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)

Leukemization in baboon B- and T-cell immunoblastomas was investigated. Immunologic identification of tumor was carried out using standard immunological and cytochemical tests, e. g. identification of several types of E-rosette forming lymphocytes, surface and cytoplasmic immunoglobulin-carrying lymphocytes and assay of such acid hydrolases as acid phosphatase, acid alpha-naphthyl acetate esterase and beta-glucuronidase in lymphoid cells. Leukemization of immunoblastomas with bone marrow infiltration by tumor immunoblasts and the appearance of the latter in peripheral blood were observed rather frequently--in 7 of 10 cases of B-cell and in all 4 cases of T-cell immunoblastoma. Immunoblastoma progression was accompanied by a rise in lymphoid element level in peripheral blood and a lesser increase in bone marrow. At terminal stage, both patterns of immunoblastoma sometimes involved the development of leukemoid reactions of a myeloid type and disturbances in bone marrow hematopoiesis which manifested themselves by mild anemia and a slightly pronounced failure to produce platelets.
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PMID:[Leukemogenesis and bone marrow hematopoietic disorders in baboons with immunoblastic malignant lymphomas of B- and T-cell types]. 387 91

Glycosidases have been demonstrated to be elevated in the interstitial fluid of tumors, sera of animals and patients with tumors, and in some tumor tissue as compared to normal adjacent tissue. Elevations of serum beta-N-acetylglucosaminidase and beta-glucuronidase most commonly have been found to occur and these enzymes have been shown to be secreted into the extracellular medium by many different tumor cell types in vitro. The mechanism of cellular release of these hydrolytic enzymes probably involves tumor lysosomal exocytosis. Increased tumor glycosidase levels may promote increased tumor cell shedding from primary tumors, local invasion and perhaps be responsible directly, or indirectly for structural changes in tumor cell surface glycoconjugates. These cell surface changes could facilitate tumor cell thrombus formation, secondary site implantation and attachment in the microcirculation to endothelial cells and/or subendothelial basement membrane components. Other studies have demonstrated a correlation between metastatic cell potential and increased endoglycosidase and polysaccharide lyase activity. Generally, metastatic tumor cell variants have been found to be more invasive and capable of degrading proteoglycan basement membrane components, in part due to these increased levels of degradative enzymes. Hence, it is of considerable interest to develop inhibitors against these enzymes. Initial studies with glucuronidase inhibitors in the therapy of bladder tumors have been promising and with the advent of better agents and the use of appropriate in vitro metastatic models it may be possible to design and develop agents which interfere in various metastatic events and limit tumor progression.
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PMID:Glycosidases in cancer and invasion. 388 85

Human osteosarcoma specimens were sliced in a cryomicrotome under strict morphological guidance. Serial sections of ten 10 micron slices each were collected in two groups according to morphologic criteria, one containing mostly undifferentiated tumor tissue, the other predominantly well-differentiated tumor tissue. The two series were analysed chemically for alkaline phosphatase (APase) acid phosphatase (acPase), beta-glucuronidase and proteolytic activities; protein, phosphorus, hydroxyproline, hexosamine, water and collagen contents were also determined. Four different types of osteosarcoma were studied: case 1 was a highly malignant osteoblastic osteosarcoma, case 2 a small cell sclerosing osteosarcoma case 3 a well-differentiated osteosarcoma, and case 4 a highly malignant anaplastic osteosarcoma. The types of cases 1, 2 and 3 are known as osteoid-forming tumors. In their less well differentiated areas APase activity was about twice as high as in better differentiated osteosarcoma. In contrast, no APase was found in the wholly undifferentiated areas of case 4, while the enzyme showed a marked increase in the areas of incipient differentiation of this tumor. The matrix of tumors differs with regard to collagen and hexosamine contents, in accordance with the general state of differentiation. In general, increasing hexosamine contents together with decreasing hydroxyproline contents will reflect the anaplastic, dedifferentiated osteosarcoma. Calcification evident in the better differentiated areas of osteosarcoma is indicated by the phosphorus content, highest in case 2, with cases 3, 1, and 4 following in sequential order.
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PMID:Biological characterization of human bone tumors. V. Zonal characterization of osteosarcoma: topological biochemical analysis correlated with morphology. 390 6

