Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1326912 (tumorigenesis)
 57,481 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to clarify the role of gut microflora in tumorigenesis by a comparison of tumor production between male germ-free and conventional Wistar rats given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 100 microgram/ml in drinking water. Ninety-one % of conventional MNNG-treated rats that died or were killed by Day 314 of the experiment developed tumors in the gastrointestinal tract, whereas only 17% of germ-free treated rats developed such tumors. In addition, large tumors, some 5 cm or more in diameter, were frequently observed in the conventional rats, whereas only small tumors 0.4 to 1.2 cm in diameter were present in the germ-free rats. Furthermore, multiple tumors including double tumors were often found in the conventional rats, while such tumors never appeared in the germ-free rats. The results suggest that gut microflora might exert a promoting influence on tumorigenesis by MNNG in the gastrointestinal tract. The promoting influence of the microflora in conventional rats might not be of a simple nature, since the influence of a variety of factors modified by the micorflora on tumorigenesis by MNNG p.o. is unavoidable.
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PMID:Gastrointestinal carcinogenesis in germ-free rats given N-methyl-N'-nitro-N-nitrosoguanidine in drinking water. 44 76

The lethal effects in Marsh mice for a range of DL-6-OH-DOPA levels were ascertained and exceeded those previously reported for 6-OH-DA under comparable conditions. The addition of vitamin "C" to the 6-OH-DOPA solution given intraperitoneally increased the lethal effect, as did the intraperitionel route of injection over that of the subcutaneous. Increased water consumption developed the fourth day for those surviving toxic levels of 6-OH-DOPA given subcutaneously as compared with controls. For all mice initially surviving administration of 6-OH-DOPA, tumorigenesis and long-term survival were of the same order as that of the controls. The toxicity of 6-OH-DOPA relating to ferric heme formation more likely involves metmyoglobin than methemoglobin. The combination of direct damage to sympathetic adrenergic cardiac innervation and metmyoglobin formation appears sufficient to account for the lethal effects of 6-OH-DOPA.
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PMID:Short- and long-term effects of graduated doses of DL-6-OH-DOPA upon marsh mice. 50 88

Aqueous solutions of molecular oxygen, per se, or in combination with either pyrogallol or 6-azauracil increased tumorigenesis in Nicotiana suaveolens X Nicotiana langsdorffii seedlings relative to control seedlings. The biological activities of the organic chemicals were O2-dependent, because the substitution of N2 or O2 or the degassing of 0.1-1 mM solutions of the compounds eliminated or greatly reduced their tumorigenic effects. Rates of tumorigenesis exceeded 95% for 0.5 mM solutions of either pyrogallol or 6-azauracil solutions in the presence of l mM O2. Although tumors developed in 20% of seedlings in the presence of 1 mM O2, alone, 4-5 times more tumors were induced by the organic chemical--O2-H2O systems. Dinitrophenol and ascorbic acid, compounds which affect cellular respiration or redox systems, strongly inhibited the chemically-mediated tumorigenesis. Dinitrophenol was equally effective at one-tenth of the molar concentrations of ascorbic acid that were required for the suppressions of oncogenesis. Dehydroascorbic acid was much less inhibitory than ascorbic acid.
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PMID:Oxygen-dependent chemical tumorigenesis in a Nicotiana hybrid: inhibition by ascorbic acid and dinitrophenol. 57 9

Diethylnitrosamine (DEN), at a concentration of 100 parts/10(6) in drinking water for 14 days, caused the development, by 48 weeks, of very few liver tumours in 5 of 18 (27%) male F=344 rats fed control diet. When the DEN treatment was followed one week later by continuous feeding of the hypolipidemic hepatic peroxisome proliferator, Wy-14,643, at 0.1% dietary level, all of 28 rats (100%) developed, between 38 and 48 weeks, a significantly higher number of liver tumours. Furthermore, laparotomy at 22 weeks revealed that several rats fed Wy-14,643 after DEN initiation had developed visible liver nodules, suggesting that Wy-14,643 also accelerates the appearance of these tumours. Administration of another peroxisome proliferator, clofibrate, at 0.5% level in the diet after DEN initiation, also caused a substantial enhancement of liver tumorigenesis. The enhancement of liver-tumour development by clofibrate, however, was less than that by Wy-14,643. The marked enhancing effect of Wy-14,643 may be due to its profound hepatomegalic and peroxisome proliferative properties.
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PMID:Enhancement by Wy-14,643, a hepatic peroxisome proliferator, of diethylnitrosamine-initiated hepatic tumorigenesis in the rat. 72 41

