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)

Adrenocortical adenoma, nodular hyperplasia, or carcinoma was diagnosed in 50 ferrets. Thirty-five (70%) ferrets were female and 15 (30%) were male. The mean age at which clinical signs were first noticed was 3.4 years (range, 1 to 7 years). Clinical signs included large vulva (n = 31; 89% of females), alopecia (n = 43; 86%), pruritus (n = 20; 40%), and increased consumption of water and increased urine output (n = 4; 8%). A mass was palpated at the cranial pole of the kidney during physical examination of 17 (34%) ferrets. Ultrasonography, performed on 39 of 50 ferrets, revealed a unilateral adrenal gland mass in 19 (49%). Four ferrets were anemic, and 2 ferrets were thrombocytopenic. Baseline plasma concentrations of cortisol and corticosterone were within or below the reference range in all 17 ferrets tested, whereas baseline plasma estradiol concentrations were high in 4 of the 11 ferrets (36%) tested. AFter adrenocorticotropic hormone (ACTH) administration, only 1 ferret had a slightly exaggerated response on the basis of plasma cortisol concentrations, and all 17 had normal responses on the basis of plasma corticosterone concentrations. There was little or no increase in plasma estradiol concentrations after ACTH administration. Of the 50 ferrets, 39 were treated by adrenalectomy. Unilateral adrenalectomy was performed in 34 ferrets in which 1 adrenal gland was large, whereas subtotal bilateral adrenalectomy was performed in 5 ferrets with bilateral adrenal disease. Five ferrets died in the immediate postoperative period, and follow-up information was available for the remaining 34, 1 to 34 months after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperadrenocorticism associated with adrenocortical tumor or nodular hyperplasia of the adrenal gland in ferrets: 50 cases (1987-1991). 840 89

Ca2+ and Ca(2+)-binding proteins are involved in running the cell cycle. Ca2+ spikes and signals from integrin-activated focal adhesion complexes and Ca2+ receptors on the cell surface along with cyclic AMP begin the cycle of cyclin-dependent protein kinases (PKs). These transiently expressed PKs stimulate the coordinate expression of DNA-replicating enzymes, activate replication enzymes, inactivate replication suppressors (e.g., retinoblastoma susceptibility protein), activate the replicator complexes at the end of the G1 build-up, and when replication is complete they and a Ca2+ spike trigger mitotic prophase. Another Ca2+ surge at the end of metaphase triggers the destruction of the prophase-stimulating PKs and starts anaphase. Ca2+ finally stimulates cytoplasmic division (cytokinesis). However, Ca2+ does more than this in epithelial cells, such as those lining the colon, and skin keratinocytes. These cells also need Ca2+, integrin signals, and only a small amount (e.g., 0.05-0.1 mM) of external Ca2+ to start DNA replication. Signals from their surface Ca2+ receptors trigger a combination of differentiation and apoptosis ("diffpoptosis") when external Ca2+ concentration reaches their setpoints. The skin's steep, upwardly directed, Ca2+ gradient has a low concentration in the basal layer to allow stem and precursor keratinocytes to proliferate, and higher concentrations in the suprabasal layers to trigger the differentiation-apoptosis ("diffpoptosis") mechanism that converts granular cells into protective, hard-shelled, dead corneocytes. A similar Ca2+ gradient may exist in the colon crypt allowing the stem cell and its amplifying transit or precursor offspring to cycle in the lower parts of the crypt, while stopping proliferation and stimulating terminal differentiation in the upper crypt and flat mucosa. Raising the amount of Ca2+ in fecal water above a critical level reduces proliferation and thus colorectal carcinogenesis in normal rats and some high-risk humans. But during carcinogenesis the Ca2+ sensors malfunction or their signals become ineffective: high Ca2+ does not stop, and may even stimulate, the proliferation of initiated mutants. Therefore, Ca2+ may either not affect, or even promote, the growth of epithelial cells in carcinogen-initiated rat colon and human adenoma patients. Clearly, a much greater understanding of how Ca2+ controls the proliferation and differentiation of epithelial cells and why initiated cells lose their responsiveness to Ca2+ are needed to assess the drawbacks and advantages of using Ca2+ as a chemopreventor.
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PMID:Calcium-cell cycle regulator, differentiator, killer, chemopreventor, and maybe, tumor promoter. 853 13

