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)

T- and T-like antigens on glycoproteins and glycolipids were examined in extracts of human urinary bladder tumors and normal tissue by Western blot analysis and reagent binding to thin layer chromatograms. Three different anti-T-reagents were used: peanut (Arachis hypogaea) lectin (PNA) and mono- and polyclonal antibodies specific for T-antigen (Gal beta(1-3)GalNAc alpha 1-O-R). Immunodetection with the T-specific reagents in nitrocellulose replicas of bladder tumor glycoproteins, separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, demonstrated tumor-specific T-antigen-bearing glycoproteins compared to normal urothelial glycoproteins. In addition, a remarkable difference in binding was found between the immunological reagents and PNA lectin. PNA showed major reactivity to a 28-kD glycoprotein extracted from tumors. Monoclonal anti-T-antibody (clone HH8) showed major reactivity with an M(r) 34,000 glycoprotein, and polyclonal anti-T-antibody showed major reactivity with an M(r) 36,000 glycoprotein. PNA agarose column affinity-purified tumor glycoproteins did not bind the antibodies. Glycoproteins, M(r) 28,000 and 34,000, were shown to be O-linked by stepwise deglycosylation. In solid phase monosaccharide inhibition tests, galactose followed by N-acetyl-galactosamine were the most potent monosaccharides inhibiting binding to immobilized bladder tumor glycoproteins. None of the anti-T-reagents reacted with glycolipids extracted from tumor tissue. It is concluded that PNA lectin, in addition to the T-disaccharide, reacts with other protein-anchored carbohydrate structures in carcinomas.
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PMID:Human urinary bladder carcinoma glycoconjugates expressing T-(Gal beta(1-3)GalNAc alpha 1-O-R) and T-like antigens: a comparative study using peanut agglutinin and poly- and monoclonal antibodies. 151 58

Some patients with thyrotropin (TSH)-producing pituitary tumors are more hyperthyroid than others despite similar TSH levels in serum, suggesting that qualitatively different TSH molecules with differing bioactivities may be secreted by different tumors. We used ricin and lentil lectin-affinity chromatography to test whether the TSH oligosaccharides varied among 12 patients with TSH-producing tumors. We found that each tumor secreted heterogeneous isoforms of TSH that differed in their extents of exposed galactose (Gal) residues, and their degrees of sialylation and core fucosylation. These biochemical parameters also varied markedly for TSH secreted by different tumors. Isoforms appeared to reflect poor sialyltransferase activity in two tumors and efficient sialyltransferase in the remainder. TSH secreted by tumors was more fucosylated than TSH secreted by control euthyroid persons. There was an inverse relationship between the sialylation and fucosylation of tumor TSH. No simple relationship between TSH oligosaccharide structures and bioactivity was evident, although mixtures of isoforms having the least and most sialylated TSH seemed to be the most bioactive clinically. In three patients from whom serum and medium TSH were both available, TSH in serum was more sialylated than TSH secreted by the tumor in vitro, perhaps reflecting slow clearance of sialylated isoforms from the circulation. Core fucosylation of serum TSH was less than that of medium TSH. These data prove that human tumors secrete TSH with heterogeneous oligosaccharide structures.
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PMID:Ricin and lentil lectin-affinity chromatography reveals oligosaccharide heterogeneity of thyrotropin secreted by 12 human pituitary tumors. 151 16

