Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006826 (cancer)
 1,092,456 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indomethacin was continuously administered in the drinking water of inbred C3H mice given grafts of syngeneic 3-methylcholanthrene-induced fibrosarcomas. A minor proportion of these animals died at the same time as the untreated controls, and others completely rejected their tumors; however, in most cases, the tumor growth rate was significantly slowed, and growth recommenced rapidly after drug withdrawal. This was the pattern for tumors either in their 10th to 14th transplant generation or only their third in vivo passage. Indomethacin exerted little prophylactic effect, in that it neither increased the minimal cell number required to initiate tumor growth nor significantly decreased the proportion of tumors established in drug-treated animals recieving tumor grafts. The injection of killed Corynebacterium parvum organisms into small, growing McC3-I tumors [intratumor (IT) route] caused the regression of most of these. In contrast, IT injection of BCG, ip injection of C. parvum, or IT injection of C. parvum into larger tumors had no effect. Oral administration of indomethacin enhanced BCG treatment and augmented the activity of C. parvum injected either systemically into animals with small tumors or IT into those with substantial tumor burdens. The duration of these effects was, however, often dependent on the continued administration of the drug.
J Natl Cancer Inst 1979 Jan
PMID:Tumor growth inhibition and potentiation of immunotherapy by indomethacin in mice. 28 66

Five nitrosamines, which can be considered alkyl derivatives of N-nitrosodiethylamine, were tested for carcinogenicity by administration to Sprague-Dawley rats in drinking water at approximately equimolar concentrations. N-Nitrosodi-n-propylamine was a potent carcinogen but less so than N-nitrosodiethylamine and gave the same spectrum of tumors. N-Nitrosodiisopropylamine was very much weaker than N-nitrosodiethylamine and induced only tumors of the nasal turbinates in significant incidence. At the doses given, neither N-nitrosodiisobutylamine nor N-nitrosodi-sec-butylamine was significantly carcinogenic. In contrast, the cyclic nitrosamine N-nitrosohexamethyleneimine was equally potent with N-nitrosodiethylamine and gave the same spectrum of tumors in liver, esophagus, and nasal turbinates. The results support the concept that oxidation at the alpha carbon atom of nitrosamines is a significant step in carcinogenesis.
J Natl Cancer Inst 1979 Feb
PMID:Carcinogenicity of methylated derivatives of N-nitrosodiethylamine and related compounds in Sprague-Dawley rats. 28 72

For all the 121 municipalities in Southern Norway where 60% or more of the inhabitants get water from registered water supplies, the municipal average concentration of natural fluoride in the water has been determined and the municipalities divided into three groups with fluoride level 0--0.05 mg/1, 0.06--0.10 mg/1, and 0.11--0.50 mg/1, respectively. The average, age-adjusted municipal mortality rate of cancer in the mouth and throat was then determined for each of these groups by sex. The resulting figures show that the mortality rate declines for both sexes with increasing fluoride level: For males from 4.7 deaths per 100 000 per year on the low fluoride level, to 3.9 deaths per 100 000 per year on the medium fluoride level, and to 3.1 deaths per 100 000 per year on the high fluoride level. For females the corresponding figures are 1.5, 1.3 and 0.5. Arguments to show that these figures are unbiased from different tobacco consumption habits, differences between urban and rural municipalities, and differences in population size are presented. Possible, explicatory models are discussed.
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PMID:Inverse relationship between fluoride and cancer in mouth and throat? 28 7

Six nitrosamides [ethylnitrosourea (ENU), 2-hydroxyethylnitrosourea (HENU), carboxymethylnitrosourea, 1-nitroso-5,6-dihydrouracil (NDHU), 1-nitrosohydantoin, and N-methyl-N-nitrosobenzamide (MNB)] and ethylnitrosocyanamide (ENC) were administered chronically in sodium citrate-buffered drinking water to MRC Wistar rats. ENU induced tumors of the reticuloendothelial system (RES) (50% incidence), mammary glands, and large intestine. NDHU in drinking water produced hepatocellular carcinomas (96% incidence), but NDHU injected ip caused mostly tumors at the injection sites (54% incidence). HENU produced bone tumors (38% incidence) and RES tumors (28% incidence). ENC produced nasal cavity tumors (36% incidence). Papillomas and/or carcinomas of the forestomach, tongue, and pharynx were induced by most of the compounds, with the highest incidence in the forestomach (47% for MNB); these tumors were attributed to local action when the compounds were ingested. Carcinogenicity was not quantitatively correlated with direct mutagenicity for Salmonella typhimurium TA1535.
J Natl Cancer Inst 1979 Jun
PMID:Carcinogenicity test of six nitrosamides and a nitrosocyanamide administered orally to rats. 28 23

Strain A female mice were exposed to 10 ppb dimethylnitrosamine (DMN) in their drinking water for 4 weeks before mating. Treatment was continued through pregnancy and lactation and after weaning until the progeny were 22 weeks old. The incidence of primary lung tumors among the treated progeny (23%) was significantly higher (P less than 0.021) than that among controls (8%). The effect of the DMN was greatest among the males: 32% had lung tumors, compared with 4% of the control males (P less than 0.016). The DMN-exposed females also had a higher lung tumor incidence than did the controls, but the difference was not of statistical significance. These results demonstrate carcinogenicity of DMN at a dose approaching amounts possibly encountered by the human population as a result of environmental exposure.
J Natl Cancer Inst 1979 Jun
PMID:Lung tumorigenesis in mice after chronic exposure in early life to a low dose of dimethylnitrosamine. 28 26

