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

Female A/J mice were maintained on NIH-07 diet or on NIH-07 diet containing butylated hydroxyanisole (BHA, a mixture of 2- and 3-tert-butyl-4-hydroxyanisole), 5 mg/g, for 1 week prior to and during 10 weeks of treatment with N-nitrosodimethylamine (NDMA) or N-nitrosopyrrolidine (NPYR), administered in the drinking water. Twenty weeks after nitrosamine treatment ended, mice were sacrificed and lung adenomas were counted. BHA inhibited NDMA tumorigenesis but enhanced NPYR tumorigenesis. Treatment of A/J mice for three weeks with BHA (5 mg/g) added to semisynthetic diet increased whole lung microsomal alpha-hydroxylation of NDMA and NPYR, as measured by aldehyde production, and increased lung and hepatic glutathione-S-transferase activities. No evidence was found for formation of S-methylglutathione in incubations with NDMA and hepatic supernatants obtained from BHA treated or control mice. Four h after gavage of NDMA, levels of 7-methylguanine in the lung DNA of mice treated with BHA were higher than in the lung DNA of control mice, but levels of O6-methylguanine in the two groups were the same. The results of this study indicate that BHA treatment increases the microsomal metabolic alpha hydroxylation of both NDMA and NPYR, but has differential effects on their tumorigenic activities.
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PMID:Effects of butylated hydroxyanisole on the tumorigenicity and metabolism of N-nitrosodimethylamine and N-nitrosopyrrolidine in A/J mice. 394 Jan 89

Administration of urethan (CAS: 51-79-6; carbamic acid, ethyl ester) in the drinking water of breeding female mice of the murine mammary tumor virus (MuMTV)-positive DD/Tbr strain and the MuMTV-negative DDf strain induced so-called keratinized nodules, which were demonstrable in wholemount preparations of mammary glands. It also induced squamous cell tumors (also called adenoacanthoma) at an extremely early age. The keratinized lesions appearing in the lobular areas of the mammary glands showed heavy infiltration with lymphocytes and as such were very different from hyperplastic alveolar nodules, the preneoplastic lesions for adenocarcinomas. Immunoperoxidase tests with antibodies against the MuMTV revealed that positivity of normal mammary gland epithelium in the DD/Tbr strain was not found in the keratinized nodules, which was further evidence that in squamous cell tumorigenesis of the mammary gland the MuMTV is not expressed overtly even at an early stage in tumorigenesis, in contrast to the case with adenocarcinoma tumorigenesis. These findings substantiate previous conclusions that the MuMTV is not involved in chemical carcinogenesis of the mouse mammary gland.
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PMID:Urethan-induced mammary tumorigenesis in a murine mammary tumor virus (MuMTV)-positive mouse strain: evidence for a keratinized nodule as an MuMTV-negative precursor lesion for squamous cell tumors. 609 Jul 51

The initiating and promoting effects of methapyrilene were evaluated using the hepatic enzyme-altered foci bioassay. Male Sprague-Dawley rats were partially hepatectomized and 24 hours later were administered either methapyrilene or nitrosodiethylamine by oral gavage. Subsequently, the animals were promoted with 500 ppm2 phenobarbital or 200 ppm methapyrilene in drinking water for eight weeks. Fresh frozen sections of liver were then stained and scored for gamma-glutamyl-transpeptidase (GGT)-positive foci. Methapyrilene, when tested as the nominal initiator at a single dose of 50 mg/kg or at two doses of 130 mg/kg and promoted by phenobarbital, did not induce foci above background levels. However, when substituted for phenobarbital as the promoting agent following nitrosodiethylamine initiation, methapyrilene enhanced enzyme-altered foci formation to an equal or greater extent than did the promoter phenobarbital. These results suggest that the carcinogenic effects of methapyrilene may be related to its ability to enhance hepatic tumorigenesis.
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PMID:Methapyrilene effects on initiation and promotion of gamma-glutamyl-transpeptidase positive foci in rat liver. 612 May 43