Parathyroid glands (n = 271) removed from 130 patients were examined by light and electron microscopy. A standardized method of tissue processing was employed and morphometry was performed. The aim of the paper is to provide a description of the human parathyroid chief cell ultrastructure in health and disease, with quantitative evaluation of structures involved in secretion of parathyroid hormone in a large case series, and to discuss their role in current diagnostic histopathology. The patients were euparathyroid (n = 10), or affected by primary (n = 97), secondary (n = 8), or tertiary (n = 15) hyperparathyroidism. In normal glands, solid parenchyma was composed of chief cells, large clear cells, transitional-oxyphil cells, and oxyphil cells. Chief cell hyperplasia, pseudo-adenomatous hyperplasia, adenoma, water-clear cell hyperplasia, and carcinoma were the most usual forms of parathyroid disease responsible for primary hyperparathyroidism. In chief cell hyperplasia, all the parathyroid glands were enlarged and the chief cells were in an active state of hormone secretion, with a large Golgi complex, abundant rough endoplasmic reticulum (RER), small lipid droplets, and tortuous plasma membrane. In pseudo-adenomatous hyperplasia, one gland was enlarged and the others displayed a normal size; however, electron microscopic examination and morphometric analysis showed that all the glands had active cells. Adenomas displayed a pattern similar to those of pseudo-adenomatous hyperplasia, with one gland enlarged and the others of normal size. However, ultrastructural examination and morphometry showed that the normal-size glands were hypo-active. Water-clear cell hyperplasia showed cells filled with cytoplasmic vacuoles. In these cells, structures with intermediate features between secretory granules and vacuoles were visible. Nucleo-cytoplasmic atypias were frequently visible in parathyroid carcinoma cells. In secondary and tertiary hyperplasia, active chief cells were regularly mixed with oxyphil or transitional-oxyphil cells. The tertiary hyperplasia was characterized by RER-associated structures that were not found in the normal or other pathological conditions. These results demonstrate that electron microscopy and morphometry represent useful tools in parathyroid histopathology.
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PMID:Ultrastructure of human parathyroid cells in health and disease. 858 May 10

Susceptibility to lung carcinogens and genetic changes in neoplastic lesions were investigated in transgenic mice carrying a human hybrid c-Ha-ras gene, encoding a prototype p21 gene product. Nine-week-old male and female transgenic mice and non-transgenic littermates were injected i.p. with 6-nitrochrysene (6NC) three times biweekly or administered urethane in their drinking water for 3 weeks. Control mice were given dimethylsulfoxide (DMSO), the solvent for 6NC, alone. The incidences of lung adenocarcinomas were four out of seven female (57%) transgenic mice treated with 6NC and three out of three males (100%) and three out of three females (100%) receiving urethane. No adenocarcinomas were observed in control animals or non-transgenic mice. Adenomas developed in all treated groups, but the incidence and multiplicity were higher in transgenic animals than in their non-transgenic counterparts. In the 6NC-treated group, forestomach papillomas and squamous cell carcinomas were also observed in both male (25 and 50%) and female (56 and 33%) transgenic mice. PCR-SSCP and DNA sequence analysis of these induced lesions revealed point mutations at codon 61 of transgenic human c-Has-ras, from CAG (Gln) to CTG (Leu) or CAG (Gln) to AAG (Lyn) in lung hyperplasias (two out of three), an adenoma (one out of two), adenocarcinomas (five out of seven) and forestomach squamous cell carcinomas (four out of five). Mutations were not observed in forestomach papillomas. No changes in mouse Ha-ras or Ki-ras were found in any lesions. Furthermore, p21 overexpression was not evident in lung or forestomach tumors on immunohistochemical analysis. These findings indicate a high sensitivity to lung carcinogens in transgenic mice carrying the human c-Ha-ras gene and that this might be effected by mutational activation.
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PMID:Chemically induced lung and forestomach neoplasias in transgenic mice carry mutant forms of the human c-Ha-ras transgene. 862 61

