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)

Lectin histochemical studies of human fetal notochord, ecchordosis physaliphora, and eight chordomas were performed. Ecchordosis physaliphora and eight chordomas were stained with Ricinus communis type I, Canavalia ensiformis, Triticum vulgaris, and Limax flavus. Ricinus communis type I, T vulgaris, and L flavus reacted with both tumor cells and the extracellular mucinous matrix, while C ensiformis mainly reacted with the cytoplasm of tumor cells. Thus, tumor cells were most recognizable with the C ensiformis stain. After neuraminidase treatment, ecchordosis physaliphora and chordomas invariably showed positivities for Arachis hypogaea. The lectin-binding patterns of chordomas closely reflected those of the human fetal notochord. Chordomas were completely sialylated regardless of either the clinical course or histopathological findings. Among the eight lectins, C ensiformis heavily labeled chordoma cells but not extracellular space. This was probably because asparagine-linked N-glycosylation was active in the chordomas, while the high-mannose-type oligosaccharides were apt to remain in the cytoplasm.
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PMID:Lectin histochemistry of human fetal notochord, ecchordosis physaliphora, and chordomas. 173 35

A study is presented of the sensitivity of freshly isolated cells (13 cases) to lysis due to natural killers (NK) depending on their malignancy grade and degree of their membrane sialization. The diagnoses were verified histologically (I-II grade gliomas-4 cases, grade III gliomas-3 cases, grade IV gliomas-6 cases). It was established that grade IV gliomas were most sensitive to NK-lysis. Treatment of tumor cells with neuraminidase increased the sensitivity to NK-lysis of grade I-III glioma cells and did not influence the sensitivity of grade IV gliomas. It is suggested that glycoprotein oligosaccharides of glial tumour cell membranes may play the role of target structures for lymphocytes-killers.
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PMID:[Sensitivity of human glial tumor cells of different grade of anaplasia to lysis due to natural killers depending on some characteristics of the glycoprotein structure of tumor cell membranes]. 178 88

112 cases of normal, dysplastic and neoplastic cervical epithelium were studied with a panel of twelve various lectins and ABC technique. The results showed that: (1) ConA and WGA receptors were relative to Squamous epithelial origin of the Cervix. (2) PNA, UEA-1, BSL and PHA receptors correlated with the tumorigenicity of cervical squamous epithelium. (3) WGA receptor correlated with the cell differentiation of squamous carcinomas. (4) DBA receptor was related with tumor invasion. (5) ConA and SJA receptors were related to the tumorigenicity of columnar epithelium of the endocervical glands. (6) Applications of neuraminidase caused compositional changes of glycoconjugates in the receptors of normal, dysplastic and malignant cervical epithelium and this may be of some value in clinical practice.
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PMID:[Distribution of lectin-receptors in normal, dysplastic and neoplastic cervical epithelium]. 181 64

Characteristics of placental-like alkaline phosphatase (PLAP-like enzyme) in seminoma was studied. By use of lectin affinity chromatography, PLAP-like enzyme in seminoma revealed extra sugar chains compared to placental alkaline phosphatase (PLAP), indicating heterogeneity of the carbohydrate moiety. However, the glycosylation patterns were found to be essentially similar between seminoma and normal testis. On isoelectric focusing, differences in migration patterns were revealed between seminoma-derived and normal testis-derived PLAP-like enzyme as well as between PLAP-like enzyme and PLAP. The differences in charge were mainly due to differences in sialylation of the molecules. The complex pattern of PLAP-like enzyme from seminoma on isoelectric focusing was not altered by neuraminidase treatment, indicating a considerable charge heterogeneity within the population of the enzyme molecules from the tumor.
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PMID:Characterization of seminoma-derived placental-like alkaline phosphatase. 194 90

Wheat germ agglutinin binding to a rat hepatoma cell line dRLa 74 treated with concanavalin A was studied. It increased depending on the concanavalin A concentration in the culture medium. The cells exhibited about twofold increase in wheat germ agglutinin-binding when pretreated with 50 micrograms/ml of concanavalin A for 48 h. The wheat germ agglutinin binding sites were shown to be localized at the cell surface by lectin-histochemistry. Wheat germ agglutinin blotting of microsomal membrane proteins showed a broad wheat germ agglutinin-reactive band with an apparent molecular weight of 90 to 100 kDa. Loss of wheat germ agglutinin binding to dRLa 74 cells and the glycoprotein after neuraminidase treatment suggested that wheat germ agglutinin reacted with cell surface sialyl residues of dRLa 74 cells. The induced change was reversible. Increased wheat germ agglutinin binding returned to the pretreatment level when the concanavalin A-treated cells were subcultured in the absence of concanavalin A. These observations suggest that environmental factors interacting with tumor cell surface sugar moieties may induce reversible epigenetic changes on cell surface carbohydrate structures.
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PMID:Increase in cell surface wheat germ agglutinin binding in a rat hepatoma cell line dRLa 74 treated with concanavalin A. 196 34

