Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effect of neuraminidase injection in rat's tumor at different doses: 5,10,50,100, 500 U and we concluded that: There was no difference between the rats treated with 5,10,50 U and the controls. The y died 3 weeks after the injection. But the rats treated by 100 at 500 U of NA died quickley, in the week, of long metastases.
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PMID:[Effect of intratumoral injection of bacterial and viral neuraminidase in rats]. 0 91

A transplantable murine osteosarcoma is described. Following transplantation into a syngeneic mouse the tumor grows rapidly and kills the mouse with pulmonary metastases simulating human osteosarcoma. A cell-mediated antibody response is evoked in the host mouse as demonstrated by in vivo and in vitro tests. The number of pulmonary metastases may be decreased with adjunctive immunotherapy following excision of the primary tumor. Immunotherapeutic materials include BCG and isologous cells treated with Vibrio cholerae neuraminidase.
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PMID:Immunological studies in murine osteosarcoma. Immunogenicity, growth kinetics, and immunotherapy. 106 29

Lymphocyte cytotoxicity, serum cytotoxicity, and the ability of the serum to inhibit lymphocyte cytotoxicity (blocking effect) were studied in a melanoma patient treated with six monthly injections of her own (autologous) tumor cells incubated with neuraminidase to increase their antigenicity. The same tumor cells grown in tissue culture were used as target cells for the cytotoxicity test. Large fluctuations of blocking effect in the serum were found, which correlated with the clinical course of tumor removal, recurrence, and regression. After the fifth injection of autologous tumor cells, the blocking effect disappeared from the serum (unblocking). In general, changes in serum cytotoxicity corresponded with changes in the amount of blocking effect produced by the serum. The results suggest that active immunotherapy may play a role in the prevention of metastases and, that when used within the autologous system, the cytotoxicity test is valuable in studying response to this type of therapy.
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PMID:Cytotoxicity reactions during immunotherapy of melanoma with neuraminidase altered autologous tumor cells. 124 39

Serine proteases, such as alpha-chymotrypsin or elastase, caused an aggregation of rat ascites tumour cell lines, AH-130, AH-109A and YS, in a protein free medium which preserved the cell viability. This aggregation, which was monitored spectrophotometrically, was dependent upon the protease activities and was resistant to treatment with either a calcium chelating reagent (EDTA) or neuraminidase. However, the tumour cell aggregates were redispersed by treatment with deoxyribonuclease I (DNase I). This dispersal effect was dependent upon the DNase activity. A possible relationship between the tumour cell aggregation and development of blood-borne metastasis was studied. An intravenous inoculation in rats of tumour cell aggregates performed by the alpha-chymotrypsin treatment resulted in significantly higher numbers of lung metastatic foci than an injection of single cells. When the re-separated single cells, prepared in vitro by treatment with DNase I following alpha-chymotrypsin treatment, were injected instead of the aggregates, the enhancement of metastasis was reversed. These enhancement and reversal effects were mimicked in vivo by intravenous injections of protease and nuclease following inoculation of a single cell suspension. That is, the number of metastatic foci caused by single cell inoculation followed by an intravenous alpha-chymotrypsin injection, was higher than that in a control group receiving PBS instead of alpha-chymotrypsin. Again, this augmentation was reversed by an injection of DNase I following alpha-chymotrypsin injection. Furthermore, an injection of DNase I alone itself reduced the starting number of metastases resulting from injection of the single tumour cell suspension. These data suggest that the metastatic behaviour of tumour cells may be increased by protease inducible DNA dependent cell aggregation should it occur in the blood stream.
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PMID:Serine protease-induced enhancement of blood-borne metastasis of rat ascites tumour cells and its prevention with deoxyribonuclease. 212 Dec 20

