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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of carcinoma of the sigmoid colon arising 26 years after ureterosigmoidostomy for a benign condition is presented. This is the 31st reported instance of neoplasia complicating ureterosigmoid diversion. Possible etiologic mechanisms include surgical trauma, constant irritation of the transplanted ureter, alteration of local tissue dynamics, and urine carcinogenesis.
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PMID:Neoplasia of the colon: a late complication of ureterosigmoidostomy. 126 17

Urinary bladder lesions induced by administration of thymine or melamine were investigated in male F344 rats. Animals, 6 weeks old at the beginning of the experiment, received either 3.0 or 1.0% thymine or 3.0, 1.0 or 0.3% melamine in the diet for 36 weeks followed by a 4 week period without chemicals, the total observation time being 40 weeks. Carcinomas of the urinary bladder were observed in 1/20 (5%) rats in each of the 3.0% thymine and 1.0% melamine groups, and in 15/19 (79%) animals given the 3.0% melamine treatment. Papillomas were induced in 9/20 (45%), 12/19 (63%) and 1/20 (5%) among rats receiving the 3.0% thymine, 3.0% and 1.0% melamine treatments respectively. Exploratory laparotomy at the end of week 36 revealed calculus formation in 9/10 (90%), 10/10 (100%) and 7/10 (70%) rats in these groups. In the ureter of the 3.0% melamine treated group, a carcinoma and papillomas were induced in 1/19 (5%) and 3/19 (16%) animals respectively. However, no tumors were observed in the renal pelvis in any of the other treated groups. Thus, administration of 3.0% thymine in the diet results in calculus formation in the urinary bladder of F344 rats, and is associated with development of tumors. It was also confirmed that a 3.0% dose level of melamine in the diet induces tumors in both the urinary bladder and the ureter.
Carcinogenesis 1992 Jun
PMID:Relationship between calculus formation and carcinogenesis in the urinary bladder of rats administered the non-genotoxic agents thymine or melamine. 160 Jun 9

Tissue-specific formation and short-term persistence of alkylated DNA bases have been studied immunocytochemically in Syrian hamsters and rats killed 3-48 h after a single s.c. or oral dose of N-nitrosobis(2-oxopropyl)amine (BOP). Antisera specific for O6-(m)ethylguanine and for 7-(m)ethylguanine were used. Strong nuclear staining, indicative of a high level of DNA alkylation, was observed at all time points in the intra- and interlobular duct cells and in the centroacinar cells of the hamster pancreas, the main target organ of BOP-induced carcinogenesis. Acinar cells were weakly stained for up to 24 h. In the liver, nuclear staining was strong in all cell types, and more pronounced in the periportal than in the central venous area. Both O6-alkylguanine and 7-alkylguanine preferentially disappeared from the centrilobular area of the liver which is in agreement with the high O6-methyltransferase activity of liver and the unusually high levels of 7-methylguanine DNA glycosylase activity in hamster tissues. Strong staining was observed throughout the experiment in the tubular cells of the renal cortex and in bronchiolar Clara and alveolar type II cells of the lung. The staining intensity of the cells of the thyroid follicles and of the columnar epithelial cells of the colon was moderate. In the rat, nuclear staining was strong in the nasal cavity (Bowman glands), the epithelium lining the thyroid follicles, the lung, liver and in the fibroblasts of the ureter intima and adventitia. The epithelial cell nuclei of the colon and ureter were moderately stained. In the pancreas, staining was weak in acinar, duct and islet cells; no acinar staining remained at 48 h. In the liver, nuclear staining was strong all over the lobule. O6-Alkylguanine was preferentially removed from the centrilobular area. The renal tubular cells were only weakly stained. From the present study we can conclude that--with the exception of hamster kidney and rat liver--high levels of DNA alkylation and stability of the alkylated products were related to a high tumor incidence.
Carcinogenesis 1991 Apr
PMID:Cell specific DNA alkylation in target and non-target organs of N-nitrosobis(2-oxopropyl)amine-induced carcinogenesis in hamster and rat. 201 23

In Bulgaria, the frequency of tumors of the renal pelvis and of the ureter is very high in the regions affected by Balkan nephritis. An increased frequency of these tumors is also reported in Yugoslavia, though to a lesser extent; however, these urothelial tumors are frequent in the endemic regions affected by Balkan nephritis, but a less significant frequency of cases is also noted in neighboring, non-endemic regions. The geographic distribution of these diseases of the urinary tract is studied, as well as the related issues of urothelial carcinogenesis.
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PMID:[Balkan nephropathy and urothelial cancer]. 217 57

Thyroid hormone participates in numerous cellular functions besides thermogenesis and metabolism. Several studies, including the recent identification of the product of an oncogene, c-erb-A, as a thyroid-hormone receptor, have shown possible involvement of thyroid hormone in the process of carcinogenesis. A recent anecdotal observation of an unusually high incidence of thyroid dysfunction in women with renal cell carcinoma led to a retrospective review of the incidence and distribution of thyroid disorders in women with renal cell carcinoma compared with a control group of women with transitional cell carcinoma of the renal pelvis, ureter, bladder, or urethra. Women with renal cell carcinoma had a statistically significantly higher percentage of hypothyroidism, thyroid disease in general, and the use of thyroid-hormone supplements as compared with the control group (P = 0.033, P = 0.005, P = 0.041, respectively). The nature of the relationship, however, could not be determined. These findings add a new dimension to renal cell carcinoma, and prospective studies are encouraged to define the contribution of thyroid hormone to renal cell carcinogenesis.
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PMID:Relationship of thyroid disease to renal cell carcinoma. An epidemiologic study. 235 76

