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)

Exocrine pancreatic neoplasms developed in the guppy Poecilia reticulata following a single brief exposure to methylazoxymethanol acetate [(MAM-Ac) CAS: 592-62-1]. Fish 6-10 days old were exposed to concentrations of MAM-Ac up to 100 mg/liter for 2 hours. Exposed specimens were transferred to carcinogen-free water and sampled periodically for tumor development. Pancreatic neoplasms occurred in approximately 9% of histologically examined individuals exposed to 10 mg MAM-Ac/liter or less. Neoplastic lesions were not found in 122 control specimens. The neoplasms included 6 cases diagnosed as adenoma, 7 cases diagnosed as acinar cell carcinoma, and 2 cases diagnosed as adenocarcinoma. Adenomas consisted mainly of well-differentiated acinar cells that were filled with zymogen granules. Two adenomas also contained foci of atypical, less-differentiated acinar cells possessing basophilic, fibrillar cytoplasm. Acinar cell carcinomas occurred in several cellular patterns that ranged from well-differentiated to more anaplastic lesions; however, none exhibited areas of ductular proliferation. Adenocarcinomas, on the other hand, exhibited a glandular growth pattern and contained numerous ductlike structures. Both types of carcinomas appear to arise from primary acinar cells. Thus lesions probably progress from adenomas to acinar cell carcinomas and adenocarcinomas. The findings of carcinogen-induced pancreatic neoplasms in guppies further strengthen the usefulness of small fish species in carcinogen testing and provide an additional model for pancreatic tumors.
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PMID:Exocrine pancreatic neoplasms induced by methylazoxymethanol acetate in the guppy Poecilia reticulata. 347 May 47

The influence of dietary selenium and cabbage on the formation of colon tumors in female Swiss mice treated with 1,2-dimethylhydrazine [(DMH) CAS: 540-73-8] was reported. Mice received a control diet (laboratory chow), the control diet plus selenium in the drinking water (1 mg/liter), or the control diet with added cabbage (12.8 g/100 g diet). They also received 8 weekly sc injections of DMH. The experiment was divided into two time periods: a) from 5 weeks before the first injection until 3 days after the last one (initiation period), and b) the subsequent 19.5 weeks until sacrifice of the mice (promotion period). Selenium had a strong protective effect when given during the initiation period; adenomas were reduced to a much greater extent than adenocarcinomas. The only effect of selenium supplementation in the promotion period was a small decrease in adenomas. Cabbage apparently had two opposing actions. It increased tumor incidence, particularly adenocarcinomas, if given in the initiation period, but it reduced adenoma formation considerably when given in the promotion period.
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PMID:Selenium and cabbage and colon carcinogenesis in mice. 347 39

Female Swiss mice were exposed to sodium arsenite or sodium aresenate in the drinking water for 15 weeks at concentrations ranging from 0 to 100 micrograms/mL arsenic content. After three weeks of the 15 week exposure period, the mice were administered urethan (1.5 mg/g) intraperitoneally. Pulmonary adenoma formation was evaluated 12 weeks later. Arsenic exposure produced a protective effect with respect to tumor development. Both forms of arsenic reduced the size and number of pulmonary adenomas observed per mouse. In addition, urethan-induced sleeping times which reflect the rate of urethan metabolism or excretion remained unchanged. This suggests that arsenic exposure does not alter urethan excretion and is not a factor influencing subsequent adenoma formation of these levels of exposure.
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PMID:The effect of arsenic on urethan-induced adenoma formation in Swiss mice. 360 54

Female Swiss were exposed to sodium selenite (3 micrograms/ml selenium content) and sodium arsenate (80 micrograms/ml arsenic content) in the drinking water individually or in combination on alternate days for 15 weeks. Comparable water consumption was observed in all individual or combined metal-exposure groups. After 3 weeks of metal exposure, the mice were administered urethan (1.5 mg/g) intraperitoneally. Pulmonary adenoma formation was evaluated 12 weeks later. Arsenic exposure reduced the tumor incidence (P = 0.0046) and tumor size (P less than 0.0001). Selenium exposure did not alter the tumor incidence but caused a reduction in tumor size (P = 0.022). No selenium-arsenic interactions associated with tumor size or number were observed. Urethan-induced sleeping times were unaffected by exposure to selenium (P = 0.832) or arsenic (P = 0.42), although combined metal exposure reduced the duration of urethan-induced sleep (P = 0.029) as compared to the individual metal exposures. This metal-metal interaction, which appeared to enhance the rate of urethan elimination as indicated by the reduced sleeping time, did not influence adenoma formation significantly.
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PMID:Alterations in urethan-induced adenoma formation in mice exposed to selenium and arsenic. 360 32

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.
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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