The effects of selenium of mouse mammary tumorigenesis were examined in 2 systems. BALB/cfC3H (MuMTV-S positive) given 2 and 6 ppm selenium in the drinking water and maintained as breeding mice, had significantly lower incidences of mammary tumors (48% and 12%, respectively) than untreated control mice (82%). Selenium at 4 ppm inhibited the tumor-producing capabilities of only 1 of 4 preneoplastic outgrowth lines maintained in BALB/c (MuMTV-S negative) mice. Selenium at 2, 4 and 6 ppm had no effect on the growth rate of primary mammary tumors transplanted subcutaneously in BALB/c mice. Selenium inhibited mammary tumorigenesis without interference of normal reproductive function and weight gain.
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PMID:Selenium-mediated inhibition of mouse mammary tumorigenesis. 626 42

Urethane administrated in the drinking water of breeding female mice of five inbred strains (DDf, KF, C3Hf, ddY and C57BL) leads to a higher incidence of mammary tumors at an extremely early age in four of these strains (DDf, KF, C3Hf and ddY). In the case of the DDf strain the tumors are adenoacanthomas, but in the case of the other strains adenocarcinomas are also observed. The effect of urethane in the drinking water on expression of endogenous retroviral structural proteins of the B and C type (MTV and MuLV) was studied in the milk by an immunodiffusion test and in organ extracts by radioimmunoassays (for MTVp27, MTVgp52 and MuLVp30). Organs tested include salivary glands, thymus and spleen from female and male animals. In addition, prostate and seminal vesicles were tested in male animals and uterus and mammary glands in females. Mammary tumors induced by urethane were also treated. Urethane does not induce or enhance endogenous retroviral antigen expression, either in these organs or in the mammary gland, one of the target organs for tumorigenesis by this agent.
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PMID:Mammary tumor induction in inbred mouse strains with urethane is not accompanied by changes in expression of B- and C-type retroviral structural proteins. 628 76

Six groups of inbred male Wistar/Furth (WF) rats were castrated at 40 days of age and group I received no further treatment. Groups 3 and 5 received 5.0 mg diethylstilboestrol (DES) pellets. Groups 4 and 6 were given both DES and 5.0 mg anti-oestrogen (antiE) clomiphene citrate pellets. At 50-55 days of age groups 2, 5, and 6 were exposed daily to drinking water containing 5.0 mg N-nitrosobutylurea (NBU), for 30 days. None of the castrated rats given NBU alone developed mammary or pituitary tumours (MT, PT). When antiE was administered, both MT and PT incidences were reduced in rats given DES alone or in combination with NBU. Furthermore, in antiE-treated rats receiving DES and NBU the mean number of MT per rat was also significantly decreased. Similarly a marked reduction in the mean pituitary weight was observed in antiE-treated groups. These results indicate that antiE treatment was effective in the prevention of both mammary and pituitary tumorigenesis in rats receiving DES alone or receiving a combination of DES and NBU, and its inhibitory effect on mammary tumorigenesis may be mainly due to competitive antagonism for DES-induced pituitary tumorigenesis by antiE.
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PMID:Preventive effects of antioestrogen on mammary and pituitary tumorigenesis in rats. 649 74

The carcinogenic response of NZO/BlGd inbred mice of both sexes to oral N-nitrosohexamethyleneimine (NHEX) was investigated at 2 differing dose rates, but equal cumulative doses. Mice received 52 mg NHEX (2 mg/g body wt) in drinking water over either an 8-week period (200 mg/l) or a 32-week period (50 mg/l), and were then kept for their natural lifespans. The main sites of tumorigenesis were upper alimentary tract (oropharynx, esophagus, squamous and glandular stomach) and liver. Lymphomas and biliary epithelial tumours were also induced, but lung carcinogenic response was of marginal statistical significance. In contrast to previous reports we found responses in mice very similar to the organ pattern of NHEX carcinogenesis in rats. A comparable previous study in rats found a more marked change in response pattern at the 2 NHEX dose rates but total doses differed by up to 1.6 times in that experiment. With equal total doses of NHEX the mouse tumour patterns at the same 2 dose rates were nearly the same, but there were higher incidences of liver and lung tumours and of lymphomas at the high dose rate, in agreement with the rat study. There were no significant sex differences in carcinogenic response.
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PMID:Carcinogenesis by N-nitrosohexamethyleneimine in NZO inbred mice. 651 60

