonged survival and, in most cases, caused complete tumor regression. Significant reduction in pulmonary metastases after systemic treatment was observed when treatment was delayed for 10 days after tumor inoculation. Increases in serum IFN-gamma, TNF-alpha, and nitrogen oxides were demonstrated, exceeding those observed with IL-2 treatment. Systemic administration of anti-IFN-gamma Abs before IL-12 treatment nearly completely abrogated the antitumor effect in experiments using subcutaneous tumors or pulmonary metastases. Depletion of the individual T cell subsets CD4 and CD8 by systemic administration of mAbs diminished the effectiveness of IL-12 when administered in combination. An infiltrate composed primarily of CD8+ + cells was demonstrated by using immunohistochemical analysis of tumors after IL-12 treatment. Minimal apparent toxicity was demonstrated at effective doses (0.1 to 1.0 microgram/day) of IL-12. These results indicate that IL-12 is an effective and minimally toxic antitumor agent in murine tumor models and leads to an immune-mediated rejection involving, at least in part, IFN-gamma, CD4+, and CD8+ cells. Human clinical trials of IL-12 for the treatment of malignancy are supported by these studies.
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PMID:Recombinant IL-12 administration induces tumor regression in association with IFN-gamma production. 791 43

AO-90, a methionine-free intravenous amino acid solution (7.43%) showed to potentiate the antitumor effect of 5-fluorouracil (5-FU) when concomitantly used as the nitrogen source in total parenteral nutrition (TPN) in Yoshida sarcoma (YS)-bearing rats. In the present experiment, this potentiation mechanism was studied by determining the serum methionine level and tumor methylenetetrahydrofolate (CH2FH4) content in YS-bearing Donryu rats given AO-90 (nitrogen 0.73g/kg on the 1st day and 1.46g/kg for the remaining 6 days) by TPN for 1 week. The rats were subcutaneously inoculated with 10(4) YS cells in the dorsum 3 days before the start of TPN. Inhibition of thymidylate synthase activity in tumor tissue after dosing of AO-90 (nitrogen 0.68g/kg on the 1st day and 1.36 g/kg for the remaining 6 days) by TPN along with daily intraperitoneal dosing of 5-FU (10 mg/kg) was also evaluated with the inoculation of 10(6) tumor cells. The results were compared with those in tumor-bearing rats given TPN with a commercially available amino acid solution containing methionine. On day 5 of TPN, the tumor-bearing rats given AO-90 showed a significantly lower serum methionine level than the control rats: 101 +/- 11 mumol/l versus 29 +/- 14 mumol/l (p < 0.01); and a higher CH2FH4 content in tumor: 7.0 +/- 2.8 pmol/g protein versus 23.7 +/- 16.6 pmol/g protein (p < 0.05). Thymidylate synthase inhibition was 81.2 +/- 5.1% in the AO-90 group and 30.9 +/- 26.3% in the control group (p < 0.01). The results of the present study suggest that AO-90 potentiate the antitumor effect of 5-FU by biochemical modulation. AO-90 concomitantly given with 5-FU for 7 days was effective not only in the allogeneic tumor model, but also in WKAH and SHR rats previously inoculated with 10(6) of syngeneic KDH-8 hepatoma cells and SST-2 adenocarcinoma cells, respectively. Weight of SST-2 adenocarcinoma in SHR rats after the TPN period was significantly smaller in the AO-90 group than in the control rats given methionine-containing TPN and 5-FU: 2.66 +/- 0.91 versus 5.12 +/- 2.11 (p < 0.05).
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PMID:[The mechanism of potentiation of the antitumor effect of 5-fluorouracil by methionine-free intravenous amino acid solution (AO-90) in rats]. 808 53

Bovine mammary epithelial cells from teat and ductal tissue were isolated at necropsy and were grown in culture. Cells were characterized by the presence of cytokeratin filaments, cell morphologic features, synthesis of milk proteins, esterase activity, DNA content, and growth patterns on polystyrene, fibronectin, laminin, collagen, and reconstituted basement membrane from the Engelbreth-Holm-Swarm murine sarcoma. Cultured teat and ductal cells stained intensely for cytokeratin and had similar morphologic features. Both cell types synthesized alpha-casein, beta-casein, alpha-lactalbumin, beta-lactoglobulin, and lactoferrin to variable degrees. Cell type and culture conditions did not affect the DNA content of the cells, as indicated by similar amounts of DNA in G0G1 and G2M phases of the mitotic cycle in cultured cells and in cells from freshly isolated mammary explants. Cells cultured on polystyrene, fibronectin, laminin, and collagen formed pavement-like cell monolayers suitable for cytotoxicity and bacterial adherence studies. Cells cultured on the reconstituted basement membrane from the Engelbreth-Holm-Swarm murine sarcoma formed three-dimensional structures closely resembling lactiferous ducts and alveoli, which could be used for studying lactogenesis and galactopoiesis. Freshly isolated cells and cultured cells were stored at -70 C or in liquid nitrogen. The latter storage method affected the cells less than did freezing at -70 C.
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PMID:Bovine mammary teat and ductal epithelial cell cultures. 817 14