Treatment of cultured HeLa cells with 5 mM sodium butyrate causes an inhibition of growth as well as extensive chemical and morphological differentiation. Lysosomal enzyme activity changes have been associated with both normal and neoplastic growth as well as many aspects of the neoplastic process. The comparative ultrastructural results show that the butyrate-treated cells have a more extensive internal membranous system than the untreated cells, whereas other organelles seem unaffected by the butyrate treatment. Methods for the histochemical localization of lysosomal acid phosphatase show a twofold increase in particulate reaction product in the butyrate-treated HeLa cells. Isolation of lysosomes followed by a comparative enzyme analysis shows a two to three fold increase in acid phosphatase activity per cell after 24 h of butyrate treatment, as well as three to four fold increase in beta-glucuronidase activity. These increases reverse within 24 h of removal of the butyrate from the culture medium. These results as interpreted suggest that butyrate treatment may be preventing sublethal autolysis by arresting the leakage of the lysosomal enzymes from the lysosome into the cytosol and thus allowing the cell to chemically and morphologically differentiate.
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PMID:Sodium butyrate induced alterations in lysosomal enzyme activity. 403 Jun 22

Mechanisms of macrophage-mediated cytotoxicity against a tumor-cell line (L-929 cells) were analyzed. Culture supernatants were harvested from mouse peritoneal macrophages cultivated for 3 days in the absence or presence of the stimulating agents Escherichia coli endotoxin or zymosan. The supernatants from stimulated cultures were cytotoxic for the tumor cells, evaluated by measuring release of radio-activity during subsequent 4 days' culture of 14C-thymidine-labelled tumor cells in the supernatants. Cytotoxicity was verified by counting cells per culture. Corresponding results were obtained from co cultures of stimulated macrophages and tumor cells, in accordance with a previous study. Selective release of af lysosomal enzyme (beta-glucuronidase) was shown in the supernatants from endotoxin- or zymosan-stimulated cultures, while reduced levels of glucose were seen in all supernatants from macrophage cultures. Dialysis of supernatants against fresh medium reduced the toxic activity somewhat. Dialysis restored the glucose content to optimal levels, while the enzyme activity was unchanged. Heating of supernatants to 56 degrees C for 30 min reduced the cytotoxicity along with a reduction in enzyme activity; 70 degrees C for 30 min removed both cytotoxic activity completely. Heating had no effect on the glucose content of the supernatants. The present data indicate that macrophage-mediated tumor cytotoxicity may be performed through release of heat-labile soluble factor(s) which co-variate with the secretion of a lysosomal enzyme from stimulated macrophages.
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PMID:Cytotoxic factor(s) released from stimulated mouse peritoneal macrophages. 403 12

The activities of six glycosidases in a rat colorectal adenocarcinoma were measured and compared with those of normal colonic mucosa. The specific activities of beta-galactosidase (EC 3.2.1.23) and beta-glucuronidase (EC 3.2.1.31) in the adenocarcinoma were similar to those of the corresponding ones in the normal mucosa, whereas those of beta-N-acetylglucosaminidase (EC 3.2.1.30), alpha-L-fucosidase (EC 3.2.1.51), alpha-galactosidase (EC 3.2.1.22) and beta-glucosidase (EC 3.2.1.21) were reduced in the former as compared with those in the latter. In the case of alpha-L-fucosidase, two forms were newly detected in the tumor. The relative abundance of three forms of beta-N-acetylglucosaminidase was quite different between the adenocarcinoma and the normal mucosa, and the level of the intermediate form in the tumor was markedly reduced. However, thermostability and Km values of two forms A and B in the tumor were not different from those of the corresponding ones in the normal tissue.
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PMID:Alteration in glycosidases from well-differentiated colorectal adenocarcinoma of rat. 404 71

A histochemical procedure for beta-glucuronidase has been used to make visible the cellular genotypes of liver tumors and of surrounding normal liver clones in allophenic mice. The animals had lifelong genetic mosaicism for cells with the allele for low beta-glucuronidase activity (g/g genotype, C3H strain) and cells with the allele for high activity (G/G genotype, C57BL/6 or BALB/c strain). The former strain is also hepatoma-susceptible; both the latter are nonsusceptible. Of 12 "spontaneous" hepatomas examined, nine were entirely of susceptible-strain hepatic cells and one was of the nonsusceptible strain; the pure-strain tumors usually arose in a liver environment containing clones of each genotype. The cells therefore behave largely autonomously with respect to gene control of tumor susceptibility. However, two tumors with malignant cells of both genotypes were formed, which suggests some measure of intercellular transmission of tumor information. Alternatively, transformation might have occurred in two or more cells concurrently. Mosaic tumors in either case imply that even a hepatoma of one inbred strain, whether in a single-genotype animal or an allophenic mouse, may comprise diverse clones of transformed cells. Possibly many or all hepatomas may therefore be genetically complex entities.
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PMID:Pure-strain and genetically mosaic liver tumors histochemically identified with the -glucuronidase marker in allophenic mice. 410 64

