Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neoplastic and non-neoplastic tissues from the urinary tract and the prostate were analyzed for the presence of human papillomavirus (HPV) DNA. The analysis was performed by PCR using primers specific for HPV 6/11 and 16. HPV DNA was present in bladder, ureter, kidney and prostate, with percentages ranging between 46% and 87%. Benign and oncogenic HPV types were detected with similar frequencies both in non-neoplastic and in neoplastic biopsies, and HPV 16 was not preferentially associated with malignant lesions. In all instances, small amounts of HPV DNA were present in the tissues, suggesting the absence of productive infection. Analysis of the physical state of HPV DNA performed by 2-dimensional gel electrophoresis and Southern blot hybridization revealed that HPV 16 DNA harbored in the urinary tract can be integrated also in non-neoplastic tissues. The results indicate that HPV 16 does not seem to be associated with urinary-tract and prostate oncogenesis, but that these tissues may represent an important reservoir for the transmission of HPV types normally infecting the genital tract.
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PMID:Presence and physical state of HPV DNA in prostate and urinary-tract tissues. 132 67

Concurrent primary renoparenchymal or renal pelvic neoplasms of different histology in the same kidney appear to be unusual. We herein report on a 75-year-old man in whom a tiny renal adenoma, a transitional cell carcinoma of the renal pelvis, ipsilateral ureter papillomas and transitional carcinoma of the urinary bladder were found. The clinicopathologic findings of this patient as well as the oncogenesis of renal tumours are discussed.
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PMID:Renal adenoma incidentally found in removed kidney in a patient with transitional cell carcinoma of the renal pelvis. 408 36

The effects of unilateral hydronephrosis by ligation of the right ureter and/or multiple injections of putrescine on kidney tumorigenesis by a single intrarenal injection of N-nitrosodimethylamine (DMN) were studied. Inbred female W rats in the unilateral hydronephrotic groups given or not given putrescine developed kidney tumors and/or neoplastic or preneoplastic lesions of the liver at an incidence of 55.6%. Almost all kidney tumors developed in the contralateral kidneys, which showed hypertrophy due to unilateral hydronephrosis. Rats having unilateral hydronephrosis and subjected to long-term putrescine administration after DMN injection frequently contracted large mesenchymal cell tumors (83%), whereas the group not given putrescine developed no mesenchymal cell tumors. Histologically, epithelial cell tumors showed a marked decrease in both gamma-glutamyltransferase activity and trypan blue uptake, but mesenchymal cell tumors did not.
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PMID:Modulation of N-nitrosodimethylamine kidney tumorigenesis by unilateral hydronephrosis and multiple putrescine administrations. 613 87

In this study we examined loss of heterozygosity (LOH) on chromosome 13q12-13 in 50 tumors from BRCA2 carriers in five families showing strong evidence of linkage to BRCA2. In addition to high frequency of LOH in female breast cancer, LOH was observed in tumors of the prostate, ovary, cervix, colon, male breast, and ureter. All detected losses involved the wild-type chromosome. These results suggest that BRCA2 is a tumor suppressor gene and may be involved in the tumorigenesis of several cancer types in addition to breast cancer.
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PMID:Different tumor types from BRCA2 carriers show wild-type chromosome deletions on 13q12-q13. 758 15

We report a case of squamous cell carcinoma of the ileovesical junction 12 years following total replacement of the ureter with ileum. The uroenteric junctions, which are not exposed to the fecal stream, may be associated with cancer as in ureterosigmoidostomy. The urine infected with fecal bacterial flora combined with a healing uroenteric suture line may be responsible for the tumorigenesis. Urine cytology should be performed at least yearly beginning 10 years after ileal ureter. If any abnormality was suspected cystoscopy must be performed.
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PMID:Bladder cancer following ileal ureter. Case report. 761 44

We report here a patient who developed a variety of tumors both synchronously and metachronously over a 2-year period. The involved organs were the uterus, ureter, and small and large intestines. The patient underwent open surgery 3 times and polypectomies 6 times. Postoperative histopathologic analysis showed 2 adenomas and 8 carcinomas. Genetic analysis revealed microsatellite instabilities at the tested loci in all 10 tumors, indicating that replication errors played an essential role in the tumorigenesis. Early identification of microsatellite instability could be useful for predicting development of additional primary cancers.
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PMID:Multiple primary cancers with microsatellite instability: report of a case. 860 41