Colorectal primary carcinomas and metastases from 20 Dukes' stage C or D patients were examined for the immunohistochemical localization and contents of various fucosylated N-acetyl-lactosamine oligomers by specific monoclonal antibodies (MAbs). MAbs used were SH1, specific for Lewis X antigen; FH4, specific for dimeric Lewis X antigen; FH6, specific for sialyl-dimeric Lewis X antigen; and KH1, specific for Lewis Y-Lewis X antigen. The distribution of the carbohydrate antigens identified by these MAbs was heterogeneous within the primary tumor as well as within the metastatic lesion. Examinations of serial sections indicated that areas within an individual tumor which were stained with one MAb were not always reactive with the other MAbs, although these four MAbs identify closely related structures. The degree of MAb reactivity with carcinoma sections was classified by percentage positive carcinoma cells, and primary tumors and metastases from the same patients were compared. An equivalent or higher proportion of carcinoma cells in the metastatic lesions were reactive with MAb FH6 than in the primary colon carcinomas, but each correlation was not seen with the other MAbs. Electrophoretic separation of tumor tissue extracts followed by staining with these MAbs revealed that a component having an approximate molecular weight of 1,000,000 is the major site for the binding of MAbs, FH6, FH4, and KH1. The electrophoretic mobility of the antigenic molecule on polyacrylamide gels as shown by direct MAb bindings was slightly different from that of a major sialomucin revealed by wheat germ agglutinin in the same tissues. MAb FH6 binding to a high molecular weight component was eliminated by prior treatment of the glycoprotein with mild acid or sialidase to remove sialic acid. Simultaneously, binding of MAb SH2, specific for dimeric Lex antigen, to this component increased. An extract was prepared from a liver metastasis, and high molecular weight components were isolated by gel filtration and then fractionated by DEAE-cellulose ion exchange chromatography. A fraction eluted from DEAE-cellulose between 0.10-0.25 M sodium chloride contained most of the MAb FH6 reactivity, as shown by antibody affinity chromatography. These results support a hypothesis that high molecular weight glycoproteins produced by colorectal carcinoma tissues are heterogeneous with regard to their carbohydrate chains and their antigenic structures may change during tumor progression.
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PMID:Sialyl-dimeric Lewis-X antigen expressed on mucin-like glycoproteins in colorectal cancer metastases. 197 61

Cell surface molecules play an important role in cellular communication, migration, and adherence. Here, we show the effect of organ-derived biomatrices on endothelial cell surface glycosylation. Five different lectins (with and without neuraminidase treatment) have been used as probes in an enzyme-linked lectin assay to quantitatively detect glycoconjugates on endothelial cells (BAEC) grown on tissue culture plastic or biomatrices isolated from bovine lung, liver, and kidney. BAEC generally exhibit strong binding of concanavalin A (Con A), Ricinus communis agglutinin I (RCA-I), wheat germ agglutinin (WGA), and soybean agglutinin, and peanut agglutinin after neuraminidase pretreatment of cells (Neu-SBA and Neu-PNA), while SBA and PNA consistently bind weakly to BAEC. BAEC grown on organ-derived biomatrices exhibit significantly altered binding intensities of Con A, RCA-I, WGA, and Neu-PNA: BAEC cultured on lung- or kidney-derived biomatrices express significantly stronger binding affinities for Con A and RCA-I than BAEC grown on liver-derived biomatrix or tissue culture plastic. In contrast, BAEC binding of WGA and PNA (after treatment of cells with neuraminidase) is significantly reduced when BAEC are grown on liver- or kidney-derived biomatrix. Quantitative lectin immunogold electron microscopy reveals consistently stronger lectin binding over nuclear regions compared to junctional regions between neighboring cells. These results indicate that extracellular matrix components regulate endothelial cell surface glycoconjugate expression, which determines cellular functions, e.g., preferential adhesion of lymphocytes or metastatic tumor cells.
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PMID:Modulation of endothelial cell surface glycoconjugate expression by organ-derived biomatrices. 198 84

