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)

We reviewed the surgical statistics of the Department of Urology, Isesaki Municipal Hospital between June 1998 and May 2003. A total of 1940 surgeries were performed. These consisted of 399 surgeries on the kidney, adrenal, and pelvis, 212 on the ureter, 433 on the bladder, 256 on the prostate, 149 on the urethra and the penis, 192 on the scrotum, 255 on the arteriovenous fistula and CAPD. In September 2003, a screening program for prostate cancer was started, and the number of prostate biopsies and total prostatectomies increased. As the adaptation of many procedures to laparoscopy expanded, the number of laparoscopic surgeries increased.
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PMID:[Surgical statistics of the Department of Urology, Isesaki Municipal Hospital during a five-year period (June 1998-May 2003)]. 1568 66

Cyclic nucleotide levels are controlled through their synthesis from nucleotide triphosphates by cyclases and their degradation to 5'-monophosphates by phosphodiesterases (PDEs). Components controlling cyclic AMP-induced relaxation in the urinary tract include receptors, inhibitory and stimulatory G-proteins, isoforms of adenylyl cyclase and PDEs. The responsiveness of PDEs to a variety of physiological challenges is related to the presence of multiple families of isoenzymes with specific localization within tissues and within cells. At least 11 families of PDEs encode more than 50 PDE proteins produced in mammalian cells. In the urinary tract, characterization of PDE isoforms has lagged behind other systems and much of the literature was published prior to identification of PDE7, 8, 9, 10, 11. Specific PDE inhibitors regulate smooth muscle function in the bladder, urethra, prostate and ureter. The pharmacological potential of these inhibitors may include treatment of urge incontinence and the low compliance bladder, and treatment of prostate cancer. G-proteins also regulate cyclic AMP production. Changes in specific G- protein isoforms with aging, most prominently Gialpha2, cause decreased relaxation response in the aging bladder. As we have seen here with aging and certainly in other disease processes, levels of the components of adenylyl cyclase/phosphodiesterase/protein kinase can change and thus affect the relaxation response. By exploitation of differences in PDE expression in disease, such as the overexpression of PDEs in cancer, treatment options may present themselves.
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PMID:Regulation of cyclic nucleotides in the urinary tract. 1585 36

Inflammatory myofibroblastic tumor (IMT) of the urinary tract, also termed postoperative spindle cell nodule, inflammatory pseudotumor, and pseudosarcomatous fibromyxoid tumor, is rare and in the past was believed to reflect diverse entities. We reviewed a series of 46 IMTs arising in the ureter, bladder, and prostate, derived primarily from a large consultation practice. There were 30 male and 16 females aged 3 to 89 years (mean 53.6). Lesions were 1.2 to 12 cm (mean 4.2). There was a history of recent prior instrumentation in 8 cases. Morphology was similar to that previously described for IMT occurring in this region, with the exception of 1 case that focally appeared sarcomatous. Polypoid cystitis coexisted in 5 patients (11%). Mitoses were typically scant (0 to 20/10 hpf, mean 1). Necrosis was seen in 14 (30%) cases. Invasion of the muscularis propria was documented in 19 (41%). By immunohistochemistry (IHC), lesions at least focally expressed anaplastic lymphoma kinase (ALK) (20/35, 57%), AE1/3 (25/34, 73%), CAM5.2 (10/15, 67%), CK18 (6/6, 100%), actin (23/25, 92%), desmin (15/19, 79%), calponin (6/7, 86%), caldesmon (4/7, 57%, rare cells), p53 (10/13, 77%), and most lacked S100 (0/14), CD34 (0/13), CD117 (2/13, 15%), CD21 (0/5), and CD23 (0/3). ALK gene alterations were detected by fluorescence in situ hybridization (FISH) in 13/18 (72%) tested cases, including 2 with prior instrumentation; 13/18 (72%) showed agreement between FISH ALK results and ALK protein results by IHC. Most bladder IMTs were managed locally, but partial cystectomy was performed as the initial management in 7 cases and cystectomy in 1 (1 IMT was initially misinterpreted as carcinoma, 1 IMT was found incidentally as a separate lesion in a cystectomy specimen performed for urothelial carcinoma). Follow-up was available in 32 cases (range 3 to 120 mo; mean 33; median 24). There were 10 patients with recurrences (2 with 2 recurrences). Recurrences were unassociated with muscle invasion or with ALK alterations. In 2 cases, tumors of the urinary tract (TURs) showing IMT preceded (1 and 2 mo, respectively) TURs showing sarcomatoid carcinoma with high-grade invasive urothelial carcinoma accompanied with separate fragments of IMT. Even on re-review the IMT in these 2 cases were morphologically indistinguishable from other cases of IMT, with FISH demonstrating ALK alterations in the IMT areas in one of them. Both these patients died of their carcinomas. Lastly, there was 1 tumor with many morphological features of IMT and an ALK rearrangement, yet overtly sarcomatous. This case arose postirradiation for prostate cancer 4 years before the development of the lesion, with tumor recurrence at 4 months and death from intra-abdominal metastatic disease at 9 months. In summary, urinary tract IMTs are rare and share many features with counterparts in other sites, displaying similar morphology and immunogenotypic features whether de novo or postinstrumentation. Typical IMTs can be locally aggressive, sometimes requiring radical surgical resection, but none of our typical cases metastasized, although they can rarely arise contemporaneously with sarcomatoid urothelial carcinomas. For these reasons, close follow-up is warranted.
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PMID:Inflammatory myofibroblastic tumors of the urinary tract: a clinicopathologic study of 46 cases, including a malignant example inflammatory fibrosarcoma and a subset associated with high-grade urothelial carcinoma. 1712 5

