Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.2.13 (aldolase)
 3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Caucasian male developed florid dermatomyositis documented by serum enzyme elevation, electromyography, and histology of skin and muscle. Serum enzymes, including creatine phosphokinase (CPK), aldolase, glutamic oxaloacetic transaminase (SGOT), and lactic dehydrogenase (LDH), decreased initially during high dose systemic corticosteroid therapy, although profound muscle weakness persisted. Subsequent elevation of serum LDH and SGOT levels during treatment provided a clue to underlying neoplasia. Primary hepatoma with widespread metastases was found at necropsy.
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PMID:Aberrant serum enzyme patterns in dermatomyositis associated with hepatoma. 18 84

An ultramicrochemical technique has been adapted to the evolution of enzyme profiles within individual human mammary tumors. Tandem observation of adjacent stained and lyophilized sections permitted dissection of microgram quantities of freeze-dried material within confirmed regions of malignancy. Enzymes frequently monitored to examine glycolytic, respiratory, and metastatic capacity were microanalyzed successfully: lactic dehydrogenase (LDH), phosphoglucose isomerase (PGI), malate dehydrogenase (MDH), acid phosphatase (AP), aldolase (ALD), glucose-6-phosphate dehydrogenase (G6PDH), pyruvate kinase (PK), alpha-glycerophosphate dehydrogenase (alpha-GOPDH), hexokinase (HK), and phosphofructokinase (PRK). All enzyme activities were higher in infiltrating ductal carcinomas than in fibroadenomas. Extracts of tumor cells mixed in varying proportions with brain or muscle extracts of rat evidenced no modification of expected activity. The technical adaptation described provided a sensitive methodology to resolve problems of relication, profile analysis, sample quantity, and selectivity within heterogeneous tissues.
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PMID:Application of a microchemical technique to the elucidation of enzyme activity profiles within single human mammary tumors. 20 41

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 aldolase activity was measured using two substrates fructose-I-phosphate (FIP) and fructose-1,6-diphosphate (FDP) in the supernatant fraction of homogenates of different mice organs (liver, muscle, brain) and hepatoma tissues during growth of hepatoma 22a. Kinetic parameters Km and Vmax were calsulated. The most essential changes in the activity of aldolase were found during the latent and terminal stares of the hepatoma development. The changes in the aldolase activity observed during development of hepatoma 22a were characterized by altered substrate specificity VFDP /VFIP activity gatio). This ratio was not changed distinctly in liver tissue; in muscles the value decreased from 50 (tumor-free control) to 15 during terminal stages; in brain, to the contrary, it was increased from 20 to 50. The values of Km, Vmax and VFDP /VFIP were similar both in the hepatoma at the eleventh day and in normal brain tissue. The specific inhibition of FDP aldolase activity by ATP was found. Substitution of aldolase B by aldolase AC apparantly ossurred in hepatoma 22a. The data obtained suggest that alteration in the parameters studied may be due to variation in the ration of isozymes.
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PMID:[Change in aldolase activity in the organs of mice in the process of hepatoma 22a development]. 49 46

Evidence is presented that the antitumor agent helenalin, a sesquiterpene lactone, suppresses anaerobic glycolytic enzymes of tumor cells at a number of sites and not exclusively at glycogen synthetase and phosphofructokinase, previously proposed sites for inhibition by alpha-methylene-gamma-lactones. Of the enzymes tested, the sulfhydryl-containing enzyme hexokinase was inhibited the maximum, i.e., 83%, by helenalin treatment, whereas phosphofructokinase and glycogen synthetase were suppressed approximately 45%. Another sulfhydryl-bearing enzyme, aldolase, was decreased approximately 43%. Phosphorylase a was inhibited 65%, glucose-6-phosphatase was inhibited 46%, and succinic dehydrogenase was inhibited 59% by helenalin treatment. Mitochondrial oxidative phosphorylation processes were also significantly depressed in the presence of helenalin in vitro with either succinate or alpha-ketoglutarate as substrates. Thus, a number of enzymes of anaerobic and aerobic carbohydrate metabolism of Ehrlich ascites cells appear to be inhibited by helenalin, which supposedly can alkylate functional groups, e.g., sulfhydryl groups of these enzymes, by a rapid Michael-type addition.
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PMID:Antitumor agents XXVII: Effects of helenalin on anaerobic and aerobic metabolism of Ehrlich ascites cells. 64 68

Sections of hypernephroid carcinoma from 20 cases were investigated for aldolase isozymes A and B by a mixed aggregation immuno-cytochemical technique, and for the brush border membrane enzymes aminopeptidase and alkaline phosphatase by conventional histochemical techniques. It was found that the cases could be grouped into four types: type 1 (1 case) contained all 4 enzymes; type 2 (7 cases) contained all enzymes except aldolase-B; type 3 (7 cases) possessed aldolase-A and one brush border membrane enzyme; type 4 (5 cases) contained only aldolase-A. The aldolase-A concentration in all tumor cells was higher than that in proximal tubule cells, whereas the concentration of the two brush border enzymes was lower. In cases tydolase-B and/or higher amounts of the brush border enzymes than the surrounding cells. No correlation was observed between clear cell and granular cell hypernephroid carcinomas or the invasiveness or the nuclear polymorphism of the tumors on the one hand with their enzyme type on the other. These histological enzyme analyses suggest that most, if not all, hypernephroid carcinomas are derived from kidney proximal tubule cells and that the tumor cells then progressively lose aldolase-B, and subsequently the brush border enzymes, but at the same time producing more aldolase-A. The presence of the enzyme-rich patches suggest different patterns of proliferation and differentiation among the tumor cell population. Three tumors other than hypernephroid carcinoma were also examined in this way. The results suggest that histoenzymological analyses are of general applicability in studies of tumor progression. They should also be useful for biopsy and aspiration cytology.
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PMID:A classification of tumor development based on an analysis of enzymes in tissue sections of hypernephroid carcinoma in man. 101 98