A syngeneic model system for the study of metastases is described. The system consisted of 2 lymphoma clones (A/63-I and A/63-2) derived from a single thymoma (A/63) induced by a wild-type Abelson-Moloney viral complex. Phenotype and genotype analyses revealed that both clones were derived from transformation of early T-cell precursors. An in vivo study of the colonizing potential following intravenous (i.v.) injection of clones showed that only the A/63-I cell clone colonized the liver. This observation was confirmed by quantitative analysis of organ distribution of both cell clones consecutive to i.v. injection of 125IUdR-labelled cells. In the same way, an in vitro study of the invasive potential of both clones was performed on frozen liver sections and showed that only the A/63-I cell clone had the ability to attach to liver. This specific adhesion was inhibited by L-fucose, D-galactose, N-acetyl-D-galactosamine (D-GalNAc) and with D-galactose- and L-fucose-containing neoglycoproteins. Differences in cell surface carbohydrates of the 2 cell clones were detected using various lectins: peanut agglutinin (PNA), Dolichos biflorus (DBA), Aleuria aurantia (AAA) and Galactia tenuiflora agglutinins (GTA). A/63-I was found to react strongly with PNA, DBA and GTA, and the removal of sialic acid by neuraminidase treatment increased DBA and PNA receptor sites of A/63-2 as compared to A/63-I. The present data suggest that cell-surface GalNAc, galactosyl and fucosyl residues are responsible for the ability of the A/63-I cell clone to recognize liver tissue probably through binding to a Kupffer-cell-associated lectin.
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PMID:Fucose and galactose receptor and liver recognition by lymphoma cells. 215 78

A33 is a mouse immunoglobulin G2a (IgG2a) monoclonal antibody (mAb) that detects a heat-stable, protease- and neuraminidase-resistant epitope. The antigen is homogeneously expressed by virtually all colon cancers and in the colon mucosa but not other epithelial tissues. The biodistribution and imaging characteristics of iodine-131 (131I)-mAbA33 were studied in colorectal carcinoma patients with hepatic metastases. Antibody labeled with 2 to 5 mCi of 131I was administered intravenously (IV) 7 to 8 days before surgery at five dose levels, ranging from 0.2 mg to 50 mg, with three or more patients entered at each dose level. In addition, three patients received 2 mg 131I-mAbTA99 (an isotype-matched control mAb) together with 125I-mAbA33. Evaluation included whole-body imaging with a gamma camera, technetium-99 (99mTc)-human serum albumin blood pool scans, liver/spleen scans, abdominal computed tomographic (CT) scans, hepatic arteriograms, antibody pharmacokinetics, and assessment of antibody distribution in biopsied malignant and normal tissues. Selective mAbA33 localization to tumor tissue was demonstrated in 19 of 20 patients, and external imaging correlated with surgical inspection, pathologic examination, and tissue radioactivity. One week after antibody administration, tumor:liver ratios ranged from 6.9:1 to 100:1 and tumor:serum ratios from 4.1:1 to 25.2:1. 99mTc-albumin blood pool studies showed that liver metastases were hypovascular, emphasizing the selective localization of mAbA33 despite poor tumor-blood flow. Control mAbTA99 studies showed mAbA33 localization was antigen-specific; tumor:liver ratios were 2.3- to 45-fold higher for specific antibody. In metastatic lesions, radioisotope was localized primarily in the viable periphery; however, even the necrotic tumor core concentrated specific antibody. External imaging showed isotope visualization in some patients' large bowel; whether this represents specific antibody uptake or gastric iodine secretion is unclear.
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PMID:Quantitative analysis of antibody localization in human metastatic colon cancer: a phase I study of monoclonal antibody A33. 223 Aug 77

We used 5 syngeneic murine tumour systems for studying quantitative lectin surface binding of intact viable tumour cells. We also investigated, for 3 of the tumours, whether the lectin binding sites were susceptible to proteolytic enzyme (pronase) or neuraminidase treatment. There were significant differences between two of the tumour lines in the binding of wheat germ agglutinin (WGA), concanavalin A (ConA). peanut agglutinin (PNA), soybean agglutinin (SBA) and Ulex europeus agglutinin (UEA). There were also variations in lectin binding between the other tumor lines, but these differences were not statistically significant. Lectin binding showed no evident relationship to the malignancy or the metastasis-forming capacity of the respective tumour cell line. Proteolytic treatment, which drastically affects intravenously induced experimental metastasis formation by one of the tumours, caused a decreased binding of SBA, ConA and WGA. Neuraminidase treatment increased both PNA and SBA binding in three different cell lines, presumably by removing sialic acid masking D-galactose and N-acetyl-D-galactose-amine groups.
Invasion Metastasis 1990
PMID:Lectin binding in murine tumour lines with different malignant characteristics. Effect of enzyme (pronase, neuraminidase) treatment on lectin labelling. 226 85