Cancer cachexia is among the most dramatic situations of depletion in body energy reserves. To ascertain whether the pattern of body composition alteration during tumour development is influenced by aging as in uncomplicated starvation, we compared the difference of body composition between Yoshida sarcoma bearing rats and young (200 g, 7 weeks) and adult (400 g, 13 weeks) control rats. After the same duration of tumour bearing, mass and composition of tumours were similar in adult and young rats, indicating that they are independent of host age. Food intake decreased to a remarkably similar value in both young and adults. Body water content was elevated in hosts of both ages. The relative deficit of body lipid vs controls was similar for both, the absolute lipid deficit being therefore larger in adult than in young tumour-bearing rats (14.3 +/- 4.4 g vs 6.8 +/- 0.9 g; P < 0.01). In contrast, there was a relatively larger deficit of body protein in young rats. Paradoxically, these rats still maintained a positive nitrogen balance whereas this balance was negative in adult tumour-bearing rats. In conclusion, as previously shown in uncomplicated undernutrition, the anorexia induced by Yoshida sarcoma development is still associated with some protein accretion in young rats whereas cachexia develops in adults.
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PMID:Body protein and lipid deficit in tumour-bearing rats in relation to age. 821 4

By using a transplantable Yoshida sarcoma in a rat total parenteral nutrition model, we measured the effectiveness of an arginine-enriched amino acid solution (AI-82) in terms of leucine kinetics and nitrogen balance as indicators of host-tumor nutrition interaction compared with that of a conventional amino acid solution (Proteamin12). When tumor-bearing rats received isocaloric total parenteral nutrition solutions for 7 days, AI-82 significantly improved host nitrogen balance and significantly decreased the tumor-nitrogen trap throughout the experimental period. Leucine kinetics of whole body and tissues were also determined by a 4-hour continuous infusion of each total parenteral nutrition solution containing 14C-leucine. Significantly increased whole-body leucine oxidation (p < .01) without an increase in leucine release from normal tissues was observed in the AI-82 group. Total incorporation of 14C-leucine into whole muscle was significantly elevated (p < .05) without changes in muscle protein degradation in the AI-82 group. In the whole tumor, AI-82 tended to decrease total incorporation of 14C-leucine, but there was no difference in leucine release caused by protein breakdown between the two groups. These findings suggest that AI-82 can improve the nutritional status of the host over that of the tumor.
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PMID:Effect of arginine-enriched total parenteral nutrition on the host-tumor interaction in cancer-bearing rats. 827 64

Epithelioid sarcoma is a peculiar soft-tissue neoplasm of uncertain origin, which is characterized by an epithelioid morphology of tumor cells coexpressing epithelial (keratin) and nonepithelial (vimentin) antigens. We herein report a new cytogenetic abnormality with der(22)t(18;22)(q11;p11.2) in a case of epithelioid sarcoma that occurred in the elbow of a 75-year-old man. Histologically, the tumor demonstrated a multinodular proliferation of epithelioid cells, with positive immunostaining for keratin, epithelial membrane antigen (EMA), and vimentin. Cultured tumor cells obtained from fresh surgical materials were frozen in plastic ampules and stocked in a liquid nitrogen freezer. Six years after surgery, the cells were recovered from the freezer and utilized for both morphologic and cytogenetic analyses. These cultured cells both before and after the freezing exhibited essentially the same epithelioid morphology and immunophenotypes as those of the original tumor. A chromosome analysis, together with fluorescence in situ hybridization (FISH), demonstrated a 61-67 modal population, and a characteristic clonal abnormality with der(22)t(18;22)(q11;p11.2). Other clonal abnormalities included numerical (-3, -4, +7, -13, -14, -16, -18, +20, -22) and structural (8p+, 9p+, 12p+, i(21q)) aberrations. Some variant clones also demonstrated i(18q). Since the breakpoint at 18q11 is similar to that reported in synovial sarcoma, this finding may support the presence of a histogenetic relationship between epithelioid sarcoma and synovial sarcoma. Our study thus indicates that the storage of frozen cells is useful for both morphologic and cytogenetic analyses of soft tissue tumors.
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PMID:Epithelioid sarcoma with an 18q aberration. 890 66