Aetiology remains the main unanswered problem in Balkan endemic nephropathy (BEN) despite investigations into the roles of genetic factors, environmental agents and immune mechanisms. Evidence has accumulated that BEN is an environmentally-induced disease. Weathering of low-rank coals near to the villages where BEN is endemic produces water-soluble polycyclic aromatic hydrocarbons and aromatic amines, similar to metabolic products of acetaminophen that cause analgesic nephropathy. Many of these compounds are known to be carcinogenic and could also cause urothelial cancer. Genetic studies have supported genetic predisposition to BEN. The candidate genes have been localized to a region between 3q25 and 3q26, the 3q BEN marker being detected in both BEN patients and in some healthy relatives with initial morphological changes peculiar to BEN. Three bands with increased frequencies of spontaneous and induced aberrations contain oncogenes. The frequent association of BEN and urinary tract tumours (UTT) can be explained by the chromosomal hypothesis of oncogenesis. The results of molecular biological investigations will allow the identification of genetic markers of BEN, permitting early detection of BEN-predisposing mutations and identification of susceptible individuals who may be at risk of exposure to the environmental agents. An increased incidence of tumours of renal pelvis and ureter in patients with BEN and in population from endemic settlements has been observed. Familial clustering of the UTT was also reported. The frequency of urinary bladder tumours in BEN-endemic settlements is also increased compared with the non-endemic villages and cities. The geographic correlation between BEN and UTT supports the speculation that these diseases share a common aetiology.
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PMID:Balkan endemic nephropathy: a need for novel aetiological approaches. 979 28

Urothelial carcinoma of the renal pelvis and ureter may develop sporadically or as a manifestation of hereditary nonpolyposis colorectal cancer. The majority of hereditary nonpolyposis colorectal cancer is caused by mutation of the human DNA mismatch repair (MMR) genes and is detected by associated microsatellite instability (MSI). Seventy-three unselected urothelial carcinomas of the ureter and/or renal pelvis were screened for MSI using the National Cancer Institute-designated reference panel (plus BAT40). Instability of at least two microsatellite markers (MSI-high) was detected in 15 samples (21%). Immunohistochemical staining of the MMR proteins (hMSH2, hMLH1, or hMSH6) was absent in 13 of 15 (87%) MSI tumors, and alteration of coding sequence microsatellites (TGFbetaRII, Bax, hMSH3, and hMSH6) was found at frequencies of 7-33% in these samples. Tumors with MSI had significantly different clinical and histopathological features including higher prevalence in female patients, low tumor stage and grade, and a papillary and frequently inverted growth pattern. Our results suggest a molecular pathway of tumorigenesis that is similar to MMR-deficient colorectal cancers and consistent with the notion that the site distributions of hereditary or sporadic MSI-high tumors may reflect tissue-specific susceptibility to lesions processed by the MMR machinery.
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PMID:Frequent microsatellite instability in sporadic tumors of the upper urinary tract. 1246 Aug 87

Wilms tumor gene 1 (WT1) is essential for normal urogenital development. Mutations in WT1 are involved in Wilms tumorigenesis and several associated syndromes, such as Denys-Drash, Frasier, or Wilms tumor, aniridia, genitourinary anomalies, and mental retardation syndrome. We report a novel familial WT1 point mutation in the stop codon of exon 10 (1730A/G; X450W) in 3 members of 1 family. The index patient is a 22-year-old woman in whom Wilms tumor and ureter duplex were diagnosed at the age of 9 years and who subsequently developed slow progressive nephropathy. Her mother also had late-onset nephropathy that led to end-stage renal failure, whereas renal function in 1 brother of the index patient was not impaired. We hypothesize that this type of mutation (read-through), which leads to an elongated, but otherwise unchanged, WT1 protein, may be associated with incomplete penetrance and a relatively late onset of both Wilms tumor and nephropathy in this family.
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PMID:Novel familial WT1 read-through mutation associated with Wilms tumor and slow progressive nephropathy. 1595 41

Hereditary non-polyposis colorectal carcinoma (Lynch syndrome) is among the most common hereditary cancers in man and a model of cancers arising through deficient DNA mismatch repair (MMR). Lynch syndrome patients are predisposed to different cancers in a non-random fashion, the basis of which is poorly understood. We addressed this issue by determining the molecular profiles for different tumors from a nationwide cohort of Lynch syndrome families (approximately 150 tumors in total). We focused on some less prevalent cancers, affecting the brain (n = 7) and urinary tract (five bladder and five ureter uroepithelial cancers and four kidney adenocarcinomas), and compared their molecular characteristics to those of the most common cancers, colorectal, gastric and endometrial adenocarcinomas, from the same families. Despite origin from verified MMR gene mutation carriers, the frequency of high-level microsatellite instability in tumors varied between high (100-96% for ureter, stomach and colon), intermediate (63-60% for endometrium and bladder) and low (25-0% for kidney and brain). In contrast to gastrointestinal and endometrial carcinomas, active (nuclear) beta-catenin was rare and KRAS mutations were absent in brain and urological tumors. Compared with other tumors, frequent stabilization of p53 protein characterized urinary tract cancers. Promoter methylation of tumor suppressor genes discriminated the tumors in an organ-specific manner. Our findings suggest that different Lynch syndrome tumors develop along different routes. Uroepithelial cancers of the ureter (and bladder to lesser extent) share many characteristics of MMR deficiency-driven tumorigenesis, whereas brain tumors and kidney adenocarcinomas follow separate pathways.
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PMID:Differential cancer predisposition in Lynch syndrome: insights from molecular analysis of brain and urinary tract tumors. 1855 May 72


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