Effect of dietary indole on the urinary bladder tumorigenesis by chronic dibutylnitrosamine (DBN) treatment was evaluated in hamsters. In the first experiment, in which DBN-water and diet were given ad libitum, dietary indole significantly suppressed bladder tumor incidence. The inhibitory effect was more pronounced in males. In the second experiment, in which consumption of both diet and DBN-water was rigidly controlled by pair-feeding, dietary indole again significantly suppressed bladder tumor incidence; its effect was similar in both males and females. This suppressive effect of indole on bladder tumorigenesis contrasted markedly with its failure to suppress tumors at other sites such as nasal sinuses, trachea, esophagus, and fore-stomach.
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PMID:Suppression of dibutylnitrosamine-induced bladder carcinomas in hamsters by dietary indole. 86 59

Tetramethylhydrazine hydrochloride (TEMH) was administered in drinking water as a 0.125% solution to randomly bred Swiss mice for life beginning at 6 weeks of age. As a result of treatment, the incidence of blood vessel tumors rose from 5 to 96% in females and from 6 to 88% in males, while that of lung tumors increased from 21 to 36% in females and from 23 to 28% in males, as compared with untreated controls. The increased incidence of blood vessel tumors, but not of lung neoplasms, was statistically significant. Histopathologically, the tumors exhibited the characteristics of angiomas and angiosarcomas of blood vessels and adenomas of the lung. The investigation proved for the first time the tumorigenicity of TEMH. The possible role of increased methyl substitution on hydrazine in tumorigenesis was also discussed, as well as hydrazine derivatives as a tumor-producing class.
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PMID:Tumorigenicity of tetramethylhydrazine hydrochloride in Swiss mice. 103 21

Daily treatment for 12 months of young nulliparous C3H mice with 0.1 mg 2-bromo-alpha-ergocryptine (CB-154), an effective suppressor of prolactin secretion, significantly reduced and in some instances virtually eliminated the incidence of spontaneous mammary tumors. The CB-154-treated mice had normal body weight gains and normal estrous cycles. Ovariectomy of young nulliparous C3H mice also reduced mammary tumor incicence, but appeared to be slightly less effective than treatment with the ergot. Chronic administration of 17beta-estradiol for 12-19 months (via drinking water) to young nulliparous intact or ovariectomized-hysterectomized C3H mice significantly increased mammary tumor incidence. Concurrent administration of 0.1 mg CB-154 to the estrogen-treated mice significantly reduced the incidence of mammary tumors when compared with mice treated with the steroid alone. Chronic sc administration (0.1 mg/mouse, twice weekly for 20 months) of Enovid to young, nulliparous, intact C3H mice significantly increased mammary tumor incidence, whereas concurrent administration of 0.1 mg CB-154 to the Enovid-treated mice significantly reduced the incidence of these tumors. Thus significant inhibition of spontaneous or estrogen- or Enovid-induced mammary tumorigenesis by concurrent drug-induced prolactin suppression has been demonstrated in these studies.
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PMID:Interaction of estrogen and prolactin in spontaneous mammary tumorigenesis of the mouse. 103 5

Toxicity investigations were conducted with 4 chemicals: hydrazine, 1,2-dimethylhydrazine di HCl, phenylhydrazine HCl and Beta-N-(gamma-L(+)-glutamyl)-4-hydroxymethylphenylhydrazine in Swiss mice. Hydrazine and phenylhydrazine HCl were administered daily in drinking water, the former at 0.01% and the latter at 0.001% concentrations. The 1,2-dimethylhydrazine di HCl and Beta-N-(gamma-L(+)-glutamyl)-4-hydroxymethylphenylhydrazine were given as a single subcutaneous injection at 45 mug and 100 mug/gr. body weight basis, respectively. The findings clearly showed that all four chemicals exerted a stronger toxic effect in male than in female mice. It is, therefore, recommended in similar situations to use different doses of chemicals for each sex in the long-term tumorigenesis studies.
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PMID:Sex dependent toxicity of four chemicals. 113 20

