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)

In a patient a papilla Vateri tumor completely prevented the bile-pancreatic flow into the intestine although the pancreatic juice was secreted into the bile duct via a common channel. Consequently, the bile-pancreatic juice was possible to sample via a percutaneous transhepatic cholangiography (PTC) catheter. This made it possible to study the effect of duodenal infusion of different substances on the bile-pancreatic secretion. In repeated experiments a suppression of the secretion was observed by intraduodenal trypsin as well as the patient's own bile-pancreatic juice. In the presence the bile-pancreatic juice intraduodenal trypsin inhibitor infusion caused a marked stimulation of the secretion. The results are in accordance with the hypothesis that trypsin in the upper part of the intestine exerts a negative feedback regulation of the pancreatic secretion in man.
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PMID:Feedback regulation of pancreatic enzyme secretion by intestinal trypsin in man. 86 33

We have investigated the receptor site activity present on 6C3HED tumor cells for concanavalin A, fava, lentil and pea lectins. The binding of the tritiated lectins to the tumor cells was inhibited by methyl-alpha-D-mannoside but not by D-galactose. The number of binding sites for the lectins was 3.5-10(6)/cell for concanavalin A, 3.3-10(6)/cell for fava, 3.6-10(6)/cell for lentil and 4.8-10(6)/cell for pea. The apparent association constants were 3.6 and 1.3 muM-1 for concanavalin A, 3.9 muM-1 for fava, 4.2 muM-1 for lentil and 4.6 and 0.6 muM-1 for pea. Competitive inhibition studies showed that lentil was a good inhibitor of pea binding; concanavalin A was a poor inhibitor of pea binding; and fava was a better inhibitor than concanavalin A but not as good as lentil. Reciprocal inhibition experiments indicated that concanavalin A and pea may bind to different receptors as well as to common receptors. This was also indicated by the observation that trypsin or protease treatment of the cells decreased the binding of pea lectin by 20-40 percent whereas concanavalin A binding was unaffected.
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PMID:Studies on 6C3HED murine ascites tumor cell receptors for mannosyl-binding lectins. 95 11

Rapid degradation of ascites tumor cells damaged by the action of antibody plus complement was found to be accomplished by all proteolytic enzymes active at physiologic pH that were tested. For three types of murine ascites tumor cells (Ehrlich ascites, sarcoma-180, and L1210 leukemia), this rate of degradation at low trypsin concentrations was proportional to a high power of enzyme concentration. This suggests that the simultaneous action of two or more enzyme molecules at adjacent cell surface sites is necessary. Cell degradation was assayed by determination of cell volume distribution with a Coulter multi-channel particle size analyzer. The present study may offer clues to in vivo mechanisms of cell degradation.
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PMID:Enzymatic degradation of tumor cells damaged by antibody plus complement. 98 39

Activities of hydrolytic enzymes on the surface of monkey kidney, canine kidney, L. FM3A and various tumor cells were determined and compared with those in the cell homogenate. Although aminopeptidase (EC 3.4.11.-) activities were always detected on the surface membrane in mammalian cells, trypsin, chymotrypsin and elastase activities were not detected while slight glycosidase activity was detected in a suspension of cultured cells. The activities of alanine-, leucine-, methionine- and phenylalanine-aminopeptidases were rather high but aminopeptidase A, proline-, valine-, glycyl propline dipeptidyl-and glycyl propyl leucine-tripeptidyl-aminopeptidases showed relatively low activities. Aminopeptidase activity was also demonstrated in the isolated membrane fractions. The specific activities of enzymes in these membrane fractions were not significantly greater than in cell homogenate so it was concluded that these enzyme activities were rather loosely bound to the cell membrane. Further evidence for the localization of the aminopeptidase activities on the cell surface was obtained by using glass-bead-bound substrate and detecting the release of the terminal residues. When bestatin, a specific inhibitor against aminopeptidase B and leucine aminopeptidase, was included in the assay system for the enzyme activities on the cell surface, the enzymes were commonly inhibited in all types of cells.
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PMID:Aminopeptidase activities on the surface of mammalian cells. 99 Mar 9

