Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin converting enzyme (ACE, EC 3.4.15.1) was purified to homogeneity from human kidney and its specific antibody was raised in the rabbit. The antibody cross-reacted equally with human enzymes from kidney, lung, intestine, plasma and urine. Immunofluorescent and immunoelectron microscopic observation indicated that the enzyme was located on the plasma membrane and micropinocytic vesicles at the luminal site of vascular endothelium in the lung. It was also present on the brush border, intercellular and basal infolding membranes of proximal tubular epithelium, but was not detected on the distal tubular epithelium or vascular endothelium in the kidney. ACE was demonstrated immunocytologically in human alveolar macrophages and renal carcinoma tissues. The carcinoma tissue contained a possible isoenzyme of ACE differing in part immunologically from the enzyme of normal kidney.
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PMID:Biochemistry of human converting enzyme. 303 82

Angiotensin-converting enzyme (ACE, EC 3.4.15.1) was demonstrated in the tissue of human renal cell carcinoma and its cultured cells by immunofluorescence and immunohistochemistry using a specific rabbit antibody to human kidney ACE. The biochemical properties of the partially purified enzyme from the tumor tissue were identical with the pure enzyme from normal kidney with respect to Km, optimal pH, chloride ion activation and heat sensitivity. Catalytic activities of tumor and normal kidney enzymes were similarly inhibited by an ACE inhibitor, captopril, and by the antibody to human kidney ACE. However, double immunodiffusion analysis showed spur-forming immunoprecipitin bands between the tumor and normal kidney enzyme. These data suggest that human renal cell carcinomas have a new isozyme of ACE differing in part immunologically from the enzyme of normal kidney.
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PMID:Characterization and immunohistologic demonstration of angiotensin-converting enzyme in human renal cell carcinoma. 630 61

Many of the discoveries of multidrug resistance (MDR) have resulted from studies using drug-resistant cultured tumor cell lines as experimental models. To date, there has been no report on the detailed characterization of such a cell line from renal cell carcinoma (RCC). By long-term exposure of an established RCC (RCC8701) to increasing concentrations of adriamycin, we established a series of subcultures that were considerably more resistant to the cytotoxic effect of this drug. Biological morphology and cell cycles were analyzed by morphometry and flow cytometry. The chemoresistance index of cells were measured by methyl tetrazolium assay. For evaluation of the expression of MDR-related protein (MRP), mdr-1, glutathione transferase (GST-pi), and topoisomerase II mRNAs, the reverse transcription-polymerase chain reaction was used. Membranous expression of mdr-1-related p-glycoprotein was analyzed by immunofluorescence cytometry. The intracellular content of both glutathione (GSH) and glucose-6-phosphate dehydrogenase (G-6-PDH) were measured using a capillary electrophoresis method. Compared with parent cells, the resistant sublines had a slower growth rate and lower confluent density. They were smaller and mixed with giant cells in different sizes and with different numbers of nucleoli. Flow cytometric analyses showed that resistant cells had a greater percentage of cells in the G2/M phase. The resistant cells, RCC8701/ADR800, were 122 times more resistant to adriamycin and 238 times more resistant to epirubicin than the parent cells. The resistant cells also demonstrated cross-resistance to cisplatin and 5-fluorouracil. In addition to MRP, the contents of mRNA coding for mdr-1, GST-pi, and topoisomerase II in the MDR sublines were higher than in the native cell line. A higher content of cytoplasmic GSH and G-6-PDH were found in the resistant cells; however, the expression of the MDR-related membranous glycoprotein, p-glycoprotein, was not raised. The adriamycin-induced MDR sublines may be used as an experimental system for the search of a means to overcome drug resistance and elucidate possible mechanisms of acquired MDR involved in human renal cancer.
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PMID:Establishment and characterization of renal cell carcinoma cell lines with multidrug resistance. 1085 Jun 29

