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

Syrian golden hamsters were fed four diets in experiments designed to evaluate the effects of the interaction of dietary fat and protein on carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine [(BOP) CAS: 60599-38-4]. The diets consisted of two levels of dietary fat [4.5 g (low fat, LF) or 18 g (high fat, HF) of corn oil/385 kilocalories (kcal)]. These levels were fed with each of two levels of dietary protein [9 g low-protein (LP) and 36 g high-protein (HP) casein/385 kcal]. The four diets were fed to two separate groups of hamsters at two different periods in their life-span. For testing of the effects of diet on tumor initiation, one group received the diets from 3 to 7 weeks of age. At 8 weeks, they were given injections sc of 10 mg BOP/kg body weight and placed on a control diet [9 g corn oil (medium fat) and 18 g casein (medium protein)/385 kcal]. The other group received control diet until 8 weeks of age, at which time they were given injections of BOP and placed on the four diets. This group was designed to test the effects of the diets on tumor development. BOP-induced lesions in the lungs, liver, common bile duct, gallbladder, and kidneys are described; results in the pancreas were reported separately. In hamsters fed the four diets after BOP treatment, the LF-LP groups had the fewest tumors, the LF-HP-fed and HF-LP-fed groups had intermediate yields of tumors, and the hamsters given HF-HP diet exhibited the largest numbers of neoplasms. Several specific tumor types showed a similar pattern. For example, the pulmonary adenoma incidence, which was low in the non-BOP-treated hamsters, was higher in the HF-HP group than in those fed LF-HP diet after BOP, but it was not influenced by fat at the LP level. In addition, renal adenomas were observed at a low incidence in non-BOP-treated hamsters and in hamsters fed LF-LP levels before or after BOP treatment (0.5% incidence) but were present at an 8% incidence in all other BOP-treated groups. The incidence of biliary cystic adenomas was highest in male hamsters that received HF diets, irrespective of BOP treatment, and BOP treatment resulted in increased yields of this lesion in females only in groups given HF-LP diet.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of the interaction of dietary fat and protein on N-nitrosobis(2-oxopropyl)amine-induced carcinogenesis and spontaneous lesions in Syrian golden hamsters. 385 80

Syrian hamsters were given in a single dose of N-nitrosobis(2-oxopropyl)-amine (BOP) (40 mg/kg, s.c.) and 1 week later were fed 1 of 4 retinoid types (13-cis-retinoic acid (13-cis-RA), N-ethylretinamide (ERA), 2-hydroxyethylretinamide (OH-ERA), or 4-hydroxyphenylretinamide (PRA)) each at 3 levels (0.05, 0.1, 0.2 mM/kg diet). The pancreatic carcinoma incidence was not influenced significantly by feeding retinoids. The pancreatic adenoma incidence, however, was reduced by feeding each of the retinoids to female hamsters, with the reduction varying with the retinoid fed (13-cis-RA greater than ERA and OH-ERA greater than PRA). In male hamsters increased numbers of pancreatic adenomas were observed after feeding OH-ERA and PRA. Tumors induced in other tissues were reduced by retinoids in females, but not in males. Females fed 13-cis-RA and ERA had a lower incidence of gall bladder polyps, and feeding OH-ERA reduced the liver tumor incidence. Food consumption and serum alkaline phosphatase ans aspartate amino transferase activities were not influenced by BOP or retinoid type or level. Body and pancreas weight were influenced by retinoid level, but the effects were not consistently dose-related.
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PMID:Sex differences in the effects of retinoids on carcinogenesis by N-nitrosobis(2-oxopropyl)amine in Syrian hamsters. 645 85

The effects of dietary fat on carcinogenesis were presented, with the pancreas excluded, in randombred Syrian golden hamsters after administration of N-nitrosobis(2-oxopropyl)amine (BOP). Diets containing 4.5, 9, or 18 g corn oil/385 kilocalories [low-fat (LF), medium-fat (MF), or high-fat (HF) diet, respectively] were fed in two sequences. In the first sequence during which the effects of fat on the initiation phase of BOP carcinogenicity were examined, LF or HF diets were fed to hamsters 3-7 weeks of age and for 2 days after a single sc BOP treatment (10 mg/kg body wt) to 8-week-old hamsters. These hamsters were then given MF diet for the remainder of their lives. In the second sequence during which the role of fat on the promotional phase (development) of BOP-induced cancer was evaluated, MF diet was fed during the weeks preceding BOP treatment and LF or HF levels were given after BOP treatment. Separate groups were fed MF diet throughout both phases, and parallel animal groups received each diet sequence and were treated with saline at 8 weeks of age. Renal adenocarcinomas in males were observed only in those given HF diet either before or after BOP treatment (9% incidence). Similarly, pulmonary adenoma and intraphepatic biliary cystic adenoma (cholangioma) incidences were elevated above spontaneous rates in HF-fed groups. This study demonstrated that dietary fat enhanced BOP-induced tumorigenesis in the kidneys, lungs, and liver when fed, either during initiation (preceding carcinogen treatment) or at promotional stages (following carcinogen treatment).
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PMID:Increased tumorigenesis induced by N-nitrosobis(2-oxopropyl)amine in Syrian golden hamsters fed high-fat diets. 657 83