Phenethyl isothiocyanate (PEITC), which occurs in certain cruciferous vegetables, was tested for its ability to inhibit lung tumorigenesis in rats induced by the tobacco-specific nitrosamine 4-(methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK) in a study involving virtually lifelong administration of both compounds. In addition, two biomarkers of NNK metabolism [4-hydroxy-1-(3-pyridyl)-1-butanone-releasing hemoglobin adducts and 4-(methylnitrosamino-1-3-pyridyl-1-butanol and its glucuronide in urine] were quantified in randomly selected rats during the course of the study. The rats were assigned to groups as follows: NNK, 2 ppm in drinking water, 60 rats; NNK, 2 ppm in drinking water and PEITC, 3 micromol/g NIH-07 diet, 60 rats; PEITC, 3 micromol/g NIH-07 diet, 20 rats; and untreated controls, 20 rats. NNK was added to the drinking water for 111 weeks and PEITC to the diet for 1 prior to NNK administration and then throughout the 111-week course of treatment. There were no significant differences in body weights or survival among the groups. There were no significant effects of PEITC on blood chemistry or hematology. NNK induced lung tumors (adenoma and/or adenocarcinoma) in 70% of the rats. In the group treated with NNK plus PEITC, 5% of the rats had lung tumors, which was not different from that of control rats. PEITC also appeared to inhibit progression of benign to malignant pancreatic tumors. At intervals during the study, blood was withdrawn from selected rats, and 4-hydroxy-1-(3-pyridyl)-1-butanone-releasing hemoglobin adducts, which are formed upon metabolic activation of NNK, were quantified. The hemoglobin adducts were significantly repressed throughout the study in the rats treated with NNK plus PEITC compared to those treated with NNK. The 24-h urine sample of several rats was analyzed for 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol glucuronide. A 4-6-fold increase in the sum of these metabolites was observed in the rats treated with NNK plus PEITC compared to those treated with NNK. This is also consistent with inhibition of metabolic activation of NNK by PEITC. Collectively, the results of this study provide strong evidence for the efficacy of PEITC as a chemopreventive agent against NNK-induced pulmonary carcinogenesis in rats and indicate that two biomarkers of NNK metabolism, measurable in tobacco consumers, can be modulated in a predictable way by PEITC administration.
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PMID:Complete inhibition of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced rat lung tumorigenesis and favorable modification of biomarkers by phenethyl isothiocyanate. 882 68

Effect of high- and low-fat diets on gastric stump carcinogenesis was experimentally investigated. A total of 130 Wistar male rats weighing 250-300 g received either sham operation or Billroth II partial gastrectomy, the resection of the distal two-thirds glandular stomach and reconstruction of gastro-jejunostomy. After surgery, each group of rats was switched from a standard diet (CRF-1) to a special diet containing either 15% soybean oil (high-fat) or 0.5% soybean (low-fat), fed ad libitum and tap water, and were killed 50 weeks after surgery. Gastric tumours were observed only in the animals that underwent gastrectomy while no tumours were detected in the animals following the sham operation. Tumours located invariably at the gastrojejunostoma, were carcinomas or adenomas in histology. Carcinomas developed in 12 of 29 gastrectomy animals (41%) fed the high-fat diet and 4 of 27 gastrectomy animals (15%) fed the low-fat diet. The difference was significant (P < 0.05). The incidence of adenoma was also significantly higher in the gastrectomy animals fed the high-fat diet (38%) than that in those fed the low-fat diet (15%) (P < 0.05). A daily faecal output of bile acids was significantly greater in the gastrectomy animals fed the high-fat diet (19.0 +/- 16.4 micromol/day) than that in those fed the low-fat diet (11.2 +/- 6.2 [micromol/day; P < 0.05). This study suggests that increased fat intake is associated with a high risk of gastric stump carcinoma.
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PMID:Positive association between dietary fat intake and risk of gastric stump carcinoma in rats. 882 9

This study examined the effects of 6-phenylhexyl isothiocyanate (PHITC) on lung tumorigenesis in F344 rats induced by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Two biomarkers of NNK metabolism, 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB)-releasing hemoglobin adducts and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronide (NNAL-Gluc) in urine, were also quantified during the course of the tumor induction experiment. Rats were divided into groups as follows: (1) NNK, 2 p.p.m. in drinking water, 60 rats; (2) NNK, 2 p.p.m. in drinking water and PHITC, 1 micromol/g NIH-07 diet, 60 rats; (3) PHITC, 1 micromol/g NIH-07 diet, 20 rats; (4) control, 20 rats. PHITC was added to the diet for 1 week prior to and during 111 weeks of NNK treatment. There were no effects of PHITC on body weight, mortality, blood chemistry or hematology. Seventy percent of the rats treated with NNK had adenoma or adenocarcinoma of the lung. In the rats treated with NNK plus PHITC, the total percent incidence of lung tumors was 26% (P < 0.01 compared with NNK). PHITC had no effect on the total incidence of exocrine pancreatic tumors induced by NNK. The rats treated with PHITC and NNK had significantly lower levels of HPB-releasing hemoglobin adducts throughout the course of the bioassay than did those treated with NNK alone and significantly higher levels of NNAL plus NNAL-Gluc excreted in urine at two time points during the bioassay. These results demonstrate that near lifetime administration of PHITC to rats strongly inhibits the metabolic activation and lung tumorigenicity of NNK.
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PMID:Inhibitory effects of 6-phenylhexyl isothiocyanate on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone metabolic activation and lung tumorigenesis in rats. 882 35

