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)

A mechanism decreasing oxidative metabolism during normal cell division and growth is expected to direct substrates toward biosyntheses rather than toward complete oxidation to CO(2). Hence, any event decreasing oxidative phosphorylations (OXPHOS) could provide a proliferating advantage to a transformed or tumor cell in an oxidative tissue. To test this hypothesis, we studied mitochondrial enzymes, DNA and OXPHOS protein content in three types of renal tumors from 25 patients. Renal cell carcinomas (RCCs) of clear cell type (CCRCCs) originate from the proximal tubule and are most aggressive. Chromophilic RCCs, from similar proximal origin, are less aggressive. The benign renal oncocytomas originate from collecting duct cells. Mitochondrial enzyme and DNA contents in all tumor types or grades differed significantly from normal tissue. Mitochondrial impairment increased from the less aggressive to the most aggressive RCCs, and correlated with a considerably decreased content of OXPHOS complexes (complexes II, III, and IV of the respiratory chain, and ATPase/ATP synthase) rather than to the mitochondrial content (citrate synthase and mitochondrial (mt)DNA). In benign oncocytoma, some mitochondrial parameters (mtDNA, citrate synthase, and complex IV) were increased 4- to 7-fold, and some were slightly increased by a factor of 2 (complex V) or close to normal (complexes II and III). A low content of complex V protein was found in all CCRCC and chromophilic tumors studied. However F(1)-ATPase activity was not consistently decreased and its impairment was associated with increased aggressiveness in CCRCCs. Immunodetection of free F(1)-sector of complex V demonstrated a disturbed assembly/stability of complex V in several CCRCC and chromophilic tumors. All results are in agreement with the hypothesis that a decreased OXPHOS capacity favors faster growth or increased invasiveness.
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PMID:Low mitochondrial respiratory chain content correlates with tumor aggressiveness in renal cell carcinoma. 1201 48

This report discusses the new cytogenetic classification of renal cell carcinoma (RCC) and its biological and clinical significance. It describes the four major types (clear cell, chromophil, chromophobe, and collecting duct) as well as rarer entities, such as small cell carcinoma, cystic RCC, rhabdoid variant of RCC, and unclassified RCC. Sarcomatoid carcinomas are a diverse group representing high-grade transformation of the other types. In addition to a description of the pathologic findings, there is a discussion of tumor markers and prognostic indicators. The clinical significance of the classification is discussed, with reference to recent reports.
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PMID:Kidney pathology: current classification of renal cell carcinoma. 1208 16

The development of consensus classifications for renal epithelial neoplasia in 1996 and 1997 led to the recognition of renal adenoma, renal oncocytoma and metanephric adenoma/adenofibroma as benign tumors and conventional (clear cell) renal cell carcinoma (RCC), papillary RCC, chromophobe RCC and collecting duct carcinoma as malignant morphotypes. While the overwhelming majority of renal adenomas and metanephric adenomas are benign, malignant transformation of both types have been described and genetic predictors of malignant transformation are as yet unknown. The main groups of malignant renal tumors are associated with characteristic genetic changes; conventional RCC (-3p), papillary RCC (+7, +17, -Y), chromophobe RCC (hypodiploid). Recent studies have also shown focal loss of heterozygosity of 3p segments in papillary and chromophobe RCC, indicating that 3p mutations are not confined to the conventional RCC morphotype and suggesting the presence of an important tumor suppressor gene at this site. Sarcomatoid metaplasia may occur in any morphotype and this is associated with a poor prognosis. More recently additional varieties of conventional RCC (multilocular cystic RCC), collecting duct carcinoma (medullary renal carcinoma) and papillary RCC (Types 1 and 2), each showing a characteristic morphology, have been recognized.
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PMID:Evolving classification of renal cell neoplasia. 1211 90

To date, much progress has been made in the fields of cytogenetics and molecular genetics of renal tumors. The previous and recent findings have delineated the characteristics of the various tumors, particularly the cytogenetic and molecular differences that exist between papillary and nonpapillary clear cell renal cell carcinomas (RCCs). At the same time, new cytogenetic subtypes have emerged [e.g., t(X;1)] in subtypes of RCC, while in others (e.g., Wilms tumors) several new cytogenetic abnormalities and consequent molecular involvement have been found. In addition to Wilms tumor, papillary RCC, and clear-cell RCC, cytogenetic and fluorescence in situ hybridization analyses have been performed on several other tumors of the kidney, including chromophobic carcinoma, metanephric adenoma, collecting duct carcinoma, transitional cell carcinoma, congenital mesoblastic nephroma, and malignant rhabdoid tumors of the kidney. This review is therefore intended to present a concise update on the cytogenetic and molecular data on renal tumors, focusing mainly on the clinical usefulness of the findings reported in the literature.
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PMID:Renal cancer: cytogenetic and molecular genetic aspects. 1240 97

