Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Previous studies have shown that the 1q31-32 region frequently presents allelic imbalance (AI) in various neoplastic diseases, such as breast cancer, medulloblastoma, male germ cell tumors, and renal collecting duct carcinoma, suggesting the presence of a tumor suppressor gene in this location. We used 19 informative microsatellite markers to analyze 33 primary breast tumors for AI in the 1q31-32 region. Our results demonstrate a 10-cM critical region of AI that is present in more than 60% of the tumors. This region is located proximal to the REN locus and is flanked by the CACNL1A3 and D1S2655 markers. Most important, the critical region of AI coincides with a female hot spot of recombination, suggesting a possible correlation between the two regions.
Cancer Res 1997 Oct 01
PMID:A region of allelic imbalance in 1q31-32 in primary breast cancer coincides with a recombination hot spot. 933 Oct 79

Collecting duct carcinoma is an aggressive malignancy derived from the renal medulla. Imaging features suggestive of this diagnosis include a medullary origin, hypovascularity, and an infiltrative growth pattern. A case of collecting duct carcinoma with unsuspected contralateral renal agenesis is presented.
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PMID:Collecting duct carcinoma arising in a solitary kidney: imaging findings. 1041 89

Sarcomatoid renal carcinoma (SRC) is an aggressive neoplasm with an age and gender distribution similar to that of conventional (clear cell) renal cell carcinoma (RCC). Genetic and morphologic evidence indicates that the tumor results from de-differentiation of renal epithelial malignancy and associations with RCC, papillary renal carcinoma, chromophobe renal carcinoma and collecting duct carcinoma have been reported. The tumor is composed of sheets of malignant spindle cells that have immunohistochemical and ultrastructural features of both stromal and epithelial cells, and may contain myxoid areas containing osteoclast-like giant cells or pleomorphic sarcomatoid spindle cells resembling rhabdomyoblasts. Rare cases of osteogenic SRC have been described. The tumor shows marked proliferative activity in growth kinetic studies and is usually associated with a poor patient survival that is best predicted by staging.
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PMID:Sarcomatoid renal carcinoma: the final common dedifferentiation pathway of renal epithelial malignancies. 1050 59

MDR1 P-glycoprotein (Pgp), the product of the MDR1 gene involved in multidrug resistance in cancer cells, is also expressed in normal tissues. In the human kidney, it is localized in the mesangium, the proximal tubule, the thick ascending limb of Henle's loop, and the collecting duct. Pgp actively transports lipophilic xenobiotics, peptides, steroids, and lipids, and perhaps endogenous substrates. It has been shown previously that human mesangial cells in culture express active Pgp and that the expression of Pgp can be down-regulated by exposure to antisense oligonucleotides. Mesangial cells do not express multidrug resistance-related protein (MRP). Experiments were performed to determine whether 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (generically platelet-activating factor, PAF) is a substrate of Pgp in human mesangial cells in culture. This study found: (1) PAF C-16 and analogs inhibited Pgp-mediated efflux of rhodamine 123 by 59 to 88% in multidrug-resistant KBV-1 cells and by 85 to 97% in cultured human mesangial cells. (2) In mesangial cells stimulated with A23187, the secretion of endogenously produced PAF was inhibited by >80% by the Pgp blockers verapamil, cyclosporin A, PSC-833, vinblastine, and adriamycin. (3) Preincubation with MDR1 antisense oligonucleotides also blocked PAF secretion by human mesangial cells. PAF analogs do not modify the transport of MRP substrates in MCF-7/VP cells expressing MRP but not Pgp. These results indicate that PAF is an endogenous substrate of Pgp in human mesangial cells. Inhibition of Pgp transport may be useful in reducing glomerular damage occurring in pathologic conditions where PAF secretion is elevated.
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PMID:Secretion of platelet-activating factor is mediated by MDR1 P-glycoprotein in cultured human mesangial cells. 1054 Dec 89