Modifying effects of chlorophyllin (CHL) on the diethylnitrosamine (DEN)-phenobarbital (PB) hepatocarcinogenesis model were examined in rats. Five-week-old male F344 rats were divided into 8 groups. Groups 1 through 5 were given i.p. injections of DEN (100 mg/kg body weight) once a week for 3 weeks beginning one week after the start of the experiment, while groups 6 through 8 received vehicle treatment. Groups 1, 2, 3 and 7 received drinking water with 500 ppm PB from one week after the end of carcinogen or vehicle treatment. CHL-containing diet (2000 ppm) was given to group 2 during the initiation phase and to groups 3 and 5 during the promotion and the post-initiation phase, respectively. Group 6 was given the experimental diet alone throughout the experiment (24 weeks). Liver neoplasms were present in DEN-treated groups and PB treatment promoted liver tumorigenesis. The incidences of adenoma in groups 2 and 3 were significantly smaller than in group 1 (P<0.05 and P<0.02), although the reductions in the incidences of liver cell cancer were not significant. The average numbers of liver neoplasms/rat in group 2 were significantly smaller than in group 1 (P<0.05-P<0.005). Glutathione S-transferase placental form-positive foci were also significantly decreased by CHL treatment (P<0.05 and P<0.001). DEN and PB exposure increased liver ornithine decarboxylase activity and this increase was significantly inhibited by feeding of CHL during the initiation phase (P<0.001). These results suggest that CHL is a chemopreventive agent for liver neoplasia.
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PMID:Inhibitory effect of chlorophyllin on diethylnitrosamine and phenobarbital-induced hepatocarcinogenesis in male F344 rats. 895 62

Disease development in flounder (Platichthys flesus) was studied over a period of 3 years in three large mesocosms (40 m x 40 m x 3 m). Two of the mesocosms contained clean sand and the third, sharing a common water circulation with one of the clean-sand mesocosms, was stocked with contaminated dredged spoil. In this way, one of the clean-sand mesocosms was indirectly polluted via the water phase, and analysis of contaminant concentrations in sediments and flounder tissues showed that it had a status intermediate between the other two. Random samples of the flounder populations from the indirectly polluted and reference mesocosms were examined every 2 months for epidermal diseases (lymphocystis, skin ulcers, fin rot) and then released. In addition, every 6 months, random samples of fish from all three mesocosms were sacrificed for histological and chemical investigation. With regard to the development of epidermal disease, the results showed little difference between the reference mesocosm and the indirectly polluted mesocosm, with the exception that lymphocystis was significantly elevated in the indirectly polluted mesocosm. Although pollution may be a risk factor in the etiology of this disease, such a relationship would probably be obscured under field conditions due to variation arising from other factors. Histopathological analysis of the livers revealed in total four cases of hepatocellular adenoma (1.5% of sampled population) in fish from the polluted mesocosms, the first occurring after 2.5 years of exposure in fish from the indirectly polluted mesocosm. Furthermore, several other liver lesions, including foci of cellular alteration and hydropic vacuolated lesions, developed during the course of the experiment before tumor formation was apparent. Prevalences of these conditions were very much lower in the reference mesocosm than in the two polluted mesocosms. Densities of melanomacrophage centers in the liver showed a similar trend. The findings clearly indicate that long-term exposure to chemically contaminated dredged spoil can induce liver neoplasia and other liver lesions in flounder at contaminant levels comparable to those found in the natural environment.
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PMID:Skin and liver diseases induced in flounder (Platichthys flesus) after long-term exposure to contaminated sediments in large-scale mesocosms. 895 12

Oestrogen producing adrenocortical tumours are extremely rare. We report a 65-year-old woman who presented with abnormal vaginal bleeding, with no significant abnormalities in her uterus or ovaries, who was found to have a right adrenal mass by radiological examination. Excessive secretion of oestrogens from the tumour was demonstrated by adrenal venous sampling. Basal levels of corticosteroids were within normal limits. Adrenalectomy was performed and pathological examination revealed an adrenocortical adenoma measuring 5.5 cm in its greatest dimension, in which both clear and compact tumour cells were observed. Oestrogen levels normalized following the removal of the adrenal mass. Tissue concentrations of oestrone and oestradiol in the tumour were 6.9 (69.5 pmol/g wet tissue weight) and 34.6 (93.6 pmol/g wet tissue weight)-fold greater respectively than those of adjacent non-neoplastic adrenal cortex. Aromatase activity in the tumour tissue determined by the 3H-water method was 118.6 pmol/h/mg protein, equivalent to that of a full-term human placenta. Immunohistochemical analysis of aromatase demonstrated immunoreactivity in the tumour cells, especially in compact cells, but not in adjacent non-neoplastic adrenal cells. This is the first reported case of an oestrogen producing adrenocortical adenoma in which aromatase in the tumour cells was documented.
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PMID:Oestrogen producing adrenocortical adenoma: clinical, biochemical and immunohistochemical studies. 897 64


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