From the highly metastatic in vivo-passaged Friend leukemia cells (FLC), WGA-resistant (WR) tumor cell variants were selected. These WR FLC had lost their capacity to metastasize when injected i.v. or s.c. into DBA/2 mice. We have characterized the plasma membrane glycoproteins of the different FLC types by: (i) metabolic labelling with (3H)-galactose; (ii) surface labelling with galactose oxidase-borohydride; (iii) direct binding of (125I)-lectins on glycoproteins separated by SDS-PAGE. The ensemble of these approaches showed that the 100- to 200-kDa glycoproteins of in vivo-passaged FLC and WR FLC exhibited a very similar distribution of the terminal galactose in their oligosaccharide moieties. In contrast, the expression of terminal sialic acid was reduced in WR FLC with respect to in vivo-passaged counterparts as appreciated by: (i) binding experiments with (125I)-WGA; (ii) cathodic shift of the 100- to 200-kDa glycoproteins in 2-dimensional electrophoresis studies, and (iii) thiobarbituric acid assay after FLC treatment with neuraminidase. Moreover, binding experiments with (125I)-LPHA, (125I)-ConA and (125I)-WGA (after Smith degradation) indicated that, in the 100- to 200-kDa region, virtually identical asparagine-linked tri- or tetra-antennary complex-type oligosaccharides were expressed in both cell types. We conclude that the sialylation of high-molecular-weight surface glycoproteins (particularly in the 150-kDa region) is strongly associated with the metastatic potential of FLC, especially to the liver.
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PMID:Hyposialylation of high-molecular-weight membrane glycoproteins parallels the loss of metastatic potential in wheat-germ agglutinin-resistant Friend leukemia cells. 291 Aug 24

During hematogenous metastasis, circulating cancer cells appear to be killed in the microcirculation by a non-exclusive mechanism, involving the mechanical trauma consequent upon cancer cell interactions with the vessel wall. Various observations by others indicate that with increased cell deformability, there is decreased intravascular cell killing. We have therefore critically examined the effects of agents previously shown to modify cell deformability, on the susceptibility of Ehrlich ascites tumor and L1210 leukemia cells to mechanical damage on passage through polycarbonate membranes in vitro. Treatment with neuraminidase, trypsin or EGTA, was previously shown to increase cell deformability. However, in the present studies, neuraminidase treatment was associated with increased cell loss on filtration; trypsin treatment with small decreases in cell loss, and EGTA treatment with decreased loss. Consideration of the effects of these agents on cell deformability and membrane strength suggests that under the described experimental conditions, the latter appears more important for survival than the former. As proteolytic and glycolytic enzymes and calcium ions are involved in the release of cancer cells from tumors and invasive events, the effects described here may be relevant to the variability of cancer cells with respect to the metastatic process.
Invasion Metastasis 1986
PMID:Perturbations in cancer cell deformability and resistance to shear forces. 308 63

In 14 patients with adenocarcinoma of the colon or rectum (Duke stages A to D), positive results for neuraminidase were obtained with the isolated leukocytes at pH 6. These were tested by a cytochemical method using a chromogenic substrate for neuraminidase. Under the same conditions, normal leukocyte neuraminidase has a pH optimum of 4. The percentage of leukocytes showing neuraminidase activity increased with the progression of Duke stage and presence of liver or peritoneal metastases. Neuraminidase activity was also found in tumor and metastases specimens of these patients as well as in a human cell line derived from colonic adenocarcinoma (HT-29). Neuraminidase antibodies were found in blood and certain tumor materials. Neuraminidase inhibition tests were positive with neuraminidase inhibitors, patients' sera, N2 neuraminidase antibodies, and antisera against some type C retroviruses (GaLV and MLV), which were used because highly purified MLV preparations proved to contain biologically active neuraminidase (N2).
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PMID:Variation of leukocyte neuraminidase with Duke stage in patients with adenocarcinoma of the colon and rectum. 324 27


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