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

Metabolism of triceps, pectoralis (in the vicinity of tumor) and gastrocnemius (away from the tumor) muscles in Swiss albino mice bearing adenocarcinoma has been studied histochemically with regard to content of glycogen, lipids, phosphorylase, aldolase, lipase, succinate dehydrogenase and cytochrome oxidase in the constituent fibres. At 9-10 weeks after transplantation of adenocarcinoma, a negligible glycogen content and decreased phosphorylase and aldolase activities are observed in the white, intermediate and red fibre types in the three muscles. Hypertrophy of fibres and occurrence of targetoid fibres is distinct in the muscles of tumor-bearing mice. The red fibres demonstrate a general loss of lipids, lipase, succinate dehydrogenase and cytochrome oxidase whereas the hypertrophied fibres reveal intense localization of these parameters in their central zones. The results indicate that a decline in glycogenolysis, glycolysis, lipolysis and oxidative metabolism in the various fibre types may contribute to the muscle weakness and muscle wasting in the adenocarcinoma-bearing mice.
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PMID:Skeletal muscle metabolism in mice bearing adenocarcinoma. I. Histochemical alterations in glycogenolytic, glycolytic, lipolytic and oxidative metabolism. 298 94

A tumor-derived factor that inhibits cellular DNA synthesis was identified. The factor was extractable from a small-cell lung carcinoma cell line grown in either chemically defined medium or nu/nu mice and inhibited tritiated thymidine ([3H]dThd) incorporation by tumor cell lines of autologous, allogeneic, and xenogeneic origins. The viability of nonproliferating cells from normal tissue was not affected. Tumor extract inhibitory activity was trypsin labile but was resistant to other proteases, neuraminidase, lipase, DNase, RNase, glucosidase, extremes of pH-temperature, and reducing conditions. Inhibitory activity was reversibly bound to helix pomatia lectin but not to lentil, wheat germ, or concanavalin A lectins. Purification by size-exclusion high-performance liquid chromatography yielded a bioactive unimodal 12-kilodalton (kd) peak. The bioactive 12-kd moiety could be eluted from sodium dodecyl sulfate-polyacrylamide gels. Redosing of populations of the T-lymphoblastoid cell line CEM achieved an early (24 hr) sustained depression of pulse [3H]dThd incorporation and ultimately led to decreased population density of factor-treated populations. DNA histogram analysis demonstrated no change in cell cycle phase distribution after factor treatment. 5-Bromo-2'-deoxyuridine (BrdUrd) vs. propidium iodide with the two-parameter Fluorescence-Activated Cell Sorter analysis showed relative inhibition of non-S-phase BrdUrd uptake at 24 hours. A cell-free DNA polymerase assay demonstrated significant inhibition of non-alpha-polymerase-associated DNA synthesis in factor-treated cells. These studies suggest that this tumor-derived inhibitor of DNA synthesis represents a class of cellular products involved in the autoregulation of growth by regulation of DNA synthetic activity.
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PMID:Inhibition of DNA synthesis by a small-cell lung carcinoma-derived protein. 302 Mar 1

Rat serum, active in the hydrolysis of the tumor-promoting phorbol diester, 12-O-tetradecanoylphorbol-13-acetate (TPA), was examined with regard to lipid interferences of [3H]TPA hydrolysis and enzyme substrate specificity. The enzymatic hydrolysis of TPA could be enhanced 8-fold, over crude serum, by using a lipid-free acetone powder of rat serum. Addition of lipid to the lipid-free acetone powder produced potent inhibition of TPA hydrolysis. The inclusion of multilamallar liposomes resulted in similar inhibition, and isolation of liposomes by high-speed centrifugation showed that 95% of the radiolabeled TPA was associated with the fatty pellet. Substrate specificity studies demonstrated that the serum activity hydrolyzes the long-chain ester of TPA and the long-chain primary acyl group of diacylglycerols. TPA was hydrolyzed at approximately twice the rate of dioleoylglycerol; however, the most reactive substrates were those synthetic analogs of diacylglycerol containing a short-chain ester group at the sn-2 position. Palmitic acid was liberated from [1-14C]palmitoyl-2-acetyl-sn-glycerol and [1-14C]palmitoyl-2-butyryl-sn-glycerol at 120- and 33-times the rate of TPA hydrolysis, respectively. Lipase resistant 1-hexadecyl-2-[3H]acetylglycerol was also used as substrate, but the sn-2 ester moiety showed poor lability. The diacylglycerol analogs are new lipase substrates and, in view of their similarities to the fatty acyl portion of TPA, it is thought that these compounds could serve as protein kinase C activators.
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PMID:Hydrolysis of novel diacylglycerol analogs and phorbol diesters by serum lipase. 315 71