The effect of administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) at a dose level of 83 mg/liter in the drinking water was followed in the pyloric mucosae of male noninbred Wistar rats. Autoradiographic studies were done on animals killed after 10, 15, 26, and 36 weeks of treatment. In the normal-appearing mucosae of the rats treated with MNNG for 10 weeks, the number of epithelial cells per pit column was significantly increased over that in control rats. Simultaneously, a shift in the major zone of epithelial cell proliferation was noted in the treated rats. Along with the formation of a longer pit in MNNG-treated rats, the greatest number of DNA-synthesizing cells was displaced from the middle third of the pit in a downward direction toward the muscularis mucosa. In addition, at this early experimental time period, pits lined with more immature, cuboidal, mucus-depleted cells were recognizable. These pits not only had higher labeling indices than normal-appearing pits of the same animals but also expressed a dual nature with increased proliferative activity extending either upward to the luminal surface or further in a downward direction. Focal areas of cellular atypism were present by week 10 of treatment with a threefold to sevenfold greater DNA synthesis activity than that found in the normal-appearing mucosa of the same animal. A wide range of values in proliferative activity was found not only among invasive pyloric tumors within the same animal but also within different areas of the same tumor. The mechanism for the formation of adenomas and invasive adenocarcinomas is believed to be related to the dual character of the hyperplastic pits described.
J Natl Cancer Inst 1979 Jul
PMID:Sequential histopathology and cell kinetic changes in rat pyloric mucosa during gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine. 28 27

In vivo MSB tumor growth and cell-mediated cytotoxicity (CMC) to MSB tumor cells in vitro were studied in male C57BL/6 mice exposed to 0, 3, 30, or 300 ppm Cd as CdCl2 in their drinking water for 21 weeks prior to and during tumor growth. CMC was assessed on days 5, 12, and 19 post injection with the use of both a 51Cr release assay and a 51Cr post-label assay. Cd exposure significantly inhibited the growth of MSB tumors in vivo and enhanced the levels of CMC in the tumor-bearing hosts. Peak levels of CMC on day 12 post tumor injection were significantly increased in Cd-exposed animals. However, whereas the inhibition of tumor growth was directly dependent on the dose of Cd, the enhancement of CMC was inversely related to dosage. These data suggested that other mechanisms in addition to increased CMC were involved in tumor growth inhibition. Possible factors such as direct inhibition of tumor growth by Cd and decreased serum blocking levels in Cd-exposed animals are discussed.
J Natl Cancer Inst 1979 Aug
PMID:Effect of cadmium exposure on primary tumor growth and cell-mediated cytotoxicity in mice bearing MSB sarcomas. 28 37

Effects of 12 chemical cancerogenic agents have been studied in 910 anuran amphibia of the grass frog Rana temporaria. Tumors developed by administration of 8 of the agents studied. Dimethyl, diethyl and dibutylnitrosamines dissolved in water induced tumors in 44.2, 43.6 and 50% of animals, respectively; benzidine and 2-acetylaminofluorene administered subcutaneously and per os--in 46.6 and 41.2%, respectively, whereas p-dimethylaminoazobenzene and orthoaminoazotoluene (per os and subcutaneously)-in 30--33.3% of cases. Diethylstilbestrol-propionate induced tumors in 21% of cases. All the tumors developed within relatively short periods of time (15.6--31.9 weeks) and were located in the liver (hepatocellular cancer, hepatoadenomas) and the haemopoetic system (hemocytoblastosis). In control group of animals 3 amphibia developed multiple tumors of skin-cystadenopapillomas. The results obtained testify to the common mechanism of cancerogenesis in classes of vertebrates. In addition, the findings presented indicate to the suitability of amphibia as a new experimental object in oncology as well as to the applicability of these animals for purposes of express diagnostics of cancerogenicity. It may successfully serve as a biological indicator of environmental pollution with blastomogenic agents.
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PMID:Tumor induction by carcinogenic agents in anuran amphibian Rana temporaria. 30 91

A transient decrease in T lymphocytes in peripheral blood was observed in twelve healthy volunteers immersed in hot water baths which raised their mean rectal temperature by 1.35 C. T lymphocytes declined from 59 to 41 rel % (2p less than 0.001) or from a mean of 1990 to 1300 per mm3. T lymphocytopenia was accompanied by a relative increase in the fraction of B lymphocytes. Total lymphocyte count remained unchanged. In vitro heating alone to 39 C did not influence the total of SRBC-labelled lymphocytes. The findings are interpreted to be the result of a change in lymphocyte distribution with increased recirculation of mobile T lymphocytes.
Cancer 1978 Dec
PMID:Peripheral T lymphocytopenia under exogenous thermal stress. 31 Mar 36

When dissolved in water nitrosomorpholine induced in frogs Rana temporaria and aquarium fish adenomas and cancer, hemocytoblastosis, adenomatous polyps and adenocarcinomas of the intestine, mesenchymomas. A combined action of sodium nitrite and morpholine would induce the tumors concerned, but taken separately NN and M produced only a toxic effect. The morpholine nitration appears to proceed both endogenously and directly in water. It seems rational to use animals of the aqueous medium as an indicator of nitrosoamines and their precursors contamination of hydrosphere.
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PMID:[Possibility of using fish and amphibians for detecting the carcinogenic action of nitrosomorpholine and its chemical precursors]. 31 23


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