Four groups of inbred male WF rats were castrated and received sc implantations of diethylstilbestrol [(DES) CAS: 56-53-1; alpha,alpha'-diethyl-4,4'-stilbenediol] at 40 days of age. Group I was given no further treatment; groups II and IV were treated with antiestrogen (AntiE) clomiphene citrate simultaneously with DES treatment. At 50-55 days of age, groups III and IV were given drinking water containing N-nitrosobutylurea [(NBU) CAS: 869-01-2; 1-butyl-1-nitrosourea] for 30 days. Castrated male rats or rats castrated and treated with NBU alone developed neither hepatic tumors (HT) nor pituitary tumors (PT). When AntiE was administered, incidences of HT and PT, size and the total number of HT, and mean pituitary weight were significantly reduced in rats given DES alone and in rats given DES with NBU. AntiE treatment changed the distribution in the histologic classification of hepatocellular lesions: Neoplastic nodules, instead of hepatocellular carcinomas, were predominant. The results indicate that AntiE was effective in the inhibition of hepatic and pituitary tumorigenesis associated with DES treatment. Our previous study has shown that prolactin was not involved in this hepatic tumorigenesis. Therefore, these studies provide evidence that the carcinogenic effect of DES on the liver cell is direct and that HT are regulated in development and growth by AntiE treatment.
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PMID:Inhibitory effect of antiestrogen on hepatic tumorigenesis in WF rats treated with diethylstilbestrol alone or in combination with N-nitrosobutylurea. 658 70

The carcinogenic or cocarcinogenic effects of bile or bile acid on stomach carcinogenesis were investigated in inbred W rats. Bile or bile acid was introduced into the stomach by choledochogastrostomy or with food after the administration of N-methyl-N'-nitro-N-nitrosoguanidine [(MNNG) CAS: 70-25-7; 1-methyl-3-nitro-1-nitrosoguanidine] in drinking water. The animals that received MNNG and bile or sodium taurocholate (CAS: 145-42-6; N-choloyltaurine sodium salt) had a significantly higher incidence of hyperplastic and neoplastic lesions in the stomach mucosa than did the relevant MNNG-treated controls. The result suggested an enhancing effect of bile and sodium taurocholate in stomach tumorigenesis.
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PMID:Enhancing effect of bile and bile acid on stomach tumorigenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 659 82

17 beta-Estradiol [(E2) CAS: 50-28-2; estradiol] and diethylstilbestrol [(DES) CAS: 56-53-1; alpha-alpha'-diethyl-4,4'-stilbenediol] were compared to determine their tumor-inducing abilities in tissue. After castration at 40 days of age, inbred male WF rats received a pellet of either 5.0 mg DES or 5.0 mg E2. Approximately half of the rats that had been given DES or E2 were further given at 50-55 days of age 5.0 mg N-nitrosobutylurea [(NBU) CAS: 869-01-2; 1-butyl-1-nitrosourea] in their drinking water each day for 30 days. None of the castrated rats given E2 alone developed hepatic tumors (HT). Even further addition of NBU did not elicit any HT. Conversely, E2 treatment as well as DES treatment, whether administrated alone or in combination with NBU, resulted in an increase in the incidence of pituitary tumors (PT) and in the mean pituitary weight. The data indicate that E2 was ineffective in inducing HT in castrated male rats, whereas E2 showed an ability to induce PT similar to that of DES. In addition, E2 was not as able to induce as many mammary tumors as DES was able to induce. There was no significant synergism between E2 and NBU in contrast to that between DES and NBU in mammary tumorigenesis, whereas these two estrogens had a similar effect in causing an increase in the pituitary weight. This study, therefore, suggests that the carcinogenic effect of estrogens may not always correlate with their estrogenic effect and further confirms the noninvolvement of prolactin in hepatic tumorigenesis.
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PMID:Effects of 17 beta-estradiol and diethylstilbestrol on concurrent development of hepatic, mammary, and pituitary tumors in WF rats: evidence for differential effect on liver. 659 93


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