A 50-year-old Japanese male hospitalized with the complaint of fever and pyohematuria. An excretory pyelography revealed the right hydronephroureter due to right ureteral stone. When the ureterolithotomy was carried out, a wide-based and rice-sized tumor co-existed at the site of the epithelium of the ureter lithotomized. Resected tumor was pathologically confirmed as poorly differentiated adenocarcinoma with mitosis. Therefore, total nephroureterectomy with bladder cuff resection was done at 10 days after the first operation. However, malignant cells were not found in the surgical specimen or histologically diagnosed localized glandular ureteritis. He is alive without any evidence of recurrence. It was reported that the glandular metaplasia, a relative rare lesion in the ureter, was correlated with carcinogenesis of adenocarcinoma in urothelium. However, when the lesion is small and localized such as in this case it should be treated with ureterectomy and addition of other suitable adjuvant therapies. Furthermore, endourological techniques which have been recently dramatically progressed may become a weapon against this lesion for both treatment and follow-up.
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PMID:[Ureteritis glandularis: a case report]. 322 51

Co-administration of uracil and N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) to weanling female Fischer rats produced uracil stones in the bladder and significantly reduced the incidence of bladder tumors. Contrary to bladder tumors, the incidence of renal pelvic and ureteric tumors was increased by this regimen. Feeding of uracil alone produced bladder tumors, in addition to the hyperplasia of renal pelvis, ureter and bladder. The mechanism of uracil's effect on FANFT carcinogenesis is not known.
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PMID:Production of urinary tract tumors by co-administration of uracil and N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide in F344 rats. 382 79

The modifying effects of 17 environmental chemicals on the development of lesions in the urinary bladder of rats with unilateral ureteric ligation were investigated. Lesions were initiated by treatment of the animals with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 2 weeks, and then test chemicals were given for 22 weeks. The lesions of the urinary bladder found were preneoplastic papillary or nodular hyperplasias (PN hyperplasias) and papillomas. Additions of sodium saccharin (5%), sodium o-phenylphenate (2%), butylated hydroxyanisole (2%), and sodium L-ascorbate (5%) to the diet had significant promoting effects on the incidences and numbers of PN hyperplasias and papillomas per 10 cm of basement membrane of the urinary bladder in this system. Sodium erythorbate (5%), ethoxyquin (0.8%) and carbazole (0.6%) significantly increased the incidence of PN hyperplasias. N-Nitrosopyrrolidine (0.02%) did not affect the incidence or number of PN hyperplasias but increased those of papillomas. Sodium o-phenylphenate also induced PN hyperplasias in rats without BBN-initiation. Ascorbic acid, ascorbic stearate, three dihydroxyphenols, methylhydroquinone, pyrogallol, quinoline, and uric acid did not show promoting activity in this test system. Thus, 8 of 17 chemicals tested had various promoting effects on urinary bladder carcinogenesis. These results show that this test system of BBN-initiated, unilaterally ureter-ligated rats should be useful for the detection of new bladder carcinogens and promoters.
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PMID:Short-term screening of promoters of bladder carcinogenesis in N-butyl-N-(4-hydroxybutyl)nitrosamine-initiated, unilaterally ureter-ligated rats. 393 81

A serum-free medium (HMRI-2) has been developed for the outgrowth and subculture of epithelial cells from normal adult human ureter and bladder. Medium HMRI-2 consists of Ham's MCDB 152 with double the amounts of the essential amino acids in Stock 1, low Ca2+ (0.06 mM) and is supplemented with epithelial growth factor, 5 ng/ml; transferrin, 5 micrograms/ml; insulin, 5 micrograms/ml; ethanolamine and phosphoethanolamine, 0.1 mM each; hydrocortisone, 2.8 X 10(-6) M; and bovine pituitary extract, 126 micrograms protein/ml. The cultured cells showed ultrastructural markers of epithelial cells (prekeratin fibers, tonofilaments, surface microvilli with glycocalyx), exhibited ABO antigens, and had a normal human diploid karyotype. Primary cultures could be subcultured and also cryopreserved in HMRI-2 in liquid nitrogen. Cells in mass cultures showed a population doubling time of 40.5 +/- 4.5 h and had a maximum in vitro life span of 20 to 25 population doublings. It was observed that primary outgrowths, secondary cultures, and even cryopreserved cells all retained the capacity to respond to high Ca2+ and serum by differentiation and desquamation. This study has resulted in the availability of easily obtainable serum-free epithelial cultures from normal adult human ureter and bladder. The useful in vitro life span of these cultures may be important in future studies of carcinogenesis.
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PMID:Selective growth of normal adult human urothelial cells in serum-free medium. 400 32

The levels of aryl hydrocarbon hydroxylase (AHH) inducibility were assessed in 173 patients with cancers statistically associated with smoking, i.e., squamous cell and transitional cell carcinomas, at various sites. In 34 patients with carcinomas of the oral cavity, 41 patients with laryngeal carcinomas, and 22 patients with pulmonary carcinomas there was a highly significant overrepresentation of high inducers, whereas 30 patients with carcinomas of the renal pelvis and ureter and 46 patients with urinary bladder carcinomas did not differ significantly in this respect from a control population comprising 92 subjects with no history of neoplastic disease. The results add further support to the concept of AHH as a major activator of carcinogens belonging to the group of polycyclic aromatic hydrocarbons (PAH) when these affect the oral cavity and/or the respiratory tract. The role of AHH in urothelial carcinogenesis seems to be less explicit.
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PMID:Aryl hydrocarbon hydroxylase induction levels in patients with malignant tumors associated with smoking. 651 2


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