Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An anti-kidney antibody was demonstrated by the indirect immunofluorescence method in the serum of patients with primary tumours of the liver or kidney. The distribution of fluorescence in rabbit kidney was consistent with that of antibody to collecting ducts. The anti-collecting duct antibody (anti-CDA) could be absorbed from serum by normal adult rabbit or human kidney tissue and by one of three specimens of renal-cell carcinoma tissue. Anti-CDA differed from anti-mitochondrial antibodies and from anti-liver/kidney microsomal antibody in the pattern of fluorescent staining obtained with rabbit kidney. Two-hundred sera from patients with cancer and other diseases and forty-three from healthy hospital personnel were tested for anti-CDA. Eleven of the twenty-five positive sera were from patients with primary cancer of the liver or urinary tract, and all but six of the remainder were from patients with tumours involving the liver or with liver disorders that may be associated with nodular hyperplasia or tumour.
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PMID:Circulating antibody to renal collecting ducts in patients with hepatoma or renal-cell carcinoma. 17 72

The localization of membrane-bound gamma-glutamyltransferase with monoclonal antibody (mAb) 138H11 proved to be of value for differential diagnosis of renal cancer, since it correlated with the histogenetic profile of human epithelial renal tumors. Immunoreactive gamma-glutamyltransferase was located in the proximal tubule in all normal human kidneys (15/15) examined thus far by both ultrastructural and immunohistochemical techniques. From 68 epithelial renal cancers tested 31/31 clear-cell carcinomas and 15/16 chromophilic carcinomas expressed the target epitope of mAb 138H11. In contrast, 0/11 oncytomas, 0/9 chromophobic carcinomas, and 0/1 Duct-Bellini carcinoma were immunoreactive. These results support a model of histogenesis and classification of epithelial renal tumours, according to which clear-cell and chromophilic renal carcinomas originate from transformed proximal tubule cells, whereas oncocytomas, chromophilic and Duct-Bellini carcinomas originate from cells of the collecting duct.
Cancer Immunol Immunother 1991
PMID:Differential diagnosis of histogenetically distinct human epithelial renal tumours with a monoclonal antibody against gamma-glutamyltransferase. 167 84

Cis-dichlorodiammine platinum (II), or cisplatin, has emerged as a principal chemotherapeutic agent in the treatment of otherwise resistant solid tumors and is currently among the most widely used agents in the chemotherapy of cancer. The chief limit to its greater efficacy is its nephrotoxicity, which has made it necessary both to lower its dosage and actively hydrate patients to reduce it. The vulnerability of the kidney to cisplatin is almost certainly related to its primary role in the excretion of cisplatin. Cisplatin enters renal cells by a process that depends on normal oxygen utilization and is specifically inhibited by organic bases. Greater localization of platinum to the S3 segment of the proximal tubules suggests that the vulnerability of this segment may depend on its specific uptake of the drug. The majority of intracellular platinum is bound to macromolecules, including protein and DNA, yet a significant portion of cell platinum is biotransformed to a nonmutagenic and possibly nontoxic compound. Polyuria and hypomagnesemia, which are commonly associated with cisplatin nephrotoxicity, may be due to defects in deep nephron or collecting duct fluid and solute transport. Low single nephron glomerular filtration rates (SNGFR) during early cisplatinum-induced acute renal failure is accompanied by reduced renal blood flow and transglomerular hydrostatic pressure without elevated intratubular hydrostatic pressure, suggesting preglomerular vasoconstriction as an important determinant of renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cisplatin nephrotoxicity. 353 59

E-cadherin, a member of the cadherin family, plays a major role in cell-cell adhesion of normal epithelium. Recent studies have demonstrated that heterogeneous expression, reduction or loss of E-cadherin is involved in invasion and metastasis of cancer cells. In this study, the localization of E-cadherin in the normal human kidney and the relationship between E-cadherin expression and histopathological features in renal cell carcinomas was examined immunohistochemically. Renal cell carcinoma tissues and normal kidney counterparts were obtained from 20 patients. E-cadherin in the normal kidney was detected in the cell-cell border of the distal tubules, collecting duct and Bowman's capsule but not in the proximal tubules. E-cadherin expression was reduced in all the clear cell type renal cell carcinomas with compact or cystic configuration (n = 15), while it was well preserved in all the papillary type (n = 3) and chromophobe cell type (n = 1) renal cell carcinomas. Different expression patterns between primary site and metastasis, i.e., homogeneously weak in primary tumor and heterogeneously positive in metastatis, was observed in a case of clear cell type renal cell carcinoma. Different patterns of expression between clear and non-clear cell type, or between papillary and non-papillary type, together with strong expression in chromophobe type might reflect the origin of each type of renal cell carcinoma. Further studies will clarify whether the change in expression of E-cadherin is associated with the prognosis of renal cell carcinoma.
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PMID:[E-cadherin expression and histopathological features in renal cell carcinomas]. 748 27