Polypoid cystitis and its more chronic phase papillary cystitis, which results as a reaction to injury to the bladder mucosa, is a benign lesion mimicking various papillary urothelial neoplasms. Analogous lesions occur throughout the urothelial tract and are referred to as polypoid urethritis, polypoid ureteritis, and polypoid pyelititis when present in the urethra, ureter, and renal pelvis, respectively. For simplicity, these lesions in different sites and papillary cystitis will typically be referred to as polypoid cystitis in this manuscript. A search of the consultation files from our institution from January 2000 to July 2007 was performed. Of 155 cases diagnosed as polypoid cystitis, we identified 41 cases that were diagnosed as papillary urothelial neoplasms by contributing pathologists and only sent to us, typically at the request of the urologist after the case had be signed out. For cases where information was available, clinical symptoms included bladder obstruction (n=7), gross hematuria (n=6), colovesicular fistula (n=4), follow-up status posttreatment of bladder and ureter carcinoma (n=4), bladder/urethral stones (n=2), benign prostate hyperplasia (n=2), follow-up after radiation for prostate cancer (n=2), long-standing urinary stents (n=2), and voiding dysfunction (n=1). Original diagnoses included noninvasive low grade papillary urothelial carcinoma (n=23), noninvasive high grade papillary urothelial carcinoma (n=6), papillary urothelial neoplasm of low malignant potential (n=5), papilloma (n=3), urothelial neoplasia (n=2), carcinoma in situ (n=1), and squamous carcinoma (n=1). The mean age at diagnosis was 63 years (range, 19 to 93 y; median 63 y). Male to female ratio was 3.1 to 1. Clinical symptoms varied with the most common manifestations, including gross hematuria, bladder/urethral stones, history of prostate cancer treated with radiation, follow-up after bladder/ureter carcinoma treatment, long-term urinary stents, and colovesicular fistulas. At cystoscopy, lesions were variably described as polypoid, trabeculations, bullous polyps, and diffuse erythema and edema. The locations of polypoid cystitis were bladder (n=34), ureteral orifice (n=2), urethra (n=2), renal pelvis (n=2), and undesignated (n=1). Architecturally, 31 cases had isolated papillary fronds with in 1 case branching papillary structures. The base of the papillary stalks were characterized as both broad and narrow (n=24), only broad (n=9), and only narrow (n=3). The overlying urothelium of polypoid cystitis was diffusely and focally thickened in 8 cases and 5 cases, respectively. Umbrella cells were identified in 32 cases. Acute and chronic inflammation was present in 28 cases, moderate in 15, and mild in 13 cases. Eleven cases showed chronic inflammation, mild in 10, and moderate in 1 case. Reactive urothelial atypia was noted in 26 cases with mitotic figures present in 22 cases, frequent in 3 and rare in 19 cases. Stroma edema was seen in 32 cases with fibrosis within the polypoid stalks seen in 16 cases. The key to correctly diagnosing polypoid/papillary cystitis is to recognize at low magnification the reactive nature of the process with an inflamed background that is edematous or densely fibrous with predominantly simple, non-branching, broad-based fronds of relatively normal thickness urothelium, and not focus at higher power on the exceptional frond that may more closely resemble a urothelial neoplasm either architecturally or cytologically. In cases where the diagnosis of papillary neoplasia is not straightforward and there is a question of polypoid cystitis, pathologists should seek clinical history that might suggest a reactive process. Because the urologist can more often better recognize the inflammatory nature of the lesion than the pathologist, the pathologist should hesitate diagnosing urothelial neoplasia when the cystoscopic impression is that of an inflammatory lesion.
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PMID:Polypoid/papillary cystitis: a series of 41 cases misdiagnosed as papillary urothelial neoplasia. 1837 18

