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 54-year-old woman presented with blepharoptosis, numbness in the lower lip, dysgeusia and pain in the extremities and back. MRI showed marked meningeal thickening and multiple bone lesions accompanying a prominent enhancing effect. CT scan of the chest and abdomen appeared to be unremarkable for primary cancer. She died 3 months after the admission, and postmortem autopsy showed a mass of about 2.5 cm in diameter in the renal medulla. Histological examination including immunohistochemistry confirmed the presence of a collecting duct carcinoma (CDC). This case is of particular interest because it emphasizes the possible fulminate clinical course of a small CDC.
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PMID:Undiagnosed collecting duct carcinoma presenting as meningeal carcinomatosis and multiple bone metastases. 2068 87

Renal cell carcinomas (RCC) can be subclassified for general purposes into clear cell, papillary cell, chromophobe cell carcinomas and oncocytomas. Other tumours such as collecting duct, medullary, mucinous tubular and spindle cell and associated with Xp 11.2 translocations/TFE 3 gene fusion, are much less common. There is also a residual group of unclassified cases. Previous studies have shown that RCC has high glycolytic rates, and expresses GLUT transporters, but no distinction has been made among the different subtypes of renal cell tumours and their grades of malignancy. In clear renal cell carcinoma (cRCC) glycogen levels increase, glycolysis is activated and gluconeogenesis is reduced. The clear cell subtype of RCC is characterized histologically by a distinctive pale, glassy cytoplasm and this appearance of cRCC is due to abnormalities in carbohydrate and lipid metabolism, and this abnormality results in glycogen and sterol storage. Several isoforms of glucose carriers (GLUTs) have been identified. We show here in a panel of 80 cRCC samples a significant correlation between isoform 5 (GLUT5) and many pathological parameters such as grade of differentiation, pelvis invasion and breaking capsule. GLUT5 expression also appears to associate more strongly with the clear cell RCC subtype. These data suggest a role for the GLUT5 isoform in fructose uptake that takes place in cRCC cells and which subsequently leads to the malignant RCC progression.
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PMID:Fructose transporter GLUT5 expression in clear renal cell carcinoma. 2116 69

Renal cell carcinoma (RCC) accounts for approximately 3% of all new cancer diagnosis every year. RCC arises from the renal epithelium and represents 85% of all kidney tumors. According to histology, these neoplasms are divided into the following types: clear cell, papillary, chromophobe, oncocytoma, collecting duct, and unclassified. Approximately, 75% of RCCs are of the clear cell type and in recent years, there have been substantial advances in the understanding of its molecular biology leading to the development of effective treatments. However, there is still an area of uncertainty with regard to non-clear cell histologies. Scarce studies have been conducted testing different drugs in this patient population. Thus, most of the evidence comes from small phase II trials, retrospective analysis, or expanded access programs. Recent insights in the molecular basis of these tumors have opened a promising research field. Molecules targeting mammalian target of rapamycin, epidermal growth factor receptor, c-MET, vascular endothelial growth factor, and platelet-derived growth factor are among some of the promising drugs tested in this setting. This article reviews the mechanisms of disease on RCC and summarizes treatment options with a particular focus on patients with non-clear cell tumors.
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PMID:Non-clear cell advanced kidney cancer: is there a gold standard? 2117 5

The kidneys are responsible for the urinary excretion of uremic toxins and the regulation of several body systems such as intra and extracellular volume status, acid-base status, calcium and phosphate metabolism or erythropoiesis. They adapt quantitative and qualitative composition of the urine to keep these systems in balance. The flow of plasma is filtered in the range of 120 mL/min, and depends on the systemic and renal hemodynamics which is subject to self-regulation. The original urine will then be modified in successive segments of the nephron. The proximal nephron is to lead the massive reabsorption of water and essential elements such as sodium, bicarbonates, amino-acids and glucose. The distal nephron includes the distal convoluted tubule, the connector tube and the collecting duct. Its role is to adapt the quality composition of urine to the needs of the body.
Bull Cancer 2012 Mar 01
PMID:[Renal physiology]. 2215 16

Hyponatremia, a common electrolyte abnormality in oncology practice, may be a negative prognostic factor in cancer patients based on a systematic analysis of published studies. The largest body of evidence comes from small-cell lung cancer (SCLC), for which hyponatremia was identified as an independent risk factor for poor outcome in six of 13 studies. Hyponatremia in the cancer patient is usually caused by the syndrome of inappropriate antidiuretic hormone (SIADH), which develops more frequently with SCLC than with other malignancies. SIADH may be driven by ectopic production of arginine vasopressin (AVP) by tumors or by effects of anticancer and palliative medications on AVP production or action. Other factors may cause hypovolemic hyponatremia, including diarrhea and vomiting caused by cancer therapy. Hyponatremia may be detected on routine laboratory testing before or during cancer treatment or may be suggested by the presence of mostly neurological symptoms. Treatment depends on several factors, including symptom severity, onset timing, and extracellular volume status. Appropriate diagnosis is important because treatment differs by etiology, and choosing the wrong approach can worsen the electrolyte abnormality. When hyponatremia is caused by SIADH, hypertonic saline is indicated for acute, symptomatic cases, whereas fluid restriction is recommended to achieve a slower rate of correction for chronic asymptomatic hyponatremia. Pharmacological therapy may be necessary when fluid restriction is insufficient. The orally active, selective AVP receptor 2 (V(2))-receptor antagonist tolvaptan provides a mechanism-based option for correcting hyponatremia caused by SIADH or other conditions with inappropriate AVP elevations. By blocking AVP effects in the renal collecting duct, tolvaptan promotes aquaresis, leading to a controlled increase in serum sodium levels.
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PMID:Diagnosis and management of hyponatremia in cancer patients. 2261 70

