Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In studies designed to determine the influence of dietary Se on pancreatic carcinogenesis, Syrian golden hamsters were fed unsupplemented torula yeast diet or diet supplemented with 0.1 or 5.0 ppm Se, from sodium selenite, starting at 4 weeks of age until the termination of the study. In separate groups, hamsters were given the diet supplemented with 0.1 ppm Se until 5 days after carcinogen treatment. Then they were fed either the unsupplemented diet or the diet supplemented with 5.0 ppm Se until the end of the experiment. N-Nitrosobis(2-oxopropyl)amine (BOP; CAS; 60599-38-4) treatment was given as a single sc injection of 20 mg/kg (body wt) at 8 weeks of age, and surviving hamsters were killed 50 weeks later. As a measure of Se status, glutathione peroxidase (GSHPX) activities were determined in plasma, erythrocytes, and liver. Values were elevated in animals fed higher levels of dietary Se. BOP treatment depressed plasma GSHPX at 24 hours and elevated erythrocyte and liver values at 4 weeks. Pancreatic ductular adenoma yields were inhibited with each elevation of dietary Se in female hamsters fed the diets, both before and after BOP administration, and were further inhibited in females that were fed diets containing 0.1 ppm Se before BOP administration and that were changed to the unsupplemented or 5.0-ppm-supplemented diets after BOP was given. Pancreatic ductular adenoma yields were highest in all male groups given diets of 0.1 ppm Se before BOP administration, irrespective of the Se level after BOP was fed. Adenoma yields in males were lowest in hamsters fed unsupplemented diet, both before and after BOP treatment. Pancreatic carcinoma yields were low and not influenced by dietary Se. The incidence of hepatic necrosis was elevated in BOP-treated hamsters fed the unsupplemented diet, and that of biliary cystic adenomas was highest in the group fed 0.1 ppm Se before and after BOP treatment.
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PMID:Effects of dietary selenium on bis(2-oxopropyl)nitrosamine-induced carcinogenesis in Syrian golden hamsters. 346 17

It was previously reported that red ginseng extract inhibited carcinogenesis by urethan, DMBA, and aflatoxin B1 [Yun et al: Cancer Detect Prevent 1983; 6:515-25]. In an attempt to investigate the mechanism of the anticarcinogenic effect of ginseng, the natural killer (NK) activity and the incidence of lung adenoma were followed over a period of 48 weeks postinjection with urethan or benzo(a)pyrene. The NK activity was markedly depressed from 4 weeks to 24 weeks after injection of carcinogens. This decreased NK activity was returned to the level of controls by administration of ginseng. At the same time, a lower incidence of lung adenoma was noted following administration of ginseng to urethan-injected mice. However, the lung adenoma induced by benzo(a)pyrene began to occur at 48 weeks in which NK activity had naturally declined to a level too low to be affected by ginseng, and administration of ginseng did not decrease the incidence. In conclusion, these results suggest that the anticarcinogenic effect of ginseng may be related to the augmentation of NK activity.
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PMID:Effect of red ginseng on natural killer cell activity in mice with lung adenoma induced by urethan and benzo(a)pyrene. 348 57

One thousand cases of resected gallbladders were histologically investigated by serial step sections. Intestinal metaplasia was found at rates of 4.0% and 30.6% in the cases without and with stone, respectively. It was found at rates of 69.8% and 61.1% in the cases of dysplasia and carcinoma, respectively. The goblet cells were found at rates of 34.5% and 26.3% in the lesions of carcinoma and dysplasia, respectively. On the other hand, the dysplasia and adenoma intermingled in the tumor tissue at the rates of 22.2% and 8.3% in 36 cases of carcinoma, respectively. Although normal epithelial cells of the gallbladder contain mainly sulfomucin, the goblet cells have sialomucin. The ratio of sialomucin-containing cells increased in the tissue of dysplasia and carcinoma. As to their location, intestinal metaplasia, dysplasia, and carcinoma showed a similar distribution in the gallbladder. Accordingly, it should be considered that the sequence of intestinal metaplasia-dysplasia-carcinoma is significant. Pseudo-pyloric glandular metaplasia was found at rates of 45.5% in the cases of cholecystitis without stone, 77.2% in those with stone, 100% in those with dysplasia, and 72.3% in those with carcinoma. However, it should be considered that pseudo-pyloric glandular metaplasia has less relationship for the bases of carcinogenesis as compared with intestinal metaplasia.
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PMID:Intestinal metaplasia-dysplasia-carcinoma sequence of the gallbladder. 352 13

