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)

The effects of enzymic treatment on the interactions between Zajdela's tumor cells and various lectins. Concanavalin A (ConA); Wheat Germ Agglutinin (WGA); Robinia lectin; have been studied. (1) The number of lectin-binding sites and the affinity constants were investigated. (2) The effects of the lectins on cell growth and [3H]thymidine incorporation were studied on untreated and enzyme-treated cells. It was observed that treatment of tumor cells with neuraminidase resulted in a change in the binding characteristics of each lectin. However, additional treatment of the cells with galactose oxidase had no further effect on lectin binding. ConA and Robinia lectin induced a decrease of the untreated tumor cell growth and a stimulation of the [3H]thymidine incorporation. This paradoxal result may be explained as a consequence of the stimulation of the [3H]thymidine uptake observed in the presence of lectins. The enzymatic treatments themselves did not change the cell growth although they did induce a change in the effect of ConA and Robinia lectin on cell growth and [3H]thymidine incorporation. As a result of neuraminidase treatment, the effects of ConA were totally suppressed but those of Robinia lectin only partially. Although WGA interacted with untreated and enzyme-treated cell surfaces, it had no effect on tumor cell growth nor [3H]thymidine incorporation. The results are discussed in terms of lectin transport.
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PMID:Specific modifications of hepatoma cell-surface glycoproteins with enzymes. Effects on in vitro growth as investigated by the use of lectins. 29 48

Cell surface glycoproteins of human tumor cell lines (melanomas and astrocytomas, and ovarian, bladder, stomach, cervical, laryngeal, and renal cancers) were studied by labelling with 1) neuraminidase-galactose oxidase-[3H]borohydride, 2) galactose oxidase-[3H]borohydride, and 3) dilute periodate-[3H]borohydride. The labeled components were examined by polyacrylamide gel electrophoresis and fluorography. Each tumor type had a distinctive pattern of labeled glycoproteins when the results from both procedures 1 and 2 were considered. Cell surface glycoproteins of malignant melanoma could not be labeled by procedure 2, whereas the other cell lines had at least two major glycoproteins that could be labeled by this method. Very similar profiles of melanoma glycoproteins were labeled by procedures 1 and 3. From these results the conclusion was reached that cell surface glycoproteins of melanomas are substituted with sialic acid so that their D-galactose and/or N-acetyl-D-galactosamine residues are available for oxidation by galactose oxidase only after neuraminidase treatment. An alternative explanation that these sugars are sterically accessible to galactose oxidase only after neuraminidase treatment also has to be considered. All melanoma lines studied were characterized by having two major cell surface glycoproteins with molecular weights of 110,000 and 90,000, respectively. Lines, however, varied considerably in their expression of other components. In particular, heterogeneity was shown in the expression of gp220, a component identified as fibronectin by immunoprecipitation with a specific antiserum, and in the expression of gp37/32, a pair of glycoproteins having the characteristics of la-like antigens. Of the other cell lines studied, astrocytomas most closely resembled melanoma in their glycoprotein profiles. The brain tumors, however, had two or three glycoproteins, including gp110, which could be labeled by galactose oxidase-[3H]borohydride without neuraminidase treatment.
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PMID:Cell surface glycoproteins of human tumor cell lines: unusual characteristics of malignant melanoma. 38 52

Lymphoma L5178Y cells were treated with neuraminidase of Vibrio cholerae, potassium iodine, dithiotreitol (DTT), mercaptoethanol, glutaraldehyde, iodoacetamide, merthiolate, sodium periodate, urea, papaine, trypsine and EDTA, to increase immunoreaction in tumor cells. Mice were immunized with modified tumor cells every week for one month. Thereafter non modified tumor cells were transplanted to previously immunized mice. Only the immunization with neuraminidase-treated cells rejected the tumor. Although the immunization with cells treated with potassium iodine, DTT and mercaptoethanol did not reject tumor, prolonged significantly span of life. The other reactives had neither effect on tumor rejection nor on span of life.
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PMID:[Immunogenicity of L5178Y cells modified by different reagents]. 41 Mar 77

Active immunization has received a new impulse most recently through the treatment of tumor cells with the enzyme neuraminidase from Vibrio cholerae. There is no passive specific immunotherapy in humans. In the field of unspecific active immunotherapy there are very many, partly contradictory, findings, especially with BCG, Corynebacterium parvum and preparations from these and other organisms. A cellularly transmitted immunity has been attempted, but so far without very encouraging results. It must be emphasized that all these statements refer to humans.
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PMID:[Problems of cancer immunotherapy (author's transl)]. 41 81