Bladder tumor cell lines derived from male F344 rats treated with N-buthyl N-(4-hydroxybuthyl) nitrosamine (BBN) or N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT) have been established in vitro and characterized with respect to histology, karyotype, myc and c-Ha-ras oncogene expression or mutation, anchorage-independent growth and tumorigenicity in nude mice. This unique model system comprising 13 cell populations was employed to study common events during development of carcinogen-induced urothelial neoplasia. Differential expression of malignant phenotypes by these cell lines prompted us to examine their expression of carbohydrate structures binding peanut agglutinin (PNA), soy bean agglutinin (SBA) or leukoagglutinin (L-PHA), which are known indicators of tumor progression in rodents and humans. In the present study we analyzed the patterns of glycoproteins reactive with PNA and L-PHA by Western blotting. We also estimated quantitative differences in lectin binding to surfaces of normal rat urothelium and tumor cell lines by flow cytometry. The patterns of PNA or L-PHA reactive glycoproteins expressed by tumor cells were different from that of normal urothelium in culture. They were also different amongst the tumor cells. A unique non-sialylated, PNA binding glycoprotein (117 kD) was seen in the case of the highly tumorigenic F5 cell line and absent in normal urothelium as well as in other tumor cell lines. Normal cells did not express glycoprotein 60 kD binding PNA (only after desialylation), which was found in lysates of some but not all transformed cell lines. A very high molecular weight (much greater than 200), perhaps mucin-like sialoglycoprotein was found in normal urothelium but not in most of the tumor cell lines. Four major L-PHA reactive bands (greater than 200, 190, 100, 80 kD approximately) were found in normal urothelium. Some of those bands were overexpressed or missing in materials isolated from different tumor cell populations. Total cell surface binding of SBA and PNA by different tumor cell lines was very heterogenous (167-2% that of normal urothelium). No simple correlation between expression of the lectin binding glycoconjugates by urothelial carcinoma cells and other known functional, phenotypic or genetic alterations was found. We were also unable to demonstrate carcinogen-specific changes in expression of lectin binding to these tumor cell lines. Thus we conclude that lectin binding patterns are cell line specific. This may reflect distinct pathways of progression of individual cell lines. The potential sources of phenotypic variability between the cell lines were discussed.
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PMID:Cell line specific abnormalities in expression of PNA, SBA and L-PHA binding sites by carcinogen induced rat urothelial carcinomas. 152 17

Changes in the glycosylation of asparagine-linked oligosaccharides have been shown in various tumor cells, including human colon cancer. Attempts were made to elucidate the difference in Asn-linked oligo-saccharides attached to lysosomal membrane glycoproteins isolated from sublines of human colon carcinoma exhibiting high and low metastatic potentials in nude mice. Lysosomal membrane glycoproteins (lamp) 1 and 2 were immunoprecipitated from the cells after labeling with radioactive sugars, and the glycopeptides prepared were fractionated by serial lectin affinity chromatography employing immobilized concanavalin A, Datura stramonium agglutinin, and tomato lectin. Comparison of Asn-linked oligosaccharides from the different colonic carcinoma cells revealed the following features. First, the highly metastatic carcinoma cells express more poly-N-acetyllactosaminyl side chains with branched galactose residues than cells with low metastatic potential. Second, sialylation is more significant in the highly metastatic carcinoma cells than in the poorly metastatic ones. Conversely, N-acetyllactosamine units are less fucosylated in the highly metastatic cells than in poorly metastatic cells. These structural changes were apparently caused by the increase in sialyltransferase and the decrease in alpha 1----3 fucosyltransferase in the highly metastatic cells. The results also suggest that highly metastatic carcinoma cells express more sialyl Lex structures at the termini of poly-N-acetyllactosaminyl side chains than poorly metastatic carcinoma cells. Further, highly metastatic cells were found to express more lamp-1 and lamp-2 on the cell surface. These results were found to be correlated to the increased expression of sialyl Lex structures with high affinity binding of anti-sialyl Lex antibody on highly metastatic cells. Increased expression of sialyl Lex in the poly-N-acetyllactosamines of the cell surface may contribute to the metastatic behavior of the cells, assuming that this structure can serve as a better ligand for selectins present on endothelial cells and platelets.
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PMID:Differential glycosylation and cell surface expression of lysosomal membrane glycoproteins in sublines of a human colon cancer exhibiting distinct metastatic potentials. 154 42

SCK-29 is a tumor cell line derived from human gastric adenocarcinoma with the feature of producing lung metastases when xenografted in nude mice. Monoclonal antibodies were produced against SCK-29 tumor cells or their glycoproteins prepared by affinity chromatography on a lectin-agarose column. Five antigens defined by the monoclonal antibodies MG-1 to MG-5 were expressed in a large number of gastric or colonic adenocarcinomas. Among the antigens, MG-1 and MG-3 proved to be tumor-associated, since they were detected only occasionally in normal tissues. MG-5 antigen was often detected in normal gastric mucosa but not in other tissues. The degree of expression of MG-1. MG-3 and MG-5 antigens differed considerably in metastatic lesions. In metastatic liver lesions of gastric adenocarcinoma, expression of these MG antigens was less marked than in primary tumors. MG-1 and MG-3 antigens were abolished by neuraminidase digestion and periodate oxidation. MG-5 antigen was likely to be a protein antigen, since it was resistant to neuraminidase digestion and to periodate oxidation but was sensitive to protease digestion.
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PMID:Monoclonal antibodies against a human gastric cancer cell line with lung metastatic potential in nude mice define antigens with different expression between the primary and metastatic liver lesions. 154 89