A 78-year-old woman with renal cell carcinoma and pulmonary metastasis presented with reversible cardiomyopathy induced by gamma(gamma)-interferon. She was treated with gamma-interferon twice a week since November 1996. She presented with severe acute congestive heart failure and gamma-interferon was immediately discontinued in December 1997. Left ventricular fractional shortening was 38% before admission, 12% on admission, and improved to 31% by 40 days after discontinuation of interferon together with administration of diuretics and angiotensin converting enzyme inhibitor. We restarted the same gamma-interferon regimen because it was effective against renal cell carcinoma after 47 days. She has remained well with no significant changes of cardiac function or renal cell carcinoma for almost one year.
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PMID:[Gamma-interferon-induced cardiomyopathy during treatment of renal cell carcinoma: a case report]. 1092 66

Several studies have suggested that antihypertensive treatment may promote cancer through unknown mechanisms. Early retrospective studies implicated reserpine in breast cancer, but data from prospective studies and meta-analysis of several case-controlled studies showed only a weak association between reserpine and breast cancer which, although statistically significant, is of little clinical concern. Data from case-controlled studies and several cohort studies suggested an association between the use of a diuretic and the occurrence of renal cell cancer, particularly in women. A recent study showed an association between the use of a diuretic and the occurrence of colon cancer. Several prospective studies showed that treatment with atenolol may increase mortality from malignancy. However, other studies that analyzed data from several thousand patients could not confirm this association. In three prospective and a few case-controlled studies, angiotensin converting enzyme inhibitors were not associated with increased mortality from malignancy. In addition, a recent retrospective study showed that long-term use of angiotensin converting enzyme inhibitors had a protective effect against malignancy. Data from three large case-controlled studies and the combined data from eight randomized controlled studies and seven longitudinal studies showed a similar risk for malignancy among users and nonusers of calcium antagonists. Until further data from prospective clinical trials are available, we advise caution about long-term diuretic therapy in women. With regard to other antihypertensive drug classes, we suggest continuing the management of hypertension according to current treatment guidelines with little fear of any substantial cancer risk.
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PMID:Carcinogenicity of antihypertensive therapy. 1200 1

A 70-year-old obese, hypertensive woman taking angiotensin converting enzyme (ACE) inhibitors and chlorthalidone but with no history of corticosteroid treatment or hypothalamus-hypophyseal-adrenal disease, underwent nephrectomy and adrenalectomy under combined general and epidural anesthesia. Severe hypotension with oliguria developed during surgery and persisted during postoperative recovery, with anuria, metabolic acidosis, hyponatremia and hyperpotassemia. Although the symptoms were initially attributed to prior treatment with ACE inhibitors and diuretics together with combined anesthesia, the patient's lack of response to crystalloid, colloid and inotropic catecholamine therapy in the context of anuria, metabolic acidosis, hyponatremia and hyperpotassemia led us to consider a diagnosis of Addisonian crisis. Blood samples were taken to determine adrenocorticotropic hormone levels, and hydrocortisone treatment was started. The patient responded to treatment and cortisol levels fell, confirming the diagnosis of adrenal insufficiency. Compensatory endrocrine secretion of cortisol by the contralateral adrenal gland has been observed in patients undergoing nephrectomy and adrenalectomy for excision of a hypernephroma, and replacement therapy is therefore not recommended. Perioperative Addisonian crises have also been described in patients suffering great surgical stress, and severe hypotension has been observed in patients on long-term treatment with ACE inhibitors after induction of general anesthesia and after epidural anesthesia with local anesthetics. The combination of these factors made rapid diagnosis and start of appropriate therapy difficult.
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PMID:[Severe perioperative hypotension after nephrectomy with adrenalectomy]. 1460 83

The 31st Annual Meeting of the American Society of Nephrology, held in Philadelphia, Pennsylvania, USA, October 25-28, 1998, presented the newest advances in basic and clinical nephrology science. Several presentations discussed the results of studies with the newer immunosuppressants such as tacrolimus, sirolimus, mycophenolate mofetil and the anti-CD25 monoclonal antibodies, with the conclusion that studies on long-term use of these agents are needed. A number of other issues on immunosuppression protocols in renal transplantation were addressed during the meeting, including the subjects of steroid withdrawal and the role of TGF-beta in the development of chronic allograft nephropathy. The use of NESP in the treatment of renal anemia, the use of sildenafil to treat erectile dysfunction in hemodialysis patients, and the use of ACE inhibitors in nondiabetic renal patients were other important issues discussed at this meeting. Newer approaches to the treatment of hypertension discussed at the meeting highlighted the potential role of angiotensin II receptor antagonists in renal disease patients. Researchers also presented the promising results of a trial of a new, hybrid cell vaccine approach to the treatment of renal cell carcinoma.
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PMID:Recent advances in nephrology. 1561 34