Active immunotherapy with tumor cells treated in vitro with Vibrio cholerae neuraminidase (VCN) plus mitomycin C augments the antitumor effects of local x irradiation in the treatment of firmly established methylcholanthrene-induced fibrosarcoma, MC-43, in syngeneic C3H/HeJ female mice. In most experiments, the inhibition of tumor growth was greater when VCN-treated tumor cells were combined with local irradiation than could be achieved with VCN-treated tumor cells or local irradiation alone. Even in those experiments in which the immunotherapeutic effect of VCN-treated cells was negligible, the combination of radiotherapy and immunotherapy appeared to be greater than irradiation alone. Similarly, total permanent regression of established tumors occurred more frequently after combined therapy than after immunotherapy or radiation therapy alone.
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PMID:The combined effect of radiotherapy and neuraminidase-treated tumor cells on 3-methylcholanthrene-induced fibrosarcoma. 59 52

C3H/HeJ mice bearing MC-80 fibrosarcomas were given immunotherapy consisting of multiple injections of a Vibrio cholerae neuraminidase (VCN)-treated tumor cell vaccine at a site remote from the established tumor. In five separate experiments we were unable to show either partial or complete tumor regression or prolongation of survival for vaccine-treated mice compared to appropriate controls. Further, the use of BCG in addition to VCN-treated tumor cells failed to show any therapeutic efficacy. We could not confirm the successful immunotherapy results reported by others despite multiple efforts of reproduce the immunotherapy model as carefully and precisely as possible.
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PMID:Failure of immunotherapy with neuraminidase-treated tumor cell vaccine in mice bearing established 3-methylcholanthrene-induced sarcomas. 62 58

B16 melanoma cells were treated in vitro with muconomycin A, a long-lasting inhibitor of protein and glycoprotein synthesis, to reduce cellular sialic acid. Two i.p. inoculations of 10(7) muconomycin-treated cells into female C57BL/6 mice, followed by challenge with homologous live cells, resulted in a significant decrease in tumor incidence when compared to the results of inoculation with untreated cells (p less than 0.01). Inoculation of mice with cells treated with neuraminidase resulted in little or no decrease in tumor incidence. Effective immunity was dependent on the number of cells injected and was found only with the i.p. route of inoculation into female mice.
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PMID:Increased tumor immunity in mice inoculated with muconomycin A-treated B16 melanoma cells. 69 27

One hundred forty-four Wistar-Furth rats in 12 therapeutic groups have been studied in a long-term comparison of the effectiveness of nonspecific immunotherapy with MER (methanol extraction residue) vs active-specific immunotherapy with neuraminidase-modified tumor cells. Six months after surgical adjuvant immunotherapy a 100% improvement in survival was achieved with MER immunotherapy compared to untreated control animals. In addition, the use of MER enhanced the value of active-specific immunotherapy where both modalities were combined in sequence. The predicted value of MER-BCG (Bacillus Calmette-Guerin) for the immunotherapy of solid tumors was borne out by these results suggesting that present ongoing clinical trials of MER as adjuvant therapy for large bowel cancer should prove to be successful if properly controlled. The pattern of survival in these experiments suggests that surgical adjuvant immunotherapy is cytostatic rather than cytocidal, and implies the need for long-term, repeated immunizations.
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PMID:Surgical adjuvant immunotherapy for colorectal cancer. 73 27

Exposure of a weakly immunogenic nickel sulfide-induced Fischer rat tumor to Vibrio cholerae neuraminidase inhibited tumor growth in normal recipients. These recipients were found to be more resistent to a subsequent tumor inoculation.
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PMID:Neuraminidase effect on the growth of a transplantable nickel sulfide-induced rat tumor. 75 42

A factor responsible for stimulating an increase in ornithine decarboxylase activity in the liver of mice was found in tumor cell-free ascites fluid of mice 3 days after inoculation of tumor cells. The factor was purified about 70-fold in 25% yield from tumor cell-free ascites fluid. As little as 1 microgram of protein of purified fraction, injected intraperitoneally into normal mice, significantly increased the activity of ornithine decarboxylase in the liver. The most active preparation of the factor formed two major protein bands on analytical polyacrylamide gel electrophoresis and both these bands stained with periodic acid-Schiff's reagent. The factor was a heat-labile, alkaline-stable, acidic protein with a molecular weight of more than 300 000. It was inactivated by treatment with 10 mM dithiothreitol, 5 M urea, pronase or mixed glycosidase, but was stable on treatment with DNAase, RNAase or neuraminidase.
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PMID:Partial purificationand characterizationof a factor which stimulates an increase in ornithine decarboxylase activity in the liver from tumor cell-free ascites fluid. 76 Aug 23


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