Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adaptation of Ehrlich ascites tumor cells to serial cultivation in media with progressively elevated (hypertonic) NaCl content ("high NaCl"-tolerant cells) has resulted in progressive increases of the cellular activities of NAD-dependent glycerol-3-phosphate dehydrogenase (EC 1.1.1.8), NAD-dependent malate dehydrogenase (EC 1.1.1.37), glutamate--oxalacetate transaminase (EC 2.6.1.1), NAD (P)-dependent glutamate dehydrogenase (EC 1.4.1.3), NADP-dependent isocitrate dehydrogenase (EC 1.1.1.42). The activities of glutamate-pyruvate transaminase (EC 2.6.1.2.) and of glycolytic enzymes as phospho-fructokinase (EC 2.7.1.11), glyceraldehydephosphate dehydrogenase (EC 1.2.1.12) and lactate dehydrogenase (EC 1.1.1.27) were only slightly and not in progressive manner (in response to the progressive increase of the environmental NaCl concentration) affected. These changes are discussed with respect to a metabolic pattern of these "high NaCl"-tolerant cells which is compatible with increased energy requirements, especially for active cation transport. It is suggested that these increased cellular enzyme activities reflect an increased transfer of reducing equivalents across mitochondrial membranes (via the "glycerophosphate cycle and the malate-aspartate shuttle") and possibly a stimulated lipid metabolism. These alterations in the level of enzyme activities must be regarded asan adaptive cellular response to the "high NaCl" environment, since readaptation to growth in regular isotonic media resulted in a reversion to the enzyme pattern characteristic of the parent cells.
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PMID:Changes in enzyme pattern of Ehrlich ascites tumor cells following serial cultivation in media with increased (hypertonic) NaCl content. 12 1

Aspartate aminotransferase (EC 2.6.1.1) activity and the distribution of its isoenzymes in human liver were examined. Rabbit antiserum against porcin soluble (i.e., non-mitochondrial) enzyme cross-reacted with the soluble enzyme of human origin and was used in an immunoprecipitation assay to quantitate the soluble and mitochondrial isoenzymes. These were separated by rapid, semiquantitative electrophoresis on cellulose acetate and by three other quantitative techniques: isoelectric focusing and anion-and cation-exchange chromatography. The mitochrondrial enzyme averaged 81% of the total activity in normal adult human liver (n = 4). Its contribution was dramatically reduced in single specimens of human fetal liver (56% of total activity) and hepatoblastoma tissue (38%). Total enzyme activities (mumol min-1 per gram of tissue) were: adult, 150; fetal, 38; tumor, 6. Total enzyme concentrations (micromoles of enzyme per kilogram of tissue) found were: adult, 10.8; fetal, 2.7; tumor, 0.4. The concentrations and isoenzyme distribution in human liver are compared to those in various animal model systems. Other methods for quantitative estimation of the isoenzymes and their adaptability for use in estimating concentrations in serum are reviewed.
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PMID:Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. 21 6

The concept of tumor markers was reviewed, and the potential uses of markers of central nervous system (CNS) tumors and methods for their evaluation were discussed. Markers examined included lactate dehydrogenase, aspartate aminotransferase, fructose-bisphosphate aldolase, the polyamines, desmosterol, and several other enzymatic, nonenzymatic, and immunologic markers. Data collated from the clinical studies surveyed showed isocitrate dehydrogenase, desmosterol, and the polyamines to have the greatest potential utility in the diagnosis of CNS tumors.
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PMID:Biochemical markers of central nervous system tumors measured in cerebrospinal fluid and their potential use in diagnosis and patient management: a review. 38 10