Involvement of the 3p14.2 region of chromosome 3 in kidney cancers was suggested 20 years ago, when a reciprocal constitutional translocation, t(3;8)(p14.2;q24), was shown to segregate with bilateral clear cell renal carcinoma in 3 generations of 1 family. The FHITgene that is interrupted at 3p14.2 by the t(3;8) translocation has been isolated, characterized, and shown to be frequently altered, mainly by internal deletion, in carcinomas or cancer-derived cell lines of the lung, stomach, pancreas, esophagus, cervix, and colon. Although up to 90% of sporadic clear cell renal carcinomas, representing 70% of adult renal carcinomas, exhibit loss of FHIT alleles, FHIT gene alterations have been documented for only a few renal cell carcinoma-derived cell lines. Nevertheless, more than 50% of clear cell carcinomas were recently shown to express little or no Fhit protein, unlike the normal kidney tubule epithelium, which is uniformly strongly positive for Fhit expression. We have extended our immunohistochemical study of expression of Fhit protein to the spectrum of histopathologic subtypes of adult renal tumors. There is an apparent continuum of Fhit expression from the 100% strongly positive oncocytomas through mostly positive papillary and chromophobe to the mostly negative clear cell and sarcomatoid to the negative or predominantly negative collecting duct renal carcinomas. This pattern of diminishing Fhit expression correlates with reported frequency of 3p allele loss in renal carcinomas and may parallel the potential for aggressive behavior of tumors, as suggested by the abundant Fhit expression in the benign oncocytomas and the near absence of Fhit expression in sarcomatoid and collecting duct RCCs.
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PMID:Loss or reduction of Fhit expression in renal neoplasias: correlation with histogenic class. 1057 5

Chromophobe renal cell carcinoma (RCC), a newly established subtype of renal neoplasm, is composed of tumor cells with characteristically cloudy, weakly eosinophilic and reticular cytoplasm. The tumor should be distinguished from the common clear cell RCC, because of the unique clinicopathological and molecular biological features. The tumor does not show gender bias. Patient ages are similar to those of clear cell RCC, but might occur in the 20- to 40-year-old age group. Grossly, the tumor tends to be beige in color, which is different from the yellowish color of common RCC. Electron microscopy and immunohistochemistry indicate the intercalated cell of the collecting duct as the cellular origin. Cytogenetic study shows non-random multiple chromosome loss, with mitochondrial DNA rearrangement. Alteration of the von Hippel-Lindau (VHL) gene, a cancer suppressor gene relating with clear cell RCC, has not yet been observed. In order to adopt the most appropriate treatment, including gene therapy, recognition and correct pathological diagnosis of chromophobe RCC are extremely important.
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PMID:Chromophobe renal cell carcinoma: clinical, pathological and molecular biological aspects. 1110 62

Renal cell carcinoma (RCC), although occurring less frequently than prostate and bladder cancer, is actually the most malignant urologic disease, killing >35% of affected patients. Therefore, investigation of the nature of premalignant lesions of the kidney is a relevant issue. Following the most recent histological classification RCC can be subdivided into four categories: conventional RCC; papillary RCC; chromophobe RCC; and collecting duct carcinoma. In contrast to many genitourinary malignancies, premalignant alterations in the kidney are scarcely described. Intratubular epithelial dysplasia has been recognized as the most common precursor of RCC. In analogy to prostatic intraepithelial neoplasia (PIN), the premalignant lesions of the kidney are described as high or low-grade renal intratubular neoplasia. In contrast, precancerous lesions have been described as part of the von Hippel-Lindau syndrome (VHL) where the evolution from a simple cyst to an atypical cyst with epithelial hyperplasia to cystic or solid conventional-type RCC is well documented. Finally, in the genesis of papillary RCC an adenoma-carcinoma sequence has been recognized with specific genetic changes. There are no data on the epidemiology of premalignant lesions of the kidney, but research into the etiology of RCC has been extended substantially. Familial and genetic factors are well documented in VHL disease, in hereditary papillary RCC, in the tuberous sclerosis complex and in familial RCC. Cigarette smoking and obesity are established risk factors for RCC. Hypertension or its medication has also been associated with an increased risk. Among dietary factors an inverse relation between risk and consumption of vegetables and fruit has been found. Occupational exposure to substances such as asbestos and solvents has been linked to an increased risk of RCC. Specific RCC variants have distinctive chromosome alterations and several genes have been implicated in the development of RCC. Loss of material from the 3p chromosome characterizes conventional RCC and the deletion of the VHL suppressor gene plays an important role in the genesis of this RCC variant. In contrast, numerical changes with trisomy of chromosomes 7 and 17 and loss of the sex chromosome are typical changes in papillary tumors, whereas papillary RCC have additional trisomies. Chromophobe RCC is characterized by loss of chromosomes with a combination of monosomies. Less consistent genetic alterations are associated with collecting duct carcinoma. The traditional treatment of RCC is surgery by radical or partial nephrectomy. The latter approach carries a risk of tumor recurrence as a result of unrecognized satellite lesions or premalignant lesions that might have been present at the time of surgery. However, the reported recurrence rates after partial nephrectomy are <1% and therefore the possible presence of premalignant disease does not alter the actual treatment strategy advocated. Although multifocality and bilateral occurrence of RCC are much more likely in cases of papillary RCC, biopsy of the renal remnant or contralateral kidney is not justified even in patients with this tumor type. Conversely, patients with RIN in a partial or radical nephrectomy specimen or in a renal biopsy taken for whatever reason should be subjected to closer follow-up with regularly repeated ultrasound. When an effective chemopreventive regimen becomes available it might be useful for patients with an inherited risk of RCC as well as in those who are at risk of tumor recurrence after intervention. Mass screening with the purpose of detecting RCC at its earliest stage is not recommended at the present time, but screening focused on certain risk groups can be advocated. Further research is needed to identify avoidable risks, develop effective chemoprevention and recognize patients at risk.
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PMID:Precancerous lesions in the kidney. 1114 93