Tumour homogenate fractions, isolated by differential centrifugation, were subfractionated by density-gradient centrifugation. Biochemical and electron microscopic analyses revealed that beta-glucuronidase and cathepsin activity were associated with a class (possibly two) of lysosomal particles of density greater than those of mitochondria and the endoplasmic reticulum. Lysosomes sedimented by low g forces were vacuolar, electron-dense, delineated by a unit membrane and about 0.2mum in diameter. beta-Glucuronidase was also apparently associated with ribosomes whereas cathepsin was bound in part to the endoplasmic reticulum. Catalase and glucose 6-phosphatase possessed slightly different density-gradient sedimentation profiles.
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PMID:The locations of cathepsin activity and beta-glucuronidase in the Guerin T8 tumour. 431 48

The phorbol ester 12-0-tetradecanoyl-phorbol-13-acetate, a potent tumor-promoting agent, caused irreversible platelet aggregation when more than 0.02 microM was stirred with human citrated or heparinized platelet-rich plasma (PRP). With washed platelets, 1 nM was effective. The alcohol phorbol, which has little tumor-promoting activity, failed to cause platelet aggregation. With all but low concentrations of phorbol ester, aggregation was succeeded by a rapid phase. The latter was prevented or reduced by enzymes which destroy ADP and by aspirin, was associated with a change in platelet shape, and was presumably due to released ADP. At higher concentrations, only a rapid phase was seen, and these inhibitors were not effective. Low concentrations did not aggregate platelets in PRP containing sufficient EDTA or EGTA to chelate ionized calcium or in PRP from thrombasthenic patients; higher concentrations caused slight aggregation. Both the primary, non-ADP-dependent aggregation and the rapid ADP-dependent aggregation were markedly inhibited by substances which increase cyclic AMP, metabolic inhibitors, and the sulfhydryl inhibitor N-ethylmaleimide. Phorbol ester reduced platelet cyclic AMP only when it had been previously elevated by prostaglandin E(1). 1 microM did not release beta-glucuronidase, lactic dehydrogenase, or inflammatory material from platelets in 4-5 min despite marked aggregation, but liberated all three in 30 min. The possibility is discussed that low phorbol ester concentrations cause primary aggregation by a direct action on platelet actomyosin.
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PMID:The tumor-promoter phorbol ester (12-O-tetradecanoyl-phorbol-13-acetate), a potent aggregating agent for blood platelets. 436 Feb 92

beta-Glucuronidase from human maxillary sinus and lung cancers and from uninvolved tissues was studied. An elevation of beta-glucuronidase activity was observed in cancerous tissues as compared with the corresponding uninvolved tissues, and this increase was significant in adenocarcinoma and squamous cell carcinoma of the lung (p less than 0.01). beta-glucuronidase preparations purified from adenocarcinoma and large cell carcinoma of lung and from normal lung showed similar kinetic properties and antigenicity. beta-Glucuronidase from lung adenocarcinoma showed considerable negative charge heterogeneity in the pI range from 4.2 to 6.2 in an experiment involving isoelectric focusing on polyacrylamide gel. Similar charge heterogeneity was observed in the enzyme from lung large cell carcinoma. Upon treatment of the adenocarcinoma enzyme with exogenous alkaline phosphatase or endoglycosidase H, the heterogeneous variant forms of the tumor enzyme appeared to partly or completely lose their negative charge and to be converted into forms similar to those of the normal lung enzyme. An experiment on the labeling of beta-glucuronidase with [32P]-phosphoric acid provided further evidence that the acidic variants found in lung cancers are extensively phosphorylated forms of the enzyme.
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PMID:[beta-Glucuronidase in human maxillary sinus and lung cancers: elevation of activity level and appearance of phosphorylated variant forms]. 609 43


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