Between 1977 and 1984 a total of 301 patients with autonomous thyroid adenoma were irradiated with an individually calculated one-time dose of 400 Gy units of 131I. Repeated follow-up tests were made in 217 patients (up to 7.2 years, mean of two years). Pre- and post-treatment diagnosis in all patients consisted of determining T3 and T4, one TRH test, one 131I two-phase test to determine treatment, including quantified scintigraphy (under suppression, if necessary), as well as post-treatment scintigraphy and (post-treatment) 99mTc scintigraphy. The treatment was successful in 98% of patients; there was no difference between compensated and decompensated forms. Euthyroid state was achieved in 87% of patients, with typical findings of compensated T3 oversecretion, as is known to occur with endemic goiter in regions of iodine deficiency. The ability of the thyroid for autoregulatory adaptation to such iodine deficiency is thus preserved. Preclinical hypothyroidism occurred in 11% of patients: it could have been avoided in about half of them. Persistent or recurring autonomous adenoma was observed in 2% of patients as a result of under-dosage. One should thus aim at a dose of 400 Gy, to obtain optimal elimination. Radiation-induced carcinogenesis was not observed: radioiodine treatment and operation are thus of equal value in the causal treatment of autonomous adenoma. Radioiodine treatment is indicated in patients aged over 40 years with additional diseases and increased risk of anaesthesia and operation. It is preferred treatment if there are multiple autonomous adenomas.
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PMID:[Iodine-131 therapy of autonomous adenoma of the thyroid. 7-year results]. 359 67

The effects of four isomeric forms of aminophenols, ortho-, meta-, para-aminophenol and acetaminophen (o-, m-, p-AP and AAP, respectively) on liver and kidney carcinogenesis initiated by N-ethyl-N-hydroxyethylnitrosamine (EHEN) were tested. Rats were given 0.1% EHEN (in their drinking water for 2 weeks) and then diet containing these compounds at concentrations of 0.8% for 49 weeks. Administration of o-AP and AAP significantly decreased the number and area of preneoplastic foci staining immunohistochemically for glutathione S-transferase placental type (GST-P) per unit area of liver section as compared with the values for rats given EHEN alone. o-AP and AAP also significantly decreased the incidence of hepatocellular carcinoma. In contrast, p-AP and AAP significantly increased quantitative values for kidney preneoplastic lesions and renal cell adenoma. It is suggested that the cytotoxic effects of these chemicals preferentially suppressed the proliferation of preneoplastic liver cells, but stimulated the mitotic activity of preneoplastic tubular lesions in the kidney.
Carcinogenesis 1987 Sep
PMID:Reciprocal modifying effects of isomeric forms of aminophenol on induction of neoplastic lesions in rat liver and kidney initiated by N-ethyl-N-hydroxyethylnitrosamine. 362 66

Toxicology and carcinogenesis studies of isophorone were conducted by administering 0, 250, or 500 mg/kg body weight per day by gavage in corn oil to groups of 50 F344/N rats and 50 B6C3F1 mice of each sex, 5 days/week, for 103 weeks. Dosed male rats developed proliferative lesions of the kidney including hyperplasia, adenoma, and adenocarcinoma of the renal tubule, and epithelial hyperplasia of the renal pelvis. Non-proliferative kidney lesions observed in dosed male rats included mineralization, and a more severe nephropathy in low dose animals than in controls or high dose animals. Carcinomas of the preputial gland occurred in high dose male rats. No isophorone-related lesions were observed in female rats. In male mice, isophorone exposure may have been associated with an increase in hepatocellular neoplasms and mesenchymal neoplasms of the integumentum in high dose animals, and with a marginally increased incidence of lymphoma in low dose male mice. In mice, no non-neoplastic lesions in males or females, or neoplastic lesions in females were considered associated with isophorone administration.
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PMID:Toxicology and carcinogenesis studies of isophorone in F344 rats and B6C3F1 mice. 370 84

5-(2-Pyrazinyl)-4-methyl-1,2-dithiol-3-thione (Oltipraz) was studied for its capacity to inhibit carcinogen-induced neoplasia in female ICR/Ha mice. When administered by oral intubation 48 h prior to benzo[a]pyrene (BP), also given by oral intubation, Oltipraz inhibited the occurrence of pulmonary adenomas and tumors of the forestomach. The ratio of the number of tumors occurring in the mice receiving Oltipraz to that of the corresponding controls was: lung, 0.36 and forestomach 0.38. Inhibition also occurred when Oltipraz was given p.o. 24 h prior to BP. In other experiments, oral administration of Oltipraz 48 h prior to p.o. administration of diethylnitrosamine or uracil mustard inhibited pulmonary adenoma formation but to a lesser extent than with BP as the carcinogen. The low toxicity of Oltipraz found previously, coupled with evidence of protective effects against chemically diverse carcinogens, suggests that this compound should be studied further for its possible use as an agent for the chemoprevention of neoplasia.
Carcinogenesis 1986 Aug
PMID:Inhibitory effects of 5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione (Oltipraz) on carcinogenesis induced by benzo[a]pyrene, diethylnitrosamine and uracil mustard. 373 91