Glyceraldehyde 3-phosphate dehydrogenase and 3-phosphoglycerate kinase are, together with some other enzymes, present on the surface of intact Ehrlich tumor cells. Aldolase, on the contrary, represents cytoplasmic enzymes not present at all on the external surface, provided 2.5 percent of bovine albumin is included in the isotonic assay medium. A flux of aldolase from the cell interior to the cell exterior could be demonstrated in the absence of albumin. Therefore, any enzymatic activity monitored when keeping the Ehrlich tumor cells in the isotonic assay medium containing 2.5 percent albumin was considered to be primarily related to the outside of the plasma membrane. Of the total glyceraldehyde 3-phosphate dehydrogenase, 0.7 percent was located on the outer surface of the tumor cell, while the corresponding figure for 3-phospoglycerate kinase was 2.7 percent. Eighty percent of this surface-located 3-phosphoglycerate kinase was released into the assay medium during incubation, while the release of glyceraldehyde 3-phosphate dehydrogenase, at the same time, was minimal. A plasma membrane preparation of Ehrlich cells, mainly consisting of vesicles, showed the presence of 3-phosphoglycerate kinase but the absence of glyceraldehyde 3-phosphate dehydrogenase. Because of the vesicular nature of the membrane preparation, it was assumed that only one side of the membrane was exposed during assay. The specific binding properties of the two enzymes to the plasma membrane, as well as possible differences in their intramembranous location, are discussed.
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PMID:Enzyme activities at the surface of intact Ehrlich tumor cells with albumin in the isotonic assay medium. 113 21

The changes in the blood cell count and in the blood chemistry (fibrinogen in the plasma, Fe and Cu in the serum) that we have found, were only seen in a late tumor state. This is also valid for the serum aldolase activity, which is said to be a screening test for a recurrency of a tumor.
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PMID:[Correlation of blood-chemistry changes and development of cancer in experimental tumor induction in the colon of rats]. 120 37

The pattern of gene expression in fetal hepatocytes transformed in culture with a hepatocarcinogen (FRL cells) is studied with respect to a range of markers which are either developmentally regulated and/or shown to be expressed at high levels in hepatoma cells. The relative abundance of the respective mRNAs is determined and immunocytochemistry is used to detect the respective proteins in cultured cells. When compared with its normal counterpart, FRL cells retain the expression of transferrin, alpha 1-acid glycoprotein, gamma-glutamyltranspeptidase, and tyrosine aminotransferase at near normal levels, while expression of the liver-specific isoenzymes of pyruvate kinase (L form) and aldolase (B form) is reduced. The cell lines are different in that they fail to express albumin, alpha-fetoprotein, thiostatin and alpha 2-macroglobulin, and they express high levels of M2-pyruvate kinase and aldolase A, markers often found in abundance in hepatoma cells. Therefore transformation has resulted in different effects on different genes. Furthermore, it is of interest to find that the cells coexpress both forms of the pyruvate kinase isoenzymes which does not occur in the normal developing hepatocyte. These results indicate that it is possible to use this model to study changes which accompany transformation of fetal rat hepatocytes. The resulting cell lines have a stable phenotype and retain the changes which result from transformation even after extended passaging. This facilitates comparisons between the precursor cell and the tumor cell, both of which can be maintained under controlled conditions which exist in culture.
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PMID:Gene expression in clonally derived cell lines produced by in vitro transformation of rat fetal hepatocytes: isolation of cell lines which retain liver-specific markers. 170 49

The serial changes in serum hepatic enzyme activities by transcatheter arterial embolization (TAE) were analyzed in 17 patients with hepatocellular carcinoma to estimate the contribution to the value by the damage of tumor or nontumorous hepatic cells. The serum levels of relatively tumor-specific fructose 1,6-diphosphate (FDP) aldolase were elevated after TAE in the cases of both superselective and nonsuperselective TAE that were performed from the segmental and the nonsegmental hepatic artery, respectively, but we found the marked elevation of FDP aldolase in the cases of the superselective TAE. In contrast, the non-tumor-specific fructose 1-phosphate (F1P) aldolase was markedly elevated only in the cases of nonsuperselective TAE. The total amount of FDP aldolase released by TAE correlated significantly with the integrated tumor tissue volume (P less than 0.005), whereas the total amount of F1P aldolase output correlated significantly with the integrated nontumorous tissue volume (P less than 0.005) as defined by lipiodol accumulation on computerized tomography scan. The consequent changes in the total nontumorous liver volumes after TAE were also analyzed by the follow-up computerized tomography scan. The nonsuperselective TAE caused the significant total nontumorous liver atrophy when compared with the superselective TAE. The progression of the total nontumorous liver atrophy correlated significantly with F1P aldolase output by TAE (P less than 0.001) but not with FDP aldolase output. These results suggest that the outputs of FDP and F1P aldolase are useful to estimate the degree of the tumorous and nontumorous tissue damage by TAE, respectively, and F1P aldolase output can be used to predict the progression of liver atrophy caused by TAE.
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PMID:Evaluation of nontumorous tissue damage by transcatheter arterial embolization for hepatocellular carcinoma. 171 51


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