Nickel subsulfide, Ni3S2, alone or combined with manganese or chromium dusts, was administered i.m. to Fischer rats to study the effects of the metals upon Ni3S2 induction of sarcomas at the injection site. The incidence of sarcomas within 2 years after injection of Ni3S2 (1.2 mg) plus manganese (1.0 mg) was 7%, versus 77% in rats that received only Ni3S2 (1.2 mg), and 80% in rats that received Ni3S2 (1.2 mg) plus chromium (1.0 mg) (p less than 0.005). No local sarcomas occurred in rats that received the injection vehicle, or in rats that received manganese or chromium without Ni3S2. Admixture of manganese diminished the solubility of 63Ni3S2 in rat serum, serum ultrafiltrate, or water, in vitro. Admixture of manganese with 63Ni3S2 did not affect the mobilization or excretion of 63Ni in vivo, nor did it alter the acute pathological reactions to Ni3S2. 63Ni concentrations in ultrafiltrates of supernatant fractions of homogenates of injection sites averaged 2.8 (S. D. +/- 0.7) ng/ml at 5 to 6 months after injection of 63Ni3S2 (1.2 mg) plus manganese (1.0 mg), versus 5.4 +/- 2.0 ng/ml after injection of only 63Ni3S2 (1.2 mg) (p less than 0.02). This study demonstrates that admixture of manganese dust and Ni3S2 inhibits Ni3S2 tumorigenesis in rats, and reveals that manganese dust affects the subcellular distribution of 63Ni derived from 63Ni3S2, without influencing 63Ni kinetics as estimated by compartmental analysis.
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PMID:Effects of manganese on carcinogenicity and metabolism of nickel subsulfide. 126 36

Two cell lines, both derived from the C3H mouse and each having different responses (oncogenic and cytotoxic) to polycyclic aromatic hydrocarbon oncogens, were studied with respect to their drug-metabolizing enzymes. The 10T1/2CL8 cells (a C3H mouse embryo fibroblastic cell line) were much more effective in converting 3-methylcholanthrene (3-MC) to 3-MC water-soluble metabolites, 3-MC phenols, and 3-MC-bound cellular macromolecules than were CVP3SC6 cells (a new line of C3H mouse adult ventral prostate fibroblasts). Basal aryl hydrocarbon hydroxylase activity was higher in 10T1/2CL8 cells than in CVP3SC6 cells, while the reverse was found for epoxide hydrase activity (using 3-methylcholanthrene-11, 12-oxide as substrate. 3-MC or benz(a)anthracene induced epoxide hydrase activity in both cell lines to about the same extent. 3-MC did not induce aryl hydrocarbon hydroxylase activity in CVP3SC6 cells. Aryl hydrocarbon hydroxylase activity was markedly induced in both cell lines by benz(a)anthracene and was slightly induced in 10T1/2CL8 cells by 3-MC. In a chemical oncogenesis cell culture system, transformation of 10T1/2CL8 cells mediated by 3-MC could be increased two- to threefold by treating the cell cultures with: either benz(a)anthracene, styrene oxide, cyclohexene oxide, or 1,2,3,4-tetrahydrona=phthalene-1,2-oxide; or with cyclohexene or 1,2-dihydrona-phthalene, alkene precursors of cyclohexene oxide and 1,2,3,4-tetrahydronaphthalene-1,2-oxide, respectively. When 10T1/2CL8 cells were treated with a combination of benz(a)anthracene and cyclohexene, 3-MC-mediated transformation was increased 7.8-fold. CVP3SC6 cells that were not transformed by 3-MC or other hydrocarbon oncogens were transformed by a combined treatment with benz(a)anthracene, 1,2-dihydronaphthalene, and 3-MC.
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PMID:The effect of modifiers of microsomal enzymes on chemical oncogenesis in cultures of C3H mouse cell lines. 126 37


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