Nicotine is recognized to be the major inducer of tobacco dependence. The smoking of cigarettes as an advantageous delivery system for nicotine, accelerates and aggravates cardiovascular disease, and is causally associated with increased risks for chronic obstructive lung disease, cancer of the lung and of the upper aerodigestive system, and cancer of the pancreas, renal pelvis, and urinary bladder. It is also associated with cancer of the liver, cancer of the uterine cervix, cancer of the nasal cavity, and myeloid leukemia. In 1950, the first large-scale epidemiological studies documented that cigarette smoking induces lung cancer and described a dose-response relationship between number of cigarettes smoked and the risk for developing lung cancer. In the following decades these observations were not only confirmed by several hundreds of prospective and case-control studies but the plausibility of this causal association was also supported by bioassays and by the identification of carcinogens in cigarette smoke. Whole smoke induces lung tumors in mice and tumors in the upper respiratory tract of hamsters. The particulate matter of the smoke elicits benign and malignant tumors on the skin of mice and rabbits, sarcoma in the connective tissue of rats, and carcinoma in the lungs of rats upon intratracheal instillation. More than 50 carcinogens have been identified, including the following classes of compounds: polynuclear aromatic hydrocarbons (PAH), aromatic amines, and N-nitrosamines. Among the latter, the tobacco-specific N-nitrosamines (TSNA) have been shown to be of special significance. Since 1950, the makeup of cigarettes and the composition of cigarette smoke have gradually changed. In the United States, the sales-weighted average "tar" and nicotine yields have declined from a high of 38 mg "tar" and 2.7 mg nicotine in 1954 to 12 mg and 0.95 mg in 1992, respectively. In the United Kingdom, the decline was from about 32 mg "tar" and 2.2 mg nicotine to less than 12 mg "tar" and 1.0 mg nicotine per cigarette. During the same time, other smoke constituents changed correspondingly. These reductions of smoke yields were primarily achieved by the introduction of filter tips, with and without perforation, selection of tobacco types and varieties, utilization of highly porous cigarette paper, and incorporation into the tobacco blend of reconstituted tobacco, opened and cut ribs, and "expanded tobacco." In most countries where tobacco blends with air-cured (burley) tobacco are used, the nitrate content of the cigarette tobacco increased. In the United States nitrate levels in cigarette tobacco rose from 0.3-0.5% to 0.6-1.35%, thereby enhancing the combustion of the tobacco. More complete combustion decreases the carcinogenic PAH, yet the increased generation of nitrogen oxides enhances the formation of the carcinogenic N-nitrosamines, especially the TSNA in the smoke. However, all analytical measures of the smoke components have been established on the basis of standardized machine smoking conditions, such as those introduced by the Federal Trade Commission, that call for 1 puff to be taken once a minute over a 2-s period with a volume of 35 ml. These smoking parameters may have simulated the way in which people used to smoke the high-yield cigarettes; however, they no longer reflect the parameters applicable to contemporary smokers, and especially not those applicable to the smoking of low- and ultra-low-yield filter cigarettes. Recent smoking assays have demonstrated that most smokers of cigarettes with low nicotine yield take between 2 and 4 puffs per minute with volumes up to 55 ml to satisfy their demands for nicotine. The overview also discusses further needs for reducing the toxicity and carcinogenicity of cigarette smoke. From a public health perspective, nicotine in the smoke needs to be lowered to a level at which there is no induction of dependence on tobacco.
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PMID:The changing cigarette, 1950-1995. 912 Aug 72

The elemental composition of a variety of tumor samples, including squamous cell lung carcinoma, sarcoma, adenoid cystic carcinoma, melanoma, and rectal carcinoma have been measured by combustion analysis. Hydrogen, carbon, nitrogen, and oxygen content have been determined. Using the elemental neutron kerma data published in ICRU Report #46 the neutron kerma factors for the various tumor samples have been calculated in the energy range 11 eV to 29 MeV. The average neutron kerma values for all tumor samples are approximately 6%-7% lower than those for average soft tissue in the energy range of interest in fast neutron therapy (energies > 1 MeV).
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PMID:The elemental composition of tumors: kerma data for neutrons. 928 46

Physicochemical, Microbial and Pharmacological studies on Fe(III)-Dacarbazine complex have been done in solid and aqueous phase. On the basis of elemental analysis, polarographic studies, amperometric titrations and IR spectral studies the probable formula for the complex has been worked out to be 1:1, Fe(III)-Dacarbazine. The metal ligand interaction has been studied using polarographic method at 25 +/- 1 degrees C and at ionic strength of mu = 1.0 (KCl). Microbial studies on the complex was done against various pathogenic bacteria viz. Pseudomonas mangiferae, Staphylococcus aureus, Salmonella typhi and Vibrio cholarae and fungi i.e. Trichothecium and Chrysosporium sp. using Raper's method. Mouse sarcoma cell line 180 and Balb/C mice were used for the anticancer screening of solid complex in vitro and in vivo respectively. The observed polarographic data, on lingane treatment revealed the formation of single (1:1) (M:L) complex with Fe(III) and dacarbazine ligands. The results of amperometric titrations of Fe(III) with dacarbazine in IM KCl supporting electrolyte pH 7.0 +/- 0.1 supported the above findings the IR data speaks of the complex formation between the metal and the dacarbazine ligand through the two nitrogen one each of primary amide and trizo groups. The results of microbial and pharmacological studies with the M:Drug complex revealed that the anticancer activity of the drug metal complex is nearly doubled as compared to the pure drug. As such Fe(III) dacarbazine complex may be recommended to the therapeutic experts for its possible use as more potent anticancer drug.
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PMID:Role of bio-metal Fe(III) in anticancer effect of dacarbazine. 1022 49

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