The most common primary malignant renal tumor is renal cell carcinoma (RCC), which accounts for 3% of all adult malignancies. Bellini duct carcinoma or collecting duct carcinoma is an unusual rare variant of RCC. This histologically distinct tumor is very rare, with less than 100 cases reported in the literature, and accounts for approximately 1% of all malignant renal epithelial tumors. We report two cases of collecting duct carcinoma and highlight the rarity of these tumors and their similarity to RCC.
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PMID:Collecting duct carcinoma: a rare renal tumor. 2280 97

Kidney cancer is not a single disease; it is made up of a number of different types of cancer, including clear cell, type 1 papillary, type 2 papillary, chromophobe, TFE3, TFEB, and oncocytoma. Sporadic, nonfamilial kidney cancer includes clear cell kidney cancer (75%), type 1 papillary kidney cancer (10%), papillary type 2 kidney cancer (including collecting duct and medullary RCC) (5%), the microphalmia-associated transcription (MiT) family translocation kidney cancers (TFE3, TFEB, and MITF), chromophobe kidney cancer (5%), and oncocytoma (5%). Each has a distinct histology, a different clinical course, responds differently to therapy, and is caused by mutation in a different gene. Genomic studies identifying the genes for kidney cancer, including the VHL, MET, FLCN, fumarate hydratase, succinate dehydrogenase, TSC1, TSC2, and TFE3 genes, have significantly altered the ways in which patients with kidney cancer are managed. While seven FDA-approved agents that target the VHL pathway have been approved for the treatment of patients with advanced kidney cancer, further genomic studies, such as whole genome sequencing, gene expression patterns, and gene copy number, will be required to gain a complete understanding of the genetic basis of kidney cancer and of the kidney cancer gene pathways and, most importantly, to provide the foundation for the development of effective forms of therapy for patients with this disease.
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PMID:Genetic basis of kidney cancer: role of genomics for the development of disease-based therapeutics. 2303 66

In December 2003, a 32-year-old man underwent puncture for right renal cyst at a clinic. Since puncture fluid was dark red color in spite of negative cytology, he was being followed, but after a while he did not show up for further examination. In November 2007, he revisited the clinic due to low-grade fever. Computed tomographic findings showed an enlarged cystic mass with a solid component invading the liver and lymph node swelling. He underwent right radical nephrectomy combined with partial liver resection and lymphadenectomy. Histological findings showed collecting duct carcinoma associated with clear cell carcinoma directly invading the liver with lymph node metastasis (pT4N2M0). Although he underwent 4 cycles of gemcitabine-cisplatin therapy and alfa interferon injection 3 times a week thereafter as adjuvant setting, multiple liver metastasis occurred 15 months after surgery. He died of cancer 31 months after surgery in spite of molecular targeted therapy including sorafenib and sunitinib.
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PMID:[A case of collecting duct carcinoma originating from renal cyst]. 2341 18

Renal cell carcinoma (RCC) is the most common malignant tumor involving the kidney. Determining the subtypes of renal cell carcinoma is among the major goals of preoperative radiological work-up. Among all modalities, magnetic resonance imaging (MRI) has several advantages, such as inherent soft tissue contrast, detection of lipid and blood products, and excellent sensitivity to detect small amounts of intravenous contrast, which facilitate the discrimination of subtypes of RCC. In this article, we review MRI and pathological features used for determining the main histologic subtypes of RCC, including clear cell, papillary, collecting duct, chromophobe, multilocular cystic, and unclassified RCC.
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PMID:Subtypes of renal cell carcinoma: MRI and pathological features. 2343 56

The recent classification of renal tumors is based on genetic evidence as well as on histologic features. Malignant tumor includes clear cell renal carcinoma (RCC), multilocular cystic RCC, papillary RCC, chromophobe RCC, carcinoma of the collecting duct of Bellini, renal carcinoma associated with Xp11.2 translocations/TFE3 gene fusions and mucinous tubular and spindle cell carcinoma. Benign tumor is subdivided into papillary adenoma, renal oncocytoma and metanephric adenoma. Recently, new disease entities such as acquired cystic disease-associated RCC, clear cell papillary RCC and renal carcinoma with t(6;11)(p21:q12) have been discovered. In this article, we briefly review and introduce the clinical, morphological and genetic features of these tumor entities.
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PMID:Recent classification of renal epithelial tumors. 2352 39


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