We have shown previously that cortisol-sensitive lymphocytes (thymocytes) have a much lower capacity than cortisol-resistant cells to catabolize cortisol. We have also shown that sera of cancer patients (CPS) possess ethanol-extractable substance(s) which can inhibit the catabolism of cortisol by lymphocytes (CCL). Recently, we noted that unsaturated fatty acids can both inhibit CCL and modulate the sensitivity of lymphocytes to cortisol. In the present study, we attempt to identify the compounds responsible for CCL inhibition and to demonstrate that inhibition of CCL may make cortisol-resistant lymphocytes vulnerable to the steroid. The enzymes DNase, RNase, pronase and lipase were added to ethanol extracts of serum as a first step in our efforts to identify the nature of the inhibitors of CCL. Only lipase had an effect on the inhibition. In fact, lipase enhanced the inhibition of CCL. This finding correlates with our previous observations that unsaturated fatty acids are potent inhibitors of CCL. Examining the effect of ethanol extracts of CPS and normal serum on the vulnerability of lymphocytes to cortisol, we noted that ethanol extracts of normal serum had no significant killing effect, whereas an ethanol extract of CPS makes lymphocytes more sensitive to cortisol. Since the adsorbance of free fatty acids of CPS by defatted albumin reduced but did not eliminate the capacity of the serum to inhibit CCL, we assume that other compounds besides free fatty acids might also be involved in CCL inhibition and modulation of the sensitivity of lymphocytes to cortisol.
Tumour Biol 1988
PMID:Effect of ethanol extract of cancer patients' serum on the vulnerability of lymphocytes to cortisol. 319 73

It is more and more clear from recent studies that both steroid and peptide (hormone and growth factor)-mediated pathways of mitogenesis are closely linked. These two pathways are intertwined into a highly regulated network. The two main points of connection are at the level of lipase and protease biosynthesis and regulating systems. Both enzymes are steroid-regulated. Furthermore, free fatty acids can be considered as positive or negative common modulators and/or messengers of the steroids and the peptide factors regulating the mitogenic processes.
Tumour Biol 1987
PMID:Nonesterified fatty acids: role in the molecular events linking endocrinology and oncology via nutrition. 332 7

A neoplasm demonstrating both pancreatic and hepatic phenotypes is described. The tumor, from a 53-year-old woman with the syndrome of subcutaneous fat necrosis and arthropathy, was studied histologically, immunohistochemically, ultrastructurally, and biochemically. The clinical features of this case can be explained by the production of large amounts of lipase by the tumor. The hepatocellular properties of the tumor included characteristic morphology and the synthesis of catalase. The pancreatic properties of the tumor included the production of pancreatic lipase. This neoplasm would appear to be analogous to animal models in which the transdifferentiation of pancreatic acinar cells and hepatocytes has been demonstrated. Although the bulk of the tumor was present in the liver, the authors believe the tumor arose from the pancreas. The distinction between differentiation and site of origin of tumors is discussed.
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PMID:A neoplasm with pancreatic and hepatocellular differentiation presenting with subcutaneous fat necrosis. 367 46