Data about second primary tumors after prostate carcinoma are controversial. Some authors emphasize an increased incidence of some cancer sites, others an overall diminution. With the aim to provide further information to define the issue, we have analyzed the frequency of second metachronous primary malignancies in patients with diagnosed prostate cancer in the Umbria region of Italy. A total of 410 metachronous cancers among 4528 prostate cancer patients were abstracted from incident cases of the RTUP, over the period 1994-2003. This cohort was compared with all cases (except prostate cancers) recorded in the RTUP archive. The expected number of cases was obtained from indirect standardization with regional incidence rates of several sites. The significance of the observed/expected ratios and the corresponding 95% confidence intervals were based on the Poisson distribution. A significant standardized incidence ratio was found for all sites but prostate, with 410/351 observed/expected cases. The significance disappears considering all sites except prostate and skin non-melanomas. Among several sites, significant standardized incidence ratios were found for skin non-melanomas, for bladder, for rectum, but not for colon cancers. Kidney, ureter and urethra showed a nonsignificant standardized incidence ratio. Nasopharynx showed a significant standardized incidence ratio, but the result was based on a very small number of cases. In our data, the increase in urinary bladder and rectal cancers, after prostate cancer diagnosis, seems to be real: it is plausible that the number of second cancers may be due to increased urologist surveillance, which, in our Region, does not seem to be reduced in elderly men.
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PMID:Metachronous malignancies in men with previous prostate cancer in Umbria, Italy, 1994-2003. 1846 27

Ectopic ureters are rare congenital malformations of the renal system that most commonly present in females. It is extremely rare to encounter an ectopic ureter in an older man undergoing radical prostatectomy. We report herein a case of a 66-year-old man with prostate cancer and a complete duplication of the left renal collecting system, with an upper pole ectopic ureter and associated normal functioning renal parenchyma entering into the prostatic urethra. This anomaly was incidentally discovered on preoperative magnetic resonance imaging of the prostate. Open radical retropubic prostatectomy and a left ureteroureterostomy were performed.
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PMID:Management of localized prostate cancer and an incidental ureteral duplication with upper pole ectopic ureter inserting into the prostatic urethra. 1914 74

We report a case of prostate cancer and left ectopic ureter opening to seminal vesicle with left renal agenesis. A 62-year-old man was admitted to our hospital for treatment of prostate cancer with cyst formation. On the rectal examination, a cystic tumor was palpable on the left side of prostate. The left kidney was not detected by intravenous pyelography and ultrasonography. Magnetic resonance imaging revealed a retrovesical cystic lesion in the left side. Total prostatectomy and left ureterectomy were performed under the diagnosis of clinical T1cN0M0 prostate cancer and left ectopic ureter opening to seminal vesicle with left renal agenesis. The pathological findings showed well differentiated adenocarcinoma, Gleason score 3 + 3, and left ectopic ureter entering into the seminal vesicle and left renal agenesis. The patient was well 39 months after the total prostatectomy and left ureterectomy without evidence of recurrence. There have been no cases of the association of this urogenital anomaly, such as ectopic ureter opening to seminal vesicle with renal agenesis and prostate cancer and the combined management of both. Our case seems to be first case in the Japanese literature.
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PMID:[Prostate cancer and left ectopic ureter opening to seminal vesicle with left renal agenesis: a case report]. 1922 14

