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)

Sprague-Dawley rats were given combinations of aminopyrine or oxytetracycline and sodium nitrite in drinking water. Of 30 animals receiving 0.1% (1,000 ppm) of aminopyrine and sodium nitrite for 30 weeks, 29 died with hemangioendothelial sarcomas of the liver. The same tumor caused death in 26 of 30 animals that received 0.025% (250 ppm) of both aminopyrine and sodium nitrite for 50 weeks. No animals in a control group of the same size that received 0.1% aminopyrine for 30 weeks developed this tumor, although one-half of them were still alive 2 years after the experiment was begun. After feeding a comparable dose (0.1%) of oxytetracycline and sodium nitrite for 60 weeks, liver tumors were present in 4 of 30 rats (3 hepatocellular tumors and 1 cholangioma). Since aminopyrine has been widely used for medicinal purposes in the human population, it is possible that many people have been exposed to a potent carcinogen (dimethylnitrosamine) by its formation in vivo. It is not certain whether the result of feeding oxytetracycline and sodium nitrite indicates significant carcinogenicity of this combination.
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PMID:Tumor induction in rats by feeding aminopyrine or oxytetracycline with nitrite. 16 60

Retrograde infusion of large amounts of water-soluble contrast agents into the biliary system results in only a brief hepatogram. A dense hepatogram lasting for several weeks and visualization of hepatic and celiac lymph nodes equal to that in direct lymphography can be obtained after retrograde biliary infusion of Ethiodol. In serching for metastasis from tumor in the liver, gall-bladder, bile ducts, pancreas, stomach, and duodenum, radiographic visualization of these nodes may help. If proved safe, the procedure can be performed by endocopic cannulation of the common bile duct.
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PMID:Retrograde hepatography and indirect lymphography of the liver: an experimental study in the dog. 16 16

Cellular injury was produced in Ehlrich ascites tumor cells by an inhibitor of the function of the cell membrane [10(-3M) parachloromercuribenzenesulfonic acid (PCMBS)] or by inhibitors of respiration (10(-4M) Antimycin A), glycolysis (10(-4M), iodoacetic acid, IAA), oxidative phosphorylation (10(-3M) 2,4 dinitrophenol, DNP) or by combinations of these in a medium with or without glucose. The contents of Na+, K+, Ca++, Mg++ and intracellular water in the treated cells and controls were correlated with the percentages of ultrastructural changes in the mitochondria of the cells. A moderate negative correlation (r = -0.66) was observed between K+ content of the cells and the condensation of mitochondria in selected experiments where mitochondrial swelling had not yet started. A moderate positive correlation (r = 0.44) was observed between mitochondrial condensation and Na+ content of the cells in the same experiments. K+ and Mg++ content of cells showed a moderate negative correlation (r = -0.58 and -0.65) with mitochondrial swelling in the material of all experiments and Ca++ content a moderate positive one (r = 0.58), but the Na+ content and intracellular water showed no correlation. The percentages of flocculent densities in mitochondria showed a moderate positive correlation (r = 0.43) with the Ca++ content of the cells and a moderate negative correlation (r = -0.61) with the magnesium content of the cells.
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PMID:Mitochondrial changes, ion and water shifts in the cellular injury of ehrlich ascites tumor cells. 17 Sep 4

Liver neoplasms were induced in medakas (Oryzias latipes) by the addition of diethylnitrosamine (DENA) to their aquarium water at levels of 15-135 ppm for 8 weeks. After 13 weeks, 21 to 32 fish had developed hepatomas. Medakas are useful for further studies because they are highly susceptible to the carcinogenic effect of DENA, and the time for tumor induction is relatively short. Histologic type differed in the lesions of different fish and also within individual tumors. Some were typical trabecular hepatomas, others were anaplastic hepatomas or cholangiomas, or mixtures of these. Electron microscopy revealed an extensive rough-surfaced endoplasmic reticulum in a lamellar pattern, many mitochondria, and several round lysosomes in tumor cells. A few fat droplets with occasional crystalline ghosts were sometimes in the cytoplasm. The Golgi apparatus was not conspicuous. Some cells had highly developed microvilli that showed differentiation toward structures resembling bile capillaries.
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PMID:Histologic and electron microscopy observations on diethylnitrosamine-induced hepatomas in small aquarium fish (Oryzias latipes). 17 29

We have studied the effects of demeclocycline on the water metabolism of a patient with the syndrome of inappropriate antidiuretic hormone (ADH) secretion who presented with a serum sodium concentration of 110 meq/litre. Free water clearance was studied before, during, and after treatment with demeclocycline. This study shows that demeclocycline (900 mg/day) can at least partially inhibit the action of ADH in the setting of tumor-induced ADH secretion, with the production of a reversible, partial nephrogenic diabetes insipidus, and with few or no side effects. Demeclocycline may be useful in the treatment of chronic inappropriate ADH secretion.
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PMID:Demeclocycline treatment in the syndrome of inappropriate antidiuretic hormone secretion. 17 18

