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)

Cyclophosphamide treatment has been associated with bladder cancer in a number of case reports but no causal relationship has been proved since nearly all of these patients were treated with the drug for malignant disease. We describe a patient who received cyclophosphamide after cadaveric renal transplantation to prevent rejection. Transitional cell carcinoma developed in the native bladder and in the donor transplanted ureter (20-year-old donor) 13 years later despite no identifiable risk factors. This case strengthens the argument that cyclophosphamide has a carcinogenic potential on the urinary tract epithelium.
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PMID:Evidence for cyclophosphamide-induced transitional cell carcinoma in a renal transplant patient. 305 Jan 50

Chronic irritation or infection may cause a neoplastic change in the uroepithelium. Our recent experience with two cases of transitional cell carcinoma associated with such stimuli is reported. A 58-year-old woman was found to have a staghorn stone in the left kidney and underwent nephrectomy because of an atrophic kidney. Transitional cell carcinoma was incidentally identified microscopically on the renal pelvis of the removed kidney. Subsequently surgery was elected to remove the residual ureter and the retroperitoneal lymph nodes, both of which turned out to be non-malignant. Then, she was treated by combination chemotherapy with CTX, ADR and CDDP. The second case was a 77-year-old woman who had had a 15-year history of an indwelling ureter catheter after gynecological surgery. Because of purulent discharge without any urine production, she underwent nephrectomy for a contracted kidney. Histology revealed transitional cell carcinoma on the pelviureteral junction. The postoperative courses were uneventful in both cases: they were followed up for 6 months and 9 months respectively without any recurrence of the disease. 90 cases of renal pelvic tumors associated with renal stones were collected from the Japanese literature and reviewed.
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PMID:[Transitional cell carcinoma developed in association with renal stone and ureter catheter: report of two cases]. 376 45

1. The aim of this study was to assess the role of sarcoplasmic reticulum (SR) calcium (Ca2+) in the smooth muscle relaxant and hyperpolarizing actions of calcitonin gene-related peptide (CGRP) in the guinea-pig ureter. 2. CGRP (0.1 microM) rapidly and transiently reduced myogenic phasic contractions (twitches) produced by electrical field stimulation (EFS). Approximately 70% of the response to CGRP was antagonized by glibenclamide (1 microM). 3. Cyclopiazonic acid (CPA, 10 microM), ryanodine (100 microM) and thapsigargin (1 microM) reduced only the glibenclamide-sensitive component of the response to CGRP (0.1 microM) but did not modify the mechano-inhibitory effect of cromakalim (3 microM). A low concentration of CPA (1 microM), assumed to produce a limited impairment of Ca2+ uptake from the stores, prolonged the duration of the inhibitory response to CGRP. Pre-exposure to caffeine (5 mM) inhibited the suppression of twitches by CGRP or cromakalim. 4. When the frequency of EFS was increased, the suppression of twitches by CGRP was reduced. Under these conditions, CPA (1 microM) again prolonged the duration of the inhibitory response to CGRP. 5. CGRP (0.1 microM) and cromakalim (3 microM) markedly depressed the phasic component of contractions to 80 mM KCl. CPA (10 microM) antagonized the inhibitory effect of CGRP but not that of cromakalim. Inhibition of the tonic contraction to 80 mM KCl by CGRP was insensitive to CPA. 6. In sucrose gap experiments, a 5 min exposure to CGRP (0.1 microM) or cromakalim (3 microM) produced a sustained membrane hyperpolarization. Caffeine (5 mM) produced a glibenclamide-sensitive transient hyperpolarization followed by a sustained depolarization. When tested in a Ca(2+)-free medium the hyperpolarization produced by CGRP, cromakalim or caffeine was reduced. In normal Krebs, pre-exposure to CPA (10 microM, 60 min) only abolished the hyperpolarization induced by CGRP. In contrast, 5 min after a caffeine challenge (5 mM) the hyperpolarizations induced by CGRP or cromakalim were reduced. The CGRP-induced hyperpolarization was insensitive to apamin (0.1 microM) or charybdotoxin (0.1 microM). 7. We conclude that the K channel-opening action of CGRP in the guinea-pig ureter requires the mobilization of intracellular Ca2+ from a caffeine- and CPA-sensitive store, leading to transient activation of glibenclamide-sensitive K channels. The K channel-opening action of caffeine appears to involve Ca2+ mobilization from a store which is insensitive to depletion by CPA.
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PMID:Role of intracellular Ca2+ in the K channel opener action of CGRP in the guinea-pig ureter. 883 77