We here report the incidence of different types of genitourinary cancers among the Iranian population according to the records of the Iran Ministry of Health and Medical Education. In a population-based cancer-registry study in 2005, all recorded data in pathology laboratories, freestanding cancer clinics and treatment centers, physician offices, and other state central registries were obtained with the assistance of Iran Universities of Medical Sciences and sent to the Diseases Management Center in the Health Ministry. The prevalences of urological cancers were as follows: bladder cancer 48.3%; prostate cancer 33.4%; renal cell carcinoma 10.3%; renal pelvis and ureter cancer 0.75%; testicular cancer 6.15%; penile cancer 0.15%; urethral cancer 0.45%; and other unspecified urinary cancers 0.43%. The male to female ratios for the various common urological cancers varied between 1.69 (renal cell carcinoma) and 7.75 (unspecified urinary cancers). The incidence of prostate cancer among our population was dramatically higher than in other countries of Asia. However, bladder cancer was found to be the commonest of the genitourinary cancers, especially in elderly patients, among our population.
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PMID:Incidence of genitourinary cancers in the Islamic Republic of Iran: a survey in 2005. 1925 36

The role of pelvic lymph node dissection (PLND) in prostate cancer, in which patients and to what extent it should be performed, remains a controversial topic. Preoperative diagnostic methods are more or less unreliable for lymph node staging and PLND remains the most reliable and accurate method. PLND is indicated in all patients with a PSA value >10 ng/ml and in those with a PSA <10 ng/ml if the Gleason score is > or = 7. If PLND is performed then it should always include the tissue along the external iliac vein, in the obturator fossa and on either side of the internal iliac vessels, up to where the ureter crosses the common iliac vessels. In conjunction with RRP extended PLND may increase staging accuracy, influence decision making with respect to adjuvant therapy and possibly impact outcome.
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PMID:Regional lymph node staging in prostate cancer: prognostic and therapeutic implications. 1926 8

Protein kinase C-related kinases are regulated by phosphatidylinositol-3-kinase and Rho family GTPases. The isoform PRK1 has been characterized in detail in prostate cancer, but not in other carcinomas. We analyzed our prior microarray data for PRK1 gene expression in 175 carcinomas and evaluated tissue microarrays for protein expression in 251 carcinomas and a comprehensive group of normal tissues. We also used immunoblotting to determine the levels and phosphoactivation status of PRK1, PRK2, and PDK1 in 12 ovarian serous carcinomas, SKOV3 cells, and 3 samples of normal ovarian surface epithelium (OSE). The highest average level of PRK1 messenger RNA was observed in ovarian serous carcinomas compared with all other carcinomas, including those of the prostate, bladder/ureter, breast, colon, stomach/esophagus, kidney, liver, pancreas, and lung (P = .05). By immunohistochemistry, PRK1 was observed in selected normal cells, including epithelium from the gynecologic tract and hematolymphoid elements. All serous ovarian and endometrial endometrioid adenocarcinomas and mesotheliomas were immunoreactive for PRK1. The findings in nonserous ovarian and most carcinomas from the prostate, breast, and pancreas were also positive but less consistently so. In comparison with OSE, the serous carcinomas typically had greater pPRK1/total PRK1 (P = .02) as well as greater pPDK/total PDK (P = .01). The relative phosphorylation status of these 2 kinases correlated within each sample. In summary, PRK1 is present in various malignancies, but especially in serous carcinomas, where the increased activation status of PRK1 and its upstream regulator, PDK, as compared with normal OSE suggests a role in ovarian cancer development or progression.
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PMID:PRK1 distribution in normal tissues and carcinomas: overexpression and activation in ovarian serous carcinoma. 1942 17


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