Usefulness of cultured human vascular endothelial cells for the in vitro assay of cancer invasion was reviewed. Selective isolation procedures for the vascular endothelial cells from the different types of vascular tubes were described. Human umbilical cord vein is one of the most useful sources for the isolation of fresh normal endothelial cells. The cells are isolated by perfusing trypsin solution through the umbilical cord vein and successively subcultivated up to 80 population doubling levels as in vitro life span. In case of human thoracic aorta, endothelial cells were removed from endothelium layer of aorta ring by a jet flow of collagenase solution through a needle. Purity of these cells as endothelial cells can be determined by indirect staining of the cytoplasma with anti-endothelin antibody. Usefulness of these cultured endothelial cells has been proved in the studies of regulation of endothelin biosynthesis, ageing of vascular cell, isolation of some new growth factors, interaction with other blood cells, etc. In addition to these studies, we consider that interaction of tumor cells with endothelial cells plays an important role in tumor metastasis. So we established in vitro invasion assay system through the interaction with endothelial cells to examine the invasion and adhesion of tumor cells. Human umbilical cord endothelial cells (HUVEC) were cultured on porous membranes coated with laminin (LN). HT1080 fibrosarcoma cells were seeded onto HUVEC, and HT 1080 cells passed through the membrane were counted. HUVEC were easily distinguished from tumor cells by specific staining of endothelial cells with UEA-1 lectin. Using scanning electron microscopy, we confirmed that HT1080 cells invaded between HUVEC. Roles of adhesion molecules induced by some cytokines on invasion of cancer cells through the endothelial cells-matrix membrane system were discussed.
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PMID:[Cell culture and its application. Application of cultured vascular endothelial cells to the in vitro assay for the invasion of cancer cells through endothelium-matrix membrane system]. 155 8

We have shown previously that an IgM mAb (A10) recognizing Ehrlich tumor (ET) cell surface carbohydrates, inhibits in vivo ET growth by a macrophage-dependent mechanism. The inhibition mechanism involving both IgM and macrophages was unclear because receptors for IgM on macrophages are controversial and another monoclonal IgM (E1), also recognizing ET cell surface carbohydrates, was completely unable to show any protective effect. Here we show that A10, but not E1, was able to promote adhesion between macrophages and ET cells by a receptor for IgM-independent mechanism. Immunofluorescence studies showed that A10, but not E1, did react with macrophages if these cells were preincubated with a source of Ag spontaneously released from ET cells. This Ag release appeared to be required for A10-mediated adhesion, because adhesion was not obtained when ET cells fixed with paraformaldehyde were used. Cytostasis studies performed with macrophages stimulated with L-929 conditioned medium and ET cells showed that A10, but not E1 nor unrelated IgM, was able to inhibit ET cell proliferation in vitro by a mechanism involving cell contact between both cell populations. Therefore, IgM inhibition of ET growth, both in vivo and in vitro, could be explained by a lectin-like mechanism, where IgM, recognizing Ag of tumor origin, bridges macrophages to tumor cells.
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PMID:Tumor cytostasis mediated by a monoclonal IgM antibody promoting adhesion between macrophages and tumor cells. Evidence for a lectin-like behavior. 156 Feb 14

With the purpose of studying changes in the expression of glycoconjugate structures in nonmalignant and cancerous lesions of urothelium the lectins ConA, TKA, PNA, DBA, STA, LFA, UEA, MPA, RCA, LCA, GSA1, SBA, GSA2, WGA, PHA and Lot were tested in formalin-fixed, paraffin-embedded tissue sections of (1) cold biopsies from normal urothelium and bladder cancer of different grades (G1-G3) in humans, (2) normal transitional epithelium and N-butyl-N(4-hydroxybutyl)nitrosamine (BBN)-induced bladder cancer in animal experiments (Wistar rat), and (3) human transitional cancer cell line HT 1376. In human urothelium TKA and SBA were positive markers demonstrating positive staining reactions in all tumor grades without binding to normal epithelium. They stained also the human transitional carcinoma cell line HT 1376 (G3). In Wistar rats DBA, ConA, LCA, SBA, GSA2 and WGA had a specific affinity to BBN-induced carcinoma. Findings of positive lectin marker in transitional cell cancer may offer progress in diagnostics and therapy.
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PMID:Lectins in diagnosis of bladder carcinoma. 158 9