A large amount of triacylglycerol lipase activity was present in the circulating blood of normal mice, and this activity decreased with development of Sarcoma 180 inoculated intraperitoneally. Triacylglycerol lipase in plasma of both normal and tumor-bearing mice was retained on the heparin-Sepharose columns and over 90% of the activity was eluted with 0.75 M NaCl. This enzyme had similar properties to hepatic triacylglycerol lipase and hydrolyzed very-low-density lipoprotein (VLDL)-triacylglycerol. Hepatic triacylglycerol lipase in plasma of normal mice hydrolyzed tricaprin and trilaurin most readily and better than 1-monoacylglycerols with the same acyl chain length. The hydrolyzing activities decreased with increase in the acyl chain length. The activity toward triolein was also higher than that toward 1-monoolein. 1-Monomyristin was hydrolyzed better than trimyristin. In contrast, hepatic triacylglycerol lipase in plasma of mice on day 4 after tumor inoculation hydrolyzed 1-monoacylglycerols better than triacylglycerols with the same acyl chain length. Hydrolysis of triolein by hepatic triacylglycerol lipase in plasma of both normal and tumor-bearing mice was reduced in the presence of 1-monoacylglycerols in the reaction mixture. The orders of their inhibitory effects coincided with the orders of the hydrolyzing activities toward 1-monoacylglycerols.
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PMID:Hepatic triacylglycerol lipase in circulating blood of normal and tumor-bearing mice and its hydrolysis of very-low-density lipoprotein and synthetic acylglycerols. 377 23

On rare occasions, excessive lipase production by functioning pancreatic acinar cell carcinoma results in subcutaneous and intraosseous fat necrosis. A patient with subcutaneous nodules and osteolytic lesions from metastatic fat necrosis associated with this malignancy is reported. Prompt recognition of the syndrome led to complete resection of the otherwise asymptomatic neoplasm of the exocrine pancreas.
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PMID:Pancreatic acinar cell carcinoma with subcutaneous and intraosseous fat necrosis. 394 Apr

The contents of apolipoproteins of plasma and ascites fluid of mice with Sarcoma 180 were measured. The apolipoprotein A-I contents of plasma decreased with development of the tumor. The apolipoprotein C-II and C-III contents of plasma reached a maximum on day 7 after tumor inoculation and then decreased. The apolipoprotein A-I content of the ascites fluid was lower than that of normal mouse plasma. In contrast, the apolipoprotein C-II and C-III contents of the ascites fluid were higher than those of normal mouse plasma. The ascites fluid of mice with Sarcoma 180 was found to contain at least two lipases. One had a pH optimum of 5.5-7.0 and was strongly inhibited by chlorpromazine. The other had an alkaline pH optimum and was inhibited only slightly by chlorpromazine. When the ascites fluid was applied to a heparin-Sepharose column 40-45% of the applied triglyceride lipase activity was retained on the column, which was eluted with 0.75 M NaCl. This fraction was inhibited by heat-inactivated (56 degrees C, 10 min) human serum, and was relatively resistant to l M NaCl. These results suggest that one of the lipolytic enzymes present in the ascites fluid of mice with Sarcoma 180 is hepatic triglyceride lipase.
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PMID:Demonstration of hepatic triglyceride lipase-like activity in ascites fluid of mice with sarcoma 180. 401 14

Supernatants from freshly disaggregated human ovarian carcinomas maintained in vitro for 24 hr, from primary ovarian carcinoma cultures (4-6 days in culture) and from established ovarian cancer cell lines were examined for chemotactic activity on blood monocytes in blind-well chemotaxis chambers. Tumor-cell culture supernatants induced migration of peripheral blood monocytes across polycarbonate filters with considerable heterogeneity among different tumors. Induction of migration occurred only in the presence of a gradient between the lower and upper compartments of the chamber. Chemotactic activity was characterized by means of supernatants from primary ovarian carcinoma cultures. Chemotactic factor(s) was (were) produced in serum-free conditions and the production was inhibited by emetine but not by mitomycin C. The activity was destroyed by exposure to proteolytic enzymes and by heating at 100 degrees C but was unaffected by RNase, DNase, lipase and exposure to extreme pH values or heating at 56 degrees C. Upon fractionation on Sephadex G 75, the activity eluted as a single peak in the cytochrome C region, corresponding to an apparent molecular weight of about 12 kd. The percentage of macrophages was assessed in 25 freshly disaggregated tumor specimens. Ovarian carcinomas were heterogeneous in their macrophage content with values ranging from 4 to 36%. A significant (r = 0.62; p = 0.00097), though far from absolute, correlation was found between chemotactic activity of culture supernatants and percentage of tumor-associated macrophages. Tumor-derived chemotactic factor(s) could be one of the mechanisms involved in the regulation of the macrophage content of human ovarian carcinomas.
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PMID:Tumor-derived chemotactic factor(s) from human ovarian carcinoma: evidence for a role in the regulation of macrophage content of neoplastic tissues. 401 9


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