Partial or total loss of chromosome 22 is often associated with tumors of the central nervous system and in particular with meningiomas. As in the case of other tumors, the ganglioside pattern is modified in transformed tissues. Cytogenetic analysis of 30 human meningiomas has been performed and the results compared to biochemical analysis of ganglioside distribution on the membrane surface. The meningiomas were divided into 2 groups on the basis of the presence or absence of chromosome 22. Thirteen tumors exhibited partial or total monosomy of the chromosome, whereas 17 were normal or showed other chromosomal anomalies. The GM3 and GD3 content of the meningiomas belonging to the 2 groups revealed a significant correlation between amount and reciprocal ratio of these 2 gangliosides and cytogenetic data. Tumors with monosomy 22 had a higher content of ganglioside GD3 than samples without monosomy 22, where the main ganglioside was GM3. Other gangliosides such as GM1, GD1a, GD1b and GT were present in various amounts in the 2 groups. Considering the biosynthetic pathway of gangliosides, we hypothesize the involvement of a gene located on chromosome 22 in the regulation of the enzymes which catalyze either GD3 synthesis (sialyltransferase 2, SAT-2) or its degradation to GM3 (neuraminidase).
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PMID:Correlation between cytogenetic data and ganglioside pattern in human meningiomas. 199 40

The mechanism whereby cytolytic lymphocytes protect themselves from killing mediated by their own cytotoxic protein, perforin, was studied. By using a competition assay, we demonstrated that the resistance of cells to perforin-mediated cytolysis is inversely correlated with their ability to absorb perforin, with tumor cells and noncytotoxic lymphocytes that are susceptible to perforin-mediated lysis being able to absorb perforin from the supernatant much better than CTL. The evidence implies that there is molecule on cytolytic lymphocytes that interferes with perforin-binding activity, resulting in the inability of perforin to lyse these cells. The molecule is most likely a surface protein or complex of proteins because its activity decreases after CTL treatment with the proteolytic enzymes trypsin and papain, and the activity can be recovered by incubation of the treated CTL cells at 37 degrees C for 6 h. The recovery can be blocked by emetine, cycloheximide, and actinomycin D, inhibitors of protein and RNA/DNA synthesis. The protein contains carbohydrate groups that play an important role in the function of the protein, as indicated by the fact that inhibition of glycosylation by tunicamycin and cleavage of sialic acid from the protein with neuraminidase result in a significant increase of perforin binding to CTL. Cross-linkage of CTL membrane proteins with glutaraldehyde and formaldehyde and blockage of the functional domains of the protein with an antiserum against CTL also inhibit the activity of this protein. Temperature-dependence studies that allow for a dissociation of the binding and pore-forming stages of perforin-mediated hemolysis suggest that the protective protein interferes at the perforin-binding stage.
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PMID:Resistance of cytolytic lymphocytes to perforin-mediated killing. Inhibition of perforin binding activity by surface membrane proteins. 210 15

Evidence is presented that a wide variety of cell types are capable of presenting class I alloantigens to purified unprimed CD8+ cells in the absence of added help. These cells include dendritic cells, a population of Ia- Thy 1- cells in spleen, peritoneal exudate cells and one of three T-tumor lines. Some cell types, e.g. T-blast cells and overnight-adherent peritoneal exudate cells (OA-PEC) only expressed antigen-presenting cell (APC) function in the presence of added lymphokines. Stimulation of OA-PEC with small concentrations of lipopolysaccharide or treatment of T-blast cells with neuraminidase (N'dase) strongly enhanced the APC function of these cells and led to helper-independent responses. N'dase treatment of small resting T stimulators caused partial restoration of APC function: strong responses were observed but only in the presence of exogenous lymphokines. Studies with T-tumor lines preincubated with IFN-gamma suggested that APC function correlates closely with antigen (class I) expression. Collectively, the data support the view that APC function depends upon a multiplicity of factors including antigen density, the level of accessory (adhesion) molecules and net surface charge. It is suggested that the potency of APC function is largely a reflection of the overall avidity of T-APC interaction: high-avidity binding leads to helper-independent responses whereas weaker binding results in helper-dependent responses.
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PMID:Antigen-presenting cells for CD8+ T cells. 212 7


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