N-Nitrosopyrrolidine and two of its derivatives were prepared and fed in drinking water to Sprague-Dawley rats to compare the effects of substituents on the carcinogenicity of the N-nitrosopyrrolidine molecule. 3,4-Dichloro-N-nitrosopyrrolidine induced esophageal tumors in 13 of 14 animals, olfactory carcinomas in 4, and a hepatocellular tumor in 1. All animals that received this compound were dead at 55 weeks after the start of the experiments. N-Nitrosopyrrolidine induced hepatocellular tumors in 26 of 29 animals and induced 1 olfactory carcinoma. Not all animals in this group were dead until 104 weeks of the experiment. 2,5-Dimethyl-N-nitrosopyrrolidine induced only 2 hepatocellular tumors in 29 animals. The alpha-methyl substitution diminished the liver carcinogenicity, while the beta chlorine substitution affected a different target organ, the esophagus, and greatly reduced the time to death with tumors.
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PMID:The effect of substituents on the carcinogenicity of n-nitrosopyrrolidine in Sprague-Dawley rats. 17 38

Three groups of ACI/N rats of both sexes received continuous administration of 66 (Group I), 30 Group II), or 13(Group III) ppm solution of 1-methyl-3-acetyl-1-nitrosourea (Ac-MNU) in their drinking water. Tumors were found most frequently in the stomach and nervous system. The former was more frequently found in the male than in the female. The incidence was highest in males of Group II, 28/30 (93%), and lowest in females of Group I, 4/30 (13%). Histologically, all epithelial tumors of the stomach were benign adenomas except 5 adenocarcinomas. Neurogenous tumors were more frequently seen in the female than in the male. The incidence was highest in females of Group I, 29/30 (97%), and lowest in males of Group III, 6/28 (21%). The tumors were predominant in the central nervous system, especially in the hemispheres. Transplantation studies were done in some of these tumors. Although gastric tumors failed to get positive transplantation, all the neurogenous tumors transplanted were positive.
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PMID:Induction of tumors in the stomach and nervous system of the ACI/N rat by continuous oral administration of 1-methyl-3-acetyl-1-nitrosourea. 18 Jul 5

Lifetime tests were done in NZR inbred rats of dimethylnitramine (DMNO) by addition to the drinking water (average dose 1.83 g/kg body weight) and in NZO mice by repeated subcutaneous injection from birth to 7 months of age followed by administration in drinking water (total average dose 4.72 g/kg body weight). Rats developed hepatocellular carcinomas (85%), some of which metastasized. Mice developed hepatocellular carcinomas (81%) and renal adenocarcinomas (48%). Statistically significant increases of other tumor types also occurred in mice. The main targets for DMNO carcinogenesis appeared to be the liver cell epithelium and, at higher dose rates, renal tubular epithelium.
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PMID:Carcinogenicity of dimethylnitramine in NZR rats in NZO mice. 18 4

Daily sc injections of 8 mg N6, O2'-dibutyryl 3',5'-cyclic AMP (DBcAMP) beginning 1 day after tumor implantation significantly increased the growth rate of R32230AC rat mammary adenocarcinomas, which nearly doubled in in situ volume by day 40 compared to similarly implanted tumors in saline-injected controls. Weights of excised tumors, intact, drained, and dried all increased approximately 80%, which suggested that the increase in tumor size was not due to accumulation of secreted fluid or tissue water. Injections of 17beta-estradiol valerate (0.1 mg/wk) from day 1 or of DBcAMP from day 22 resulted in insignificant changes in growth--28% and 35% increases in tumor volume and a 5% decrease and an 18% increase, respectively, in drained wet weight. Electron microscopic examination revealed that estrogen and DBcAMP caused differentiation of the tumor cells into two different states: Estrogen-treated tumors resembled lactating mammary glands; they contained large lipid droplets, organized rough endoplasmic reticulum, and vesicles containing electron dense granules resembling protein. DBcAMP-treated tumor cells were marked by a proliferation of the Golgi complex and numerous vesicles containing fine granular material.
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PMID:Enhancement of R3230AC rat mammary tumor growth and cellular differentiation by dibutyryl cyclic adenosine monophosphate. 19 Apr 20

Groups of male Sprague--Dawley rats were maintained on three regimens: I. basal diet plus 0.05% 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB), II. same as I plus 6 ppm selenium (Na2SeO3) in the drinking water, and III. same as I plus 6 ppm selenium added to the diet in the form of a high selenium yeast. The 3'-MeDAB was incorporated in the diet for 8 weeks and then removed. The selenium supplements in Groups II and III were continued for an additional 4 weeks. At sacrifice the liver tumor incidence from was ascertained as the ratio of animals with tumors/total number of surviving animals per group. Selenium reduced the incidence from 92% (11/12) in the Group I control, to 46% (7/15) in Group II and to 64% (9/14) in Group III.
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PMID:Effects of selenium on azo dye hepatocarcinogenesis. 19 14


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