The current classification system of renal tumors is based on morphologic criteria, as supported by genetic findings. We present a group of previously unclassified tumors with similar morphologic and genetic features, suggesting a new entity within renal neoplasms. Seven renal tumors from five patients (ages 31-67 years) were analyzed. All cases were stained with periodic acid-Schiff, Hale's colloidal iron (HCI), and Alcian blue (AB) at pH 2.5/1.0 with and without hyaluronidase (HA) digestion. Immunohistochemical (IHC) stains were performed for CK8, CK18, CK19, vimentin, villin, Tamm-Horsfall protein (THP), renal cell carcinoma marker (RCC), epithelial membrane antigen (EMA), ulex europaeus agglutinin (UEA-1), soy bean agglutinin (SBA), peanut agglutinin (PNA), and MIB-1. Comparative genomic hybridization (CGH) and loss of heterozygosity (LOH) studies were performed on all cases. All tumors showed circumscribed growth, a tubular growth pattern with focal solid areas, no significant nuclear atypia and absence of necrosis, desmoplasia, or inflammation. Abundant extracellular mucin was present. Immunohistochemistry stains support collecting duct origin (EMA+, PNA+, SBA+/-, CK 8/18/19+, vimentin+/-, UEA-1-, RCC-, villin-, THP-). The proliferative rate was low (<1%). CGH showed multiple consistent chromosomal losses (-1,-4, -6, -8, -9, -13, -14, -15, -22). Clinical outcome was favorable, with recurrences but no known distant metastases or death of disease. These findings are distinct from all previously classified renal neoplasms. Our data suggest the presence of a unique tumor entity within tumors of probable collecting duct origin: tubular-mucinous renal tumors of low malignant potential.
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PMID:Low-grade tubular-mucinous renal neoplasms: morphologic, immunohistochemical, and genetic features. 1242 95

In recent years, the concept of chromophobe renal cell carcinoma (RCC) has been established. Chromophobe RCCs account for about 4-6% of all renal tumors. Macroscopically, the cut surface of the tumor is generally grey-beige in color. Histologically, there are two variants (typical and eosinophilic). In the typical variant, large tumor cells with architecture of a compact tubulo-cystic pattern proliferate. The cytoplasm is abundant and shows a fine reticular translucent pattern. The cell border is thick, prominent and eosinophilic. In the eosinophilic variant, tumor cells are smaller and markedly eosinophilic, and a perinuclear halo is often seen. Histochemically, the tumor cells generally show a diffuse and strong reaction for Hale's colloidal iron staining. Ultrastructurally, tumor cells contain many cytoplasmic microvesicles (150-300 nm). In chromosomal analysis, a low chromosome number is characteristic of chromophobe RCCs, due to the frequent occurrence of a combined loss of chromosomes 1, 2, 6, 10, 13, 17, and 21. In differential diagnosis, histological distinction from oncocytomas, which share a common phenotype (intercalated cells of the collecting duct system), is most important. In this diagnostic setting, recent studies have given rise to several problems. Firstly, some cases of coexistent chromophobe RCC and oncocytoma (so-called renal oncocytosis) or cases of oncocytoma with metastasis have recently been reported. Secondly, the existence of chromophobe adenoma, which is the benign counterpart of chromophobe RCC, and an oncocytic variant of chromophobe RCC has recently been suggested. Therefore, further studies are needed to elucidate the relationship between chromophobe RCCs and oncocytomas, to confirm whether chromophobe adenoma actually exists or not, and to identify the key gene that causes chromophobe RCCs.
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PMID:Review of chromophobe renal cell carcinoma with focus on clinical and pathobiological aspects. 1250 96