The value of serum bile acids (SBA) in the diagnosis of hepatobiliary disease has been investigated. A modified GLC method was used, with an overall coefficient of variation of +/- 11% in the control range. Serum was obtained after a 12 hour fast, and two hours after a fatty meal from 73 patients and 14 control subjects. In controls the total fasting SBA of 2.17 +/- 0.86 mumol/l increased significantly (p less than 0.001) to 3.81 +/- 1.14 mumol/l after a meal. All icteric patients had raised SBA, but in 23 anicteric patients there was no significant difference in the detection of chronic liver disease by fasting SBA, postprandial SBA, AST, or gamma GTP. Compared with controls, serum in patients contained proportionately less deoxycholic acid (p less than 0.001), there was proportionately more cholic acid in extrahepatic obstruction (p less than 0.001), and proportionately more chenodeoxycholic acid in patients with cirrhosis, viral hepatitis, and neoplasia (p less than 0.001). In control subjects, the fasting cholic:chenodeoxycholic acid ratio ranged from 0.5-1.0, and differed significantly (p less than 0.001) from patients with extrahepatic obstruction 0.96-3.6, and cirrhosis 0.1-0.5. It is concluded that serum bile acids measured by sensitive methods can provide useful diagnostic information.
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PMID:Serum bile acids in the diagnosis of hepatobiliary disease. 59 Aug 51

Acute renal failure developed in nine of 78 patients who were subjected to hepatic artery ligation for nonresectable and extensive malignant tumor of the liver. Of those nine, six had hepatomas, one cholangiocarcinoma, one metastatic islet-cell carcinoma and one metastatic melanoma. Preoperative renal function as reflected in blood-urea-nitrogen and serum creatinine values was within normal limits. There were marked elevations of serum glutamic-oxalacetic transaminase and lactic dehydrogenase levels after hepatic artery ligation, an indication of massive ischemic injury of the tumor and the liver. A diagnosis of acute renal failure was established within 14 to 70 hours after hepatic artery ligation. In five patients, oliguric renal failure developed, and in four, high urinary output renal failure. In only three patients did systemic hypotension and hypovolemia precede acute renal failure. Seven of the nine patients died. Postmortem examination was done in five patients, and in only two was there evidence of renal tubular necrosis. The factors contributing to acute renal failure appear to be extensive involvement of the liver by tumor, presence of ascites and jaundice, occlusion of the portal vein and hyperuricemia. The presence of any one of the foregoing contraindicates the procedure.
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PMID:Acute renal failure after ligation of the hepatic artery. 95 59

Polyriboinosinic-polyribocytidylic acid (poly I - poly C), an interferon inducer, was administered in multiple doses of 0.3-75 mg/m2 to 26 patients with a variety of solid tumors, 9 with acute leukemia, and 2 with chronic myelogenous leukemia in blast crisis. Forty-four separate drug trials were comprised of various schedules and routes of administration. Toxic reactions included fever (in 66% of the trials), transient elevation of serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase (25%), minimal laboratory evidence of coagulation abnormalities (59%), and hypersensitivity (5%). These toxic manifestations did not relate to dose level or magnitude of interferon induction. Poly I - poly C administered iv induced low serum concentrations of interferon in 24/38 trials (63%), but the correlation between drug dose and peak interferon titer was not linear. Poly I - poly C administered iv or im was not effective as an inducer of interferon in the cerebrospinal fluid. Similarly, poly I - poly C administered im or by inhalation did not produce detectable serum levels of interferon. No patients experienced an objective tumor response to the administration of poly I - poly C, and most (76%) had progression of their disease while receiving the drug.
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PMID:A phase I-II trial of multiple-dose polyriboinosic-polyribocytidylic acid in patieonts with leukemia or solid tumors. 97 71