We previously reported that the mouse macrophage galacose and N-acetylgalactosamine-specific lectin (MMGL) may participate in the binding of the macrophages to tumor cells [Oda, S., Sato, M., Toyoshima, S., & Osawa, T. (1989) J. Biochem. 105, 1040-1043]. We now report the cloning and characterization of a cDNA encoding MMGL. The MMGL gene encoded a protein consisting of 304 amino acid residues with a molecular weight of 34,595. The deduced amino acid sequence indicated that MMGL had a single membrane-spanning region, three leucine zipper-like domains, and a carbohydrate recognition domain. Two N-glycosylation sites were found in the extracellular region of MMGL, corresponding to the heavy N-glycosylation in the native MMGL. Comparison of the amino acid sequence of MMGL with those of rat hepatic lectins revealed a high overall sequence homology. The sequence homology was especially high in the putative membrane-spanning region and carbohydrate recognition domain. There was, however, a region of 25 amino acids which did not exist on hepatic lectins. The MMGL cDNA without the region encoding the putative membrane-spanning region and intracellular region was expressed in Escherichia coli. The expressed protein had galactose-binding activity and its sugar-binding specificity was same as that of the native lectin.
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PMID:Molecular cloning and expression of cDNA encoding a galactose/N-acetylgalactosamine-specific lectin on mouse tumoricidal macrophages. 158 94

Image analysis was performed on 40 Feulgen-stained histologic samples and 48 Feulgen-stained cytologic preparations representing normal squamous epithelium and all grades of cervical lesions (from mild dysplasia to invasive carcinoma) in order to characterize the evolutionary progressive changes in cervical epithelial proliferative disease toward malignancy. Quantitative studies included the analysis of proliferative features, differentiation features, nuclear morphology and DNA content. The data obtained on the histologic sections showed that the various features, to a different extent, detected a gradual increase in phenotypic cellular disarrangements related to the progression of the cervical lesions toward malignancy--that is, the modifications to nuclear area, perimeter, DNA content, percentage of nuclei with nucleoli, nuclear/cytoplasmic ratio and percentage of cells with no membrane positivity for soybean agglutinin lectin were progressively greater, moving from normal epithelium and mild dysplasia toward infiltrating carcinoma. In particular, all the morphologic and histochemical features appeared to parallel a diploid reduction and the appearance of aneuploidy. The simultaneous evaluation of proliferation- and differentiation-related features, together with those of nuclear DNA content, showed two main successive preneoplastic lesions: one characterized by an increase in cell turnover without alterations in its organization and another by a true neoplastic disorder. The data obtained on sequential cytologic examinations showed that individual cell changes are detectable and seem basically to be characterized by the appearance of clusters of cells with somatic characteristics not observed in previous cytologic checks. From the results of our study, the cervical intraepithelial neoplasia (CIN) concept appears to be inaccurate. In fact, only CIN III (severe dysplasia/carcinoma in situ) lesions have the morphologic and proliferative alterations of true neoplasia. In contrast, CIN I and some cases of CIN II lesions lack these characteristics and seem to be properly classified as dysplasia, thus avoiding the term neoplasia, implicit in CIN. Moreover, the multivariate study of data sets of features related to the progressive somatic changes, both in histologically and cytologically studied cases, allows us to detect the steps of progression; they are marked by the appearance of cell clusters with qualitatively different phenotypic characters when compared to the cell populations from which they presumably arise. These results seem to provide a further argument against the CIN theory, which stresses the concept that progression is related only to a gradual numerical increase in an initially established phenotype with the characteristics of malignancy.
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PMID:Cytometric evidence that cervical intraepithelial neoplasia I and II are dysplasias rather than true neoplasias. An image analysis study of factors involved in the progression of cervical lesions. 159 Aug 97


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