Glycopeptides suggesting a complex oligosaccharide composition are present on the surface of cells from human neuroblastoma tumors and several cell lines derived from the tumors. The glycopeptides, labeled with radioactive L-fucose, were removed from the cell surface with trypsin, digested with Pronase, and examined by chromatography on Sephadex G-50. Human skin fibroblasts, brain cells, and a fibroblast line derived from neuroblastoma tumor tissue show less complex glycopeptides. Although some differences exist between the cell lines and the primary tumor cells, the similarities between these human tumors and animal tumors examined previously are striking.
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PMID:Glycopeptides from the surgace of human neuroblastoma cells. 100 Apr 97

Host DNA synthesis-suppressing factor (DSF) produced into culture fluid of cloned HeLa cells (HeLa C-9) infected with a small plaque variant of Toyoshima strain of measles virus was purified by precipitation with ammonium sulfate, chromatography on CM-cellulose and DEAE-cellulose, and gel-filtration on Sephadex G-100 and G-200. The specific activity of the finally purified DSF was 302 units/mg of protein representing approximately 300-fold purification. The molecular weight of DSF was estimated to be about 55 000. By isoelectric focusing, two kinds of DSF having isoelectric points of 4.24 and 5.24 were detectable. The purified DSF was able to suppress host DNA synthesis of HeLa cells, continuous human lymphoid cells (NC-37), mouse L cells and Meth-A cells derived from an ascitic tumor of the mouse. The activity of the purified DSF was inactivated by heating at 56 C for 30 min or by treatment with trypsin.
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PMID:Purification of host DNA synthesis-suppressing factor (DSF) produced by infection with measles virus. 101 43

Immunological studies are presented on a patient with a long clinical history suggesting the existence of a tumor-specific immune response. His tumor, first considered benign, progressed to a highly malignant osteosarcoma. Cell-mediated immune reactivity against biopsy cells and against tumor extract was detected in vitro by the autologous tumor stimulation test (ATS) and in vivo by the skin test. In one ATS-test with tumor extract, blastogenesis of T-cells was demonstrated. The amount of Ig(s) in consecutive biopsies increased. Biopsies taken in the later period of the disease stimulated only after trypsin treatment. This stimulation was inhibited by autologous serum or acid eluate of the biopsy. The inhibitory factor in the serum was not intact immunoglobin. Blood lymphocytes did not show a discriminatory or disease-related cytotoxicity, either directly or after co-cultivation with the tumor material. Lymphocytes isolated from one biopsy were non-reactive in both the ATS and the cytotoxicity test.
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PMID:Search for anti-tumor response in a bone tumor patient with a long clinical history. 106 20

Regressing and progressing Moloney sarcomas, induced in BALB/c mice by the injection of cultured sarcoma cells (MSC)1, were sampled for histologic analysis and then disaggregated using mixtures of trypsin, collagenase and DNAse or collagenase and DNAse alone. The types of inflammatory cells (IC) found in resultant cell suspensions were determined 6, 11, 14 and 18 days post inoculation. Inflammatory infiltrates were composed almost exclusively of three cell types; neutrophils, T lymphocytes and macrophages. The extent to which each was found in tumors was related to the time post inoculation. Neutrophils were part of an early acute inflammatory response seen in both developing regressing and progressing sarcomas. The onset of regression was associated histologically with the appearance within tumors of a mononuclear inflammatory infiltrate. T lymphocytes and macrophages were the principal constituents. A higher percentage of T lymphocytes was recovered at all sampling times from regressing, compared to progressing, sarcomas. During development of the mononuclear inflammatory infiltrate there were relatively more large T cells in regressing, than in progressing tumors, and the percentage of macrophages was higher. Thereafter, the proportion of macrophages in the recovered cell population was approximately the same for both types of tumor. Such equality was more apparent than real, however, since IC were restricted to the peripheries of progressing sarcomas after the acute inflammatory phase, but continued to be found throughout regressing neoplasms. The effective ratio of macrophages and T lymphocytes to tumor cells therefore was much lower in progressing sarcomas than was suggested by percentage figures. The data presented support the concept that T lymphocytes are instrumental in causing the regression of Moloney sarcomas, possibly through