Lactic dehydrogenase (LDH), glutamic-oxalacetic transaminase (GOT), and acid and alkaline phosphatase activities in bone marrow and in cubital vein serum were compared. For patients without cancer, marrow serum LDH attained levels four times as high, and GOT and alkaline phosphatase, levels twice as high as those normal for cubital vein serum; levels of acid phosphatase were the same for both sources. For patients with cancer, significant increase of enzyme levels over reference levels depends on the tumor origin and on the presence and localization of metastases. Marrow enzyme levels may become elevated with or without concurrent elevation in cubital vein serum. Concurrent elevations were found with colonic carcinoma and lymphoid leukemia, and noncurrent elevations, with prostatic cancer, myeloid leukemia, and myeloma. A nonconcurrent elevation of marrow enzymes indicates that the origin of the enzyme is in the marrow, whereas with concurrent elevation, the source of the enzyme may be another organ.
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PMID:Enzymes in peripheral and bone marrow serum in patients with cancer. 98 36

The diagnostic value of CSF lactate dehydrogenase and aspartate transaminase in cases of brain tumours (except for CSF AST in the benign tumours), congenital hydrocephalus, and brain abscess is established. Tumour cyst fluids show a higher enzymatic activity than does the CSF. The two enzyme estimations do not help in differentiating the supratentorial from the infratentorial tumours. CSF AST is superior to CSF LD in discriminating the malignant and benign tumours, in so far as the AST is increases selectively in malignancy. Estimates of CSF LD are slightly superior to those of CSF AST, both in incidence of abnormality and the degree of their rise.
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PMID:Lactate dehydrogenase and aspartete transaminase of the cerebrospinal fluid in patients with brain tumours, congenital hydrocephalus, and brain abscess. 101 Oct 18

Serum tissue polypeptide antigen (TPA) was determined in 86 cirrhotic patients who underwent a thorough clinical and laboratory evaluation. Increased serum TPA levels were found in 87.2% of the patients (81% of Child's A, 81.3% of Child's B and 97% of Child's C) with very high levels in some cases. There were significant correlations between TPA and several clinical and biochemical tests, especially AST (r = 0.678, p < 0.000001), and this enzyme was the best predictor of TPA levels. Patients with abnormal AST had also significantly higher serum levels of TPA than those with normal AST in each of the Child's class (p < 0.01 for each). TPA values were found to be more frequently abnormal than AST ones in cirrhotics (p = 0.009) and could be used as indirect markers of activity in these patients. The underlying mechanism involved in the increase in TPA in cirrhosis was probably related to the cytolytic/regenerative activity of the liver. TPA cannot be used as a tumor marker in these patients.
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PMID:A clinical and laboratory evaluation of the behavior of tissue polypeptide antigen in liver cirrhosis. 129 4

A case of non-Hodgkin's lymphoma showed a phenotypic and genotypic cell lineage switch twice during nine years of his clinical history; first, T-cell type, pleomorphic small cell lymphoma developed, followed by B-cell type, diffuse centroblastic/centrocytic lymphoma, and finally T-zone lymphoma without follicles again developed, from which AST-1 cultured cell line was established. Karyotype analysis demonstrated a shared abnormal chromosome, der(1)t(1;?)(p36;?), among the first relapsed B-cell tumor, the second relapsed T-cell tumor and AST-1 cell line. Furthermore, T-cell receptor (TCR) gamma gene rearrangement bands of the same size were observed in the first relapsed B-cell tumor and the second relapsed T-cell tumor as well as AST-1 cell line. These results suggested that both relapsed tumors of different cell lineages are derived from a common malignant clone, presumably a committed lymphoid stem cell. A unique translocation, t(2;14)(q37;q11.2), which may involve TCR delta/alpha gene complex, was observed in the second relapsed tumor and AST-1 cells. To attempt to isolate the breakpoint of this translocation, the configuration of TCR delta/alpha gene complex was studied. The result showed that two rearrangements of TCR alpha gene detected with J alpha probes were the products of the normal TCR rearrangement process, and were not involved in the translocation at this region. This patient, together with the AST-1 cell line, provided us a unique opportunity to study the development and clonal evolution of malignant lymphoma.
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PMID:Phenotypic and genotypic lineage switch of a lymphoma with shared chromosome translocation and T-cell receptor gamma gene rearrangement. 131 86


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