Mottled yellow Avy/A and agouti A/a (C3H x VY) F-1 hybrid male mice were fed untreated control diet or diet with a target dose of 500 p.p.m. sodium phenobarbital (PB) for 17-19 months. No differences in prevalence of hepatocellular adenomas or carcinomas were found between untreated yellow and agouti mice. PB treatment increased prevalence of adenomas but decreased prevalence of carcinomas. No difference in enhancement of adenoma formation by PB was observed between yellow and agouti mice bearing single adenomas. However, the proportion of PB-treated yellow mice bearing multiple adenomas (66%) was much greater than the proportion of analogous agouti mice (18%). Fatty changes in the periportal area of the liver and focal cytoplasmic vacuolization were induced to a much greater extent in PB-treated yellow mice than among treated agoutis. PB increased the prevalence and severity of focal areas of chronic inflammation in the liver considerably more in agouti than in yellow mice. The possible relation of this finding to the altered immune responses of obese yellow mice remains to be determined. The results of this study suggest that the use of yellow Avy/A and agouti A/a (C3H x VY) F-1 hybrid mice in carcinogenicity assays make make it possible to differentiate between weak and strong promoters as well as between promoters and complete carcinogens. Weak promoters should induce hepatocellular adenomas in yellow mice even if they fail to do so in agouti mice. Promoting substances which act similarly to PB may be identified in this system by simultaneously increasing adenoma prevalence and decreasing carcinoma prevalence. Complete carcinogens should increase carcinoma prevalence in the yellow mice even at low dose levels.
Carcinogenesis 1986 Nov
PMID:Amplified response to phenobarbital promotion of hepatotumorigenesis in obese yellow Avy/A (C3H x VY) F-1 hybrid mice. 376 39

Following 17-19 months of feeding 500 p.p.m. sodium phenobarbital (PB) in the diet to yellow Avy/A and agouti A/a (C3H X VY) F1 hybrid male mice, two subgroups differing in responsiveness to PB with respect to promotion of hepatocellular adenomas and body weight gain were observed within each genotype. In untreated mice of both genotypes, the presence of an adenoma at necropsy was associated with decreased body weight gain during this study. However, PB treatment inverted this association. In treated mice the presence of an adenoma at necropsy was preceded by a greater increase in body weight during the study than when no tumor was present. This increase in average body weight gain was more pronounced among the yellow mice (44%) than among the agouti mice (21%). Among yellow mice PB treatment had no effect on body weight gain unless an adenoma was present at necropsy. However, in those yellow mice in which an adenoma was found, body weight was greater than in untreated yellow controls throughout the study beginning at week 27. The mean body weight curve of treated yellow mice bearing one adenoma was slightly higher than that of treated yellow mice in which no adenoma was found. The mean body weight curve of treated yellow mice bearing multiple adenomas was significantly higher than those of yellow mice with no or only one adenoma.
Carcinogenesis 1986 Nov
PMID:Susceptible and resistant subgroups in genetically identical populations: response of mouse liver neoplasia and body weight to phenobarbital. 376 43

The skin and lung tissues from SENCAR mice used as part of the Environmental Protection Agency's (EPA's) Carcinogenesis Testing Matrix were examined. This study included SENCAR mice used in three different short-term bioassay protocols in which the skin papilloma assay was used to identify initiators, promoters, and complete carcinogens. Also included were the pathology findings from SENCAR mice used in the combined bioassay in which the skin assay and the lung adenoma assay were conducted simultaneously. The gross and microscopic features of treatment-associated and spontaneous lesions of the skin and lung of the SENCAR mouse used in these studies are defined and the lesions most commonly observed are described. Generally, gross observations and microscopic findings in both the skin and lung tissues were poorly correlated. Although there are several definite criteria on which gross interpretations of the various skin and lung lesions can be made, with the exception of pedunculated squamous cell papillomas and the classic squamous cell carcinomas, the various lesion types had a wide variety of clinical presentations that severely compromised the accuracy of gross diagnosis. Further, in the case of benign skin neoplasms, malignant transformation of these tumors most often occurred at the base of the lesion and was initially hidden from gross observation. As a result, approximately 50% of the neoplasms interpreted clinically as benign tumors (papillomas and keratoacanthomas) were actually malignant neoplasms. Moreover, many lesions determined grossly to be nontumorous were in fact found to be neoplastic when examined microscopically. The SENCAR mouse was found to be more responsive in the lung adenoma assay than other strains examined with exception of the Strain A. Although accurate interpretation of the lung lesions in the SENCAR was compromised by nonneoplastic treatment-associated and/or spontaneous lesions, the feasibility of using the SENCAR skin and lung as target tissues in two-stage combined carcinogenesis studies merits further consideration.
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PMID:Gross and microscopic lesions in the female SENCAR mouse skin and lung in tumor initiation and promotion studies. 378 Jun 37


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