There is much to find out about this fascinating and complex molecule in relation to the development and progression of asthma. Added to it are three further new asthma/allergy genes identified by positional cloning: PDH Finger Protein II (PHF11) on chromosome 13q14, which encodes NY-REN-34 a protein first described in patients with renal cell carcinoma [67]; Dipeptidyl diptidase 10 (DDP10) on chromosome 2q14 [68]; and G protein-coupled receptor for asthma susceptibility (GPRA) on chromosome 7p [69]. For each of these genes, as is the case for ADAM33, determining their normal function(s) and how these become disordered in asthma is the future challenge.
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PMID:ADAM33: a newly identified gene in the pathogenesis of asthma. 1625 31

We report three cases of metastatic renal cell carcinoma (RCC) in which combination treatment of cimetidine, cyclooxygenase-2 inhibitor and renin-angiotensin system inhibitor (angiotensin converting enzyme inhibitor or angiotensin II type 1 receptor antagonist) (CCA therapy) was effective. Case 1: A 47-year-old man who had a 12-cm right renal tumor with multiple pulmonary and hepatic metastases refused cytokine therapy for economic reasons and received CCA therapy. All of the metastases showed partial remission, which continued for 12 months. Case 2: A 62-year-old man with multiple pulmonary and mediastinal lymph node metastases from clear cell RCC refractory to interferon-alpha and interleukin-2 started CCA therapy. Partial remission has been maintained for 16 months. Case 3: A 64-year-old man with pulmonary metastases from clear cell RCC discontinued interferon-alpha treatment due to its side effects after six months and received CCA therapy. Pulmonary metastases showed partial remission for 31 months. The CCA therapy could be an alternative treatment for metastatic RCC patients unfit for cytokine therapy.
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PMID:Favorable response to combination treatment of cimetidine, cyclooxygenase-2 inhibitor and renin-angiotensin system inhibitor in metastatic renal cell carcinoma: Report of three cases. 1878 6

We report a patient with scleroderma, renal cell carcinoma (RCC) and membranous nephropathy (MN). Certain clinical and laboratory features suggested that RCC caused or enhanced the other two conditions. A 55-year-old man developed scleroderma which progressed rapidly during its first 2 years with development of hypertension and acute renal failure, peak serum creatinine (SCr) 327 micromol/l (3.7 mg/dl) and partial improvement of the renal function (SCr 239 micromol/l or 2.7 mg/dl) after initiation of an angiotensin converting enzyme inhibitor. He subsequently developed nephrotic syndrome (urine protein excretion 9 gm/24-h) and progressive renal failure, with SCr 469 +/- 18 micromol/l (5.3 +/- 0.2 mg/dl). An anti-nuclear mitotic apparatus protein (NUMA) antibody, which is uncommon in scleroderma but has been linked to certain malignancies, was found in his serum. A left upper pole RCC was removed by heminephrectomy. MN was found in the renal parenchyma adjacent to the excised tumor. In the 3.5 years following surgery, the clinical manifestations of scleroderma have been arrested while the medications prescribed for this condition have been greatly reduced. Proteinuria is consistently less than 1 gm/24-h and 42 months after surgery serum creatinine was 256 micromol/l (2.9 mg/dl). Nutrition has also improved. Although this case may represent chance occurrence of three uncommon diseases (scleroderma, RCC, MN) in the same individual, the sustained improvement of the manifestations of scleroderma and MN after resection of the RCC contrasted to the rapid course of these conditions until the surgery, and the presence in the patient's serum of an autoantibody which is uncommon in patients with scleroderma, but has been linked to malignancy, suggest a pathogenetic relationship between the three conditions.
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PMID:Association between scleroderma, renal cell carcinoma and membranous nephropathy. 1920 52


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