Renal epithelial cancers represent a heterogeneous group of neoplasms arising from the malignant transformation of presumed diverse cell lineages. We recently demonstrated that tumor-specific up-regulation of human leukocyte antigen (HLA)-G, a nonclassical HLA class Ib molecule that might be involved in immune evasion by tumor cells, frequently occurs in conventional (clear cell) renal carcinoma. We here examined whether HLA-G activation is a common process affecting all types of renal epithelial tumors. We analyzed a series of 38 paraffin-embedded tumors including clear cell, papillary, chromophobe, collecting duct carcinoma, and oncocytoma. Seven of 12 (58%) clear cell tumors were positive by immunohistochemistry, whereas all of the other subtypes of renal carcinoma were negative for HLA-G expression. Developing or adult normal renal tissue were devoid of HLA-G expression. We also observed that ectopic expression of HLA class II antigens occurs more frequently in clear cell renal carcinoma than in other subtypes of renal tumors. Moreover, in contrast to the common observation of a down-regulation of major histocompatibility complex class Ia antigens reported in various tumors, the concomitant study of the same biopsies for classical HLA class Ia antigen expression revealed a general increase of HLA class Ia expression, regardless of histological subtypes. These results provide evidence for the heterogeneity of major histocompatibility complex expression patterns in renal carcinoma and support the hypothesis that specific mechanisms underlying the malignant transformation into clear cell renal carcinoma up-regulate expression of HLA-G and to a lesser extent HLA class II molecule expression. Considering the immunotolerant role of HLA-G toward the immune response, these mechanisms may thus provide renal cell carcinoma tumor cells with additional means to escape immune surveillance.
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PMID:Altered pattern of major histocompatibility complex expression in renal carcinoma: tumor-specific expression of the nonclassical human leukocyte antigen-G molecule is restricted to clear cell carcinoma while up-regulation of other major histocompatibility complex antigens is primarily distributed in all subtypes of renal carcinoma. 1254 8

We report a case of a 72-year-old man with a chromophobe renal cell carcinoma that had both sarcomatoid and collecting duct carcinoma components. The 7-cm tumor occupied the entire lower pole of the kidney and infiltrated the renal parenchyma and the pelvic-calyceal system. Histologically, it had an area of classic chromophobe renal cell carcinoma that merged into a sarcomatoid component. Closely intermixed with the sarcomatoid component was a collecting duct carcinoma component characterized by highly pleomorphic, epithelioid cells arranged in cords, nests, and tubulomicrocystic structures. The cords, nests, and tubules were associated with a florid desmoplastic stromal response and numerous inflammatory cells. In addition, dysplastic changes were noted in adjacent nonneoplastic collecting duct epithelium. Immunohistochemical studies confirmed the presence of 3 distinct components in this patient's tumor. To the best of our knowledge, this is the first reported case of a chromophobe renal cell carcinoma with sarcomatoid and collecting duct carcinoma components.
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PMID:Renal cell carcinoma, chromophobe type, with collecting duct carcinoma and sarcomatoid components. 1256 94

International agreement was reached on the histologic classification of renal epithelial neoplasms during the last years. This classification defines malignant neoplasms as clear-cell (conventional) renal carcinoma, papillary renal carcinoma, chromophobe renal carcinoma, collecting duct carcinoma and renal cell carcinoma, unclassified. Benign neoplasms are papillary adenoma, renal oncocytoma and metanephric nephroadenoma/adenofibroma. Over the past few years, new or rare distinctive kidney tumors have been described. The aim of this review is to present examples of recently recognized clinicopathologic tumor entites and to discuss the value of immunohistochemical and molecular tests for the differential diagnosis. The following tumors will be described: mixed epithelial/stromal renal tumors, primary renal synovial sarcomas, primary renal primitive neuroectodermal tumors, low grade myxoid renal epithelial neoplasms with distal nephron differentiation and epitheloid angiomyolipoma. Detection of SYT-SSX gene fusion transcripts resulting from the t(X;18) and the EWS-FLI-1 gene fusion are described as molecular tests for the diagnosis of renal synovial sarcomas and renal primitive neuroectodermal tumors. Immunohistochemical expression of hormone receptor is helpful to diagnose mixed epithelial/stromal renal tumors. It is important to distinguish these tumor entities from adult Wilms' tumors and sarcomatoid renal cell carcinomas because of a different biological behaviour and different therapeutical approaches.
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PMID:[Renal tumors in adults: rare tumors and new tumor entities]. 1264 50

In sarcomatoid renal cell carcinoma (RCC), it is generally accepted that the sarcomatoid portion is derived from metaplastic transformation of carcinoma. Sarcomatoid RCCs account for about 1-8% of all renal tumors. Macroscopically, tumors generally form encapsulated masses and show invasive growth. Sarcomatoid RCCs originate from all subtypes of RCCs, including conventional, papillary, chromophobe, and collecting duct carcinomas. With regard to the growth pattern of the sarcomatoid component, malignant fibrous histiocytomatous, fibrosarcomatous and unclassified sarcomatous patterns are frequently seen. Immunohistochemically, sarcomatoid RCCs are generally positive for AE1/AE3, epithelial membrane antigen (EMA) and vimentin and negative for desmin, actin and S-100. Little is know about genetic alterations in sarcomatoid RCCs. Further studies are therefore needed to identify the key gene involved in sarcomatoid transformation of RCCs.
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PMID:Review of sarcomatoid renal cell carcinoma with focus on clinical and pathobiological aspects. 1264 6


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