We report a case of collecting duct carcinoma (Bellini duct carcinoma) producing carcinoembryonic antigen (CEA). A 61-year-old man visited our hospital because of a left renal mass detected by ultrasonography in an other hospital. Computed tomography showed a low density tumor measuring about 3 cm in the left kidney. Angiography demonstrated a hypovascular tumor. The serum level of CEA was increased to 20 ng/ml. (normal < 7 ng/ml). Left radical nephrectomy was performed. Histological examination revealed collecting duct carcinoma with papillary growth (T1aN1M0). Cancer cells showed a positive immunohistochemical staining for CEA. Under a diagnosis of CEA-producing collecting duct carcinoma of the left kidney, the patient underwent systemic chemotherapy (M-VAC). The serum level of CEA decreased to the normal level after the nephrectomy, but six months postoperatively, metastatic bone tumor at the left pelvic bone was revealed on the plain film and at the same time, the CEA level was increased again.
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PMID:[A case of collecting duct carcinoma (Bellini duct carcinoma) producing carcinoembryonic antigen]. 1132 60

Collecting duct carcinoma of the kidney is a rare neoplasm that arises from the medullary collecting ducts. It has an aggressive clinical course and patients usually present with metastatic disease. Treatment approaches apart from surgery have been unrewarding. Renal medullary carcinoma is also an aggressive tumour which occurs predominantly in young, black, male patients with sickle cell trait. We describe a case of collecting duct carcinoma in a 61-year-old black female who exhibited the sickle cell trait. Histopathology revealed a high-grade tubular carcinoma with marked desmoplasia, adjacent dysplastic collecting ducts and positive immunohistochemical staining for high and low molecular weight cytokeratins and epithelial membrane antigen. The association of collecting duct carcinoma with sickle cell trait has not been previously reported. This case supports the postulate that collecting duct carcinoma and renal medullary carcinoma may be part of the same spectrum of renal malignancies.
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PMID:Collecting duct carcinoma of the kidney associated with the sickle cell trait. 1150 Dec 35

cis-platinum(II) (cis-diammine dichloroplatinum; cisplatin) is a potent antitumor compound that is widely used for the treatment of many malignancies. An important side-effect of cisplatin is nephrotoxicity, which results from injury to renal tubular epithelial cells and can be manifested as either acute renal failure or a chronic syndrome characterized by renal electrolyte wasting. Recently, apoptosis has been recognized as an important mechanism of cell death mediating the antitumor effect of cisplatin. This study was undertaken to examine the mechanisms of cell death induced by cisplatin in M-1 cells, which were derived from the outer cortical collecting duct cells of SV40 transgenic mice. Treatment of M-1 cells with high concentrations of cisplatin (0.5 and 1 mM) for 2 hr led to necrotic cell death, whereas a 24-hr treatment with 5-20 microM cisplatin led to apoptosis. Antioxidants protected against cisplatin-induced necrosis, but not apoptosis, indicating that reactive oxygen species play a role in mediating necrosis but not apoptosis induced by cisplatin and that the mechanism of cell death induced by cisplatin is concentration dependent. The low concentrations of cisplatin, which induced apoptosis in M-1 cells, did not affect the expression levels of Bcl-2-related proteins and did not activate c-Jun NH2-terminal kinase (SAPK/JNK). Cisplatin induced the translocation of endogenous Bax from the cytosolic to the membrane fractions and, subsequently, the release of cytochrome c. Overexpression of Bcl-2 blocked cisplatin-induced apoptosis and Bax translocation. These observations suggest that the subcellular redistribution of Bax is a critical event in the apoptosis induced by cisplatin.
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PMID:Cisplatin-induced apoptosis by translocation of endogenous Bax in mouse collecting duct cells. 1159 70


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