Chronic exposure to phenobarbital (PB) in the drinking water of male B6C3F1 mice starting at 4 weeks of age and subsequent to a single (ip) injection of diethylnitrosamine (DENA) administered on Day 15 of age has been shown to result in the inhibition of hepatic tumor formation. In this study, we varied the time of onset of PB administration to determine if sexual maturity would affect liver tumor formation and progression. Male B6C3F1 mice were divided into eight groups. Groups 1-4 received a single (ip) dose of 5 mg/kg DENA at 15 days of age while mice in groups 5-8 received saline. At weaning (4 weeks of age), groups 1 and 5 received deionized drinking water (DDW) for 24 weeks; groups 2 and 6 received PB (500 ppm) in the drinking water (PB DW) for 16 weeks followed by DDW for 8 weeks; groups 3 and 7 received DDW for 4 weeks, PB DW for 16 weeks, and then DDW for 4 weeks; and groups 4 and 8 received DDW for 8 weeks and PB DW for 16 weeks. Mice were killed at 28 weeks of age and hepatic lesions were evaluated. Mice which did not receive DENA (groups 5-8) exhibited no liver tumors. Animals in groups 1-4 exhibited hepatocellular foci and adenomas. PB treatment in groups 2, 3, or 4 resulted in a significant decrease in the incidence of DENA-initiated hepatocellular foci and adenomas when compared to those observed in group 1. The number of foci in group 4 was significantly decreased compared to those in groups 2 and 3. There was no significant difference in the adenoma incidence among groups 2, 3, and 4. No significant differences were observed in the sizes of foci or adenomas among groups 1-4. Data from this study suggest that the inhibition of hepatocellular tumorigenesis by PB remains intact even when the start of the administration of PB is withheld up to 12 weeks of age.
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PMID:Effect of the age of B6C3F1 mice on phenobarbital promotion of diethylnitrosamine-initiated liver tumors. 362 93

Of 15 patients with primary aldosteronism, 7 had idiopathic adrenal hyperplasia (IHA) and 8 had aldosterone-producing adenoma (APA). In order to determine any renal problems involved in the treatment, the renal clearance of these patients was analyzed and the results compared with those obtained from 12 patients with essential hypertension. With water diuresis or under antidiuresis status, levels of urine volume, Cosm and CH2O in patients with APA were greater (p less than 0.05-p less than 0.001) than those of patients with essential hypertension, while the fractional tubular sodium delivery of the former patients was lower than that of the latter patients (p less than 0.001 or less than 0.05). A similar tendency was observed in clearance studies in patients with IHA, although to a lesser extent. Adrenal surgery for patients with APA normalized these values, but administration of trilostane (3 beta-hydrosteroid dehydrogenase inhibitor) to patients with IHA failed to improve these values. These results indicate that impaired urinary concentrating ability as well as reduced urinary diluting capability is a common feature of primary aldosteronism. Such impaired renal function was improved only in patients with APA after adrenal surgery.
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PMID:Evidence for a defect in urinary concentrating ability in primary aldosteronism and its reversal by adrenal surgery. 367 60

We have studied the postoperative diuresis patterns in 116 patients following the removal of a pituitary adenoma using the trans-sphenoidal approach. We observed a normal diuresis (ND) in 55 patients and a hypotonic polyuria (HP) in 61 patients, consisting of water elimination (WE = 45 cases) and transient diabetes insipidus (DI = 16 cases). We investigated the problem of predicting these patterns from eight pre-operative factors by applying stepwise logistic discriminant analysis. We demonstrated that DI was significantly associated with a posterior localization of the adenoma in the pituitary gland and that WE was more frequently observed in cases of suprasellar expansion, in young patients, and in prolactin secreting tumors. Finally, we discuss the pathogenic role of these factors in the occurrence of HP, taking into account inhibition of vasopressin secretion and possible fluid overload.
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PMID:Study of hypotonic polyuria after trans-sphenoidal pituitary adenomectomy. 370 Aug 41

We present here a series of seven children with primary hyperparathyroidism caused by parathyroid adenoma. Chief cells were the primary element in six patients and water-clear cells in one patient. A brief review of the literature on primary hyperparathyroidism in children is included. Emphasis is placed on the clinical characteristics of this rare disease in children.
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PMID:Primary hyperparathyroidism in children. 371 90

Coal tar paints are among the products used as inside coatings for water pipes and storage tanks to retard corrosion in potable water supply systems. Four different formulations of these paints were tested in earlier work by this laboratory in the Ames mutagenesis and the mouse skin carcinogenesis bioassays. The paint most active in these assays were then tested in a particulate form in the lung adenoma assay with A/J mice. The paint was applied to clean glass plates, cured, collected and homogenized in 2% Emulphor. Doses of this coal tar suspension were administered by gavage at 1.0, 10.0 and 55.0 mg in 0.2 ml per mouse 3X weekly for 8 weeks. The total doses of coal tar paint were 24, 240, and 1320 mg/mouse. Benzo[a]pyrene (BaP), administered in a parallel schedule to a total dose of 6 mg/mouse, served as positive control. A negative control group received an equivalent volume of 2% Emulphor. Animals were killed at 9 months of age (8 months after first dose) and lung adenomas counted. A dose-related response, in the average number of lung tumors per mouse, was observed with the coal tar particulate. There were also squamous cell tumors of the forestomach in 42% of the mice receiving 55.0 mg coal tar paint per application.
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PMID:Carcinogenic effects in A/J mice of particulate of a coal tar paint used in potable water systems. 380 69


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