Syrian hamsters were treated with either a low (10 mg/kg body weight) or high (40 mg/kg body weight) single dose of bis(2-oxopropyl)nitrosamine (BOP) and beginning 1 week later fed either low (0.2 mmol/kg diet) or high (0.4-1.0 mmol/kg diet) levels of one of four retinoids [13 cis retinoic acid (13-cis-RA), N-ethylretinamide (ERA), N-(2-hydroxyethyl)retinamide (OHERA) or N-(phenyl)retinamide (PRA)] for periods of 40 or 50 weeks. The high retinoid levels (0.4-1.0 mmol/kg diet) fed following the highest BOP treatment enhanced pancreatic carcinoma yields (average number/effective animal) in males fed all four retinoids, and in females fed ERA and 13-cis-RA. Enhanced adenoma yields were also seen in all groups when high retinoid levels were fed following 40 mg BOP/kg body weight. However, these retinoid levels caused an increased adenoma yield in male hamsters only and did not modify carcinoma yields when fed following 10 mg BOP/kg body weight. Similarly, tumor yields at extra-pancreatic sites were elevated in retinoid-fed hamsters of both sexes after 40 mg BOP/kg body weight and in males fed ERA and 13-cis-RA after 10 mg BOP/kg body weight when retinoids were given at the high levels (0.4-1.0 mmol/kg diet). Increased incidences of bile duct and liver tumors in particular were found in hamsters given 40 mg BOP/kg body weight. Consumption of retinoid levels of 0.4 mmol/kg diet and above was also associated with a high incidence of liver cell necrosis, ovarian cysts and ovarian hemorrhage. Retinoids (ERA, OHERA, and PRA) fed at the low level (0.2 mmol/kg diet) following the low BOP dose did not enhance carcinogenesis in the pancreas or at other sites and did not cause alterations in morphologic observations.
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PMID:Lack of inhibition by retinoids of bis(2-oxopropyl)nitrosamine-induced carcinogenesis in Syrian hamsters. 657 72

ICR mice were given four subcutaneous injections of bis(2-oxopropyl)nitrosamine (BOP) 10, 20 and 40 mg/kg body weight, respectively, on day 1, 8, 15 and 22 of age. Animals treated with BOP developed mainly tumors of the lung, liver, nasal cavity, and pancreas. Lung tumors were histologically alveolar cell adenoma or adenocarcinoma at an incidence of 41-100%, hepatocellular adenoma or carcinoma 59-96%, adenoma or adenocarcinoma of the nasal cavity 11-26%, and pancreatic acinar cell adenoma or anaplastic carcinoma 3-7%. No sex difference in response to BOP carcinogen was observed.
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PMID:Tumor induction in mice administered neonatally with bis(2-oxopropyl)nitrosamine. 773 18

Binding of a specific antibody to proliferating cell nuclear antigen (PCNA) and staining of argyrophilic proteins associated with nucleolar organizer regions (AgNORs) were investigated in proliferative lesions induced by N-nitrosobis(2-oxopropyl)amine (BOP) in the hamster kidney. Thirty male Syrian golden hamsters were given three weekly s.c. injections of BOP (10 mg/kg body wt.) and sacrificed for characterization of proliferative changes 30 weeks after the first BOP treatment. Morphologically, lesions of the tubular epithelia were classified either as tubular adenoma or dysplasia, the latter being further classified into small cluster, acidophilic cell, clear cell and cystic types. Immunohistochemistry for PCNA revealed significant increases of cell proliferation activity in adenomas and acidophilic cell types of dysplasia, along with significantly elevated mean numbers of AgNORs per nucleus. The results thus indicate that the acidophilic cell type of dysplasia may be of prime significance as the preneoplastic renal lesion induced by BOP.
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PMID:Analysis of proliferative activity in renal lesions induced by N-nitrosobis(2-oxopropyl)amine (BOP) in male Syrian golden hamsters. 791 May 17

To elucidate the pathogenesis of carcinomas in the extrahepatic bile duct, we investigated the histomorphological characteristics of adenomas and early carcinomas induced in the extrahepatic bile duct of hamsters. Syrian hamsters underwent a cholecystoduodenostomy along with a dissection of the common duct, while also being administered N-nitrosobis(2-oxopropyl)amine (BOP). The tumors that arose from the extrahepatic bile duct included 10 adenomas and 55 early carcinomas in 56 of the 156 hamsters sacrificed. All the adenomas were found to be polypoid in shape. The early carcinomas, which were restricted within the mucosal layer of the bile duct, showed the following three different growth patterns: (1) protruding type in 41 (75%), consisting of 27 polypoid and 14 papillary tumors; (2) superficial spreading type in 9 (16%); and (3) periductal glandular type in 5 (9%). There were no depressed tumors observed. Carcinomas existing either alone or associated with adenomas were evident in 12 (22%) tumors, and 11 of these were polypoid. Atypical papillary hyperplasia within the tumor mass was noted in 22 early carcinomas (40%) and was particularly prominent in papillary type tumors. These results support the concept of an adenoma-carcinoma sequence in the majority of polypoid tumors of the extrahepatic bile duct. Atypical papillary hyperplasia might also be premalignant, and these precursor lesions should reflect the growth patterns of tumors, at least in the early stage of tumorigenesis.
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PMID:Experimental study on pathogenesis and histomorphology of early carcinoma of the extrahepatic bile duct in the Syrian hamster. 1627 May 35