Collecting duct carcinoma (CDC) is a recently recognised histological variety of renal carcinoma (RC) considered to arise from the epithelium of the collecting ducts. Diagnosis of this entity depends on well defined gross and microscopic criteria and is supported by a characteristic immunostaining pattern. The clinical features of these patients, the natural course of the disease and its response to treatment have not been clearly established. Between 1980 and 1990 we treated 12 patients (median age 43 years, range 16-62) with collecting duct carcinoma of the kidney. In addition to being relatively young, each patient had a strong family history of associated malignancies. Survival was short (median 22 months) and 11 patients presented with locally advanced or metastatic disease.
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PMID:Collecting duct carcinoma of the kidney. 849 79

E- and N-cadherins are proteins involved in intercellular adhesion and are localized, e.g., in the adherens junctions of epithelial cells. Kidney tubules express these molecules in a distinctive pattern, the expression of N-cadherin being restricted to proximal tubules and that of E-cadherin to distal tubules and collecting ducts. Renal cell carcinomas (RCCs) and oncocytomas are considered to originate from these tubular epithelia. To find out whether cadherins could serve as markers for a cellular origin of these tumors, we studied the expression of E- and N-cadherins in RCCs and oncocytomas, in cell lines derived from RCCs as well as in tumors grown in nude mice. Most RCCs co-expressed E- and N-cadherins, as did 2 of the 4 cell lines studied. The expression pattern did not correlate with the histological grade of the tumors, and even the least differentiated tumors, as well as metastases, showed expression of cadherins. Renal oncocytomas expressed E-cadherin but not N-cadherin, which is in line with previous studies that have proposed a collecting duct origin for these tumors. Papillary renal neoplasms, a separate entity usually not classified as RCC, expressed neither of the cadherins studied despite the abundant expression of beta-catenin. Our results suggest that most RCCs co-express the characteristic adhesion molecules of both proximal and distal tubules, which makes it questionable whether the origin of these tumors can be reliably located to any distinct part of the renal tubule. Our results also suggest that in RCCs the increased histological grade is not directly associated with changes in the expression of either of the cadherins, indicating other mechanisms underlying the deficient capacity to form polarized tubular structures.
Int J Cancer 1995 Dec 20
PMID:Expression of E- and N-cadherin in renal cell carcinomas, in renal cell carcinoma cell lines in vitro and in their xenografts. 855 Feb 43

Tumors of varying malignant potential arise from the complex epithelial lining of the nephron. Although the molecular characteristics of renal clear cell carcinomas, which arise from the proximal tubule, have been studied, little is known about tumors that develop from other parts of the renal tubular system. To elucidate common molecular lesions that may contribute to the development or progression of nonproximal tubule renal tumors, we performed a detailed microsatellite allelotype of lesions thought to arise from the renal collecting duct. Eighteen collecting duct carcinomas (CDCs) and 13 renal oncocytomas were studied using highly informative microsatellite markers on all autosomal arms. Loss of heterozygosity (LOH) was identified on multiple chromosomal arms in CDCs and renal oncocytomas. Microsatellite analysis revealed LOH of 1q in 57% of informative CDCs. LOH was also observed on arms 6p (45%), 8p (40%), and 21q (40%). In renal oncocytomas, LOH of 1q occurred in approximately 30% of tumors, but 1p LOH was observed in 57% of informative cases analyzed. High levels of LOH were also observed on arms 8p, 14q, 19q, and 21q in the oncocytomas studied. Loss of chromosomal arm 3p was infrequent in both tumor types. Our results suggest that the molecular events that contribute to the development of distal nephron tumors are distinct from those associated with the etiology of proximal tubule renal cancers.
Cancer Res 1996 Apr 15
PMID:Distal nephron renal tumors: microsatellite allelotype. 862 May 10

Chromosome 8 loss of heterozygosity (LOH) in cancer of the urinary bladder is associated with high tumour grade and stage. We have screened 193 cases of transitional cell carcinoma (TCC) of the bladder using 30 microsatellite polymorphisms on chromosome 8. Forty three cases (22%) showed LOH on 8p, the majority of which (72%) had lost the entire short arm. Using 12 tumours with partial deletions of 8p, we have defined a minimum telomeric region of deletion between D8S264 and D8S133 (8p2l.1-pter). We also found LOH in the region 8pl1.2-12, where we have defined at least one centromeric target for deletion within a 4 cM interval. Two tumours were identified with loss of the telomeric region only, whereas all cases with loss in the centromeric region also had telomeric deletion. Chromosome 8p deletions have also been described in prostate, colorectal, hepatocellular, lung and endometrial carcinoma and collecting duct carcinoma of the kidney. It has been postulated that loss or inactivation of at least 2 tumour suppressor genes on 8p may play an important role in progression of both prostate and colorectal carcinomas. The regions of deletion we have identified in bladder tumours are compatible with these, suggesting that at least two genes on 8p may play a role in the development of many common solid tumours. Our findings significantly refine the localisation of the more centromeric of these loci.
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PMID:Deletion mapping implicates two tumor suppressor genes on chromosome 8p in the development of bladder cancer. 864

We report our experience with 40 retrograde renal brush samples of pelvic-calyceal lesions with confirmatory tissue studies. On-site cytopathologic evaluation was performed in 38 of these specimens. The final histologic diagnoses included 24 cases of transitional cell carcinoma (TCC), 17 of which were low-intermediate grade tumors. All 24 cases were diagnosed cytologically as TCC (22), or as suspicious for TCC (2). Three cases classified as collecting duct carcinomas were resected; the cytologic specimens in 2 of these cases were interpreted as TCC, and one as reactive change. There were three renal cell carcinomas (RCC); cytologically, one was considered a papillary neoplasm, one suspicious for malignancy, and one as reactive. Two cases of atypical renal cysts were reported as suspicious for malignancy in both cytologic and histologic material. There was one case of metastatic colon carcinoma identified in the brush specimen. Finally, tissue studies in the remaining 7 cases showed reactive/inflammatory changes; however, four of the corresponding pelvic brush specimens were considered abnormal. A review of the above cases is reported with the objective of presenting the cytologic features seen in collecting duct carcinoma, low-intermediate grade TCC, and diagnostically difficult cases with cyto/histomorphologic discrepancies. The contribution of on-site assessment to diagnostic accuracy is also discussed.
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PMID:Cytopathology of retrograde renal pelvis brush specimens: an analysis of 40 cases with emphasis on collecting duct carcinoma and low-intermediate grade transitional cell carcinoma. 898 87

The MN/CA9 protein is a tumor-associated antigen that has been shown to have diagnostic utility in identifying cervical dysplasia and carcinoma. MN/CA9 expression is limited to very few normal tissues. We have now extended those observations to further investigate expression of the MN/CA9 protein in histological sections and fine-needle aspiration biopsy smears of normal kidney, benign renal cell lesions, all categories of renal cell carcinomas (clear/granular/spindle cell, chromophilic cell, chromophobic cell, and collecting duct cell RCCs), metastatic RCCs, and non-renal cell clear cell adenocarcinomas. We have found that high levels of MN/CA9 expression is seen in all primary RCCs, cystic RCCs, and metastatic RCCs, with the exception of two cases of the chromophobe cell type, which were MN/CA9 negative. Identical MN/CA9 immunostaining was also observed in the aspiration cytological smears. In contrast, all benign lesions, including pyelonephritis, renal cysts, adenomas, oncocytomas, and normal kidney, did not express the MN/CA9 protein. Thus, we conclude that MN/CA9 protein expression could serve as a valuable adjunct to the cytological and histological diagnosis of benign renal cysts versus cystic RCC, adenoma versus RCC, and oncocytoma versus granular cell RCC. Diffuse membraneous staining of all RCCs (with the exception of chromophobic cell RCC) suggests that MN/CA9 protein expression might have an important clinical utility in the early detection and treatment of RCC. Absence of MN/CA9 expression in non-renal cell clear cell adenocarcinoma also indicates that MN/CA9 protein expression may be used as a differential diagnostic biomarker of metastatic clear cell RCC.
Cancer Res 1997 Jul 15
PMID:Identification of the MN/CA9 protein as a reliable diagnostic biomarker of clear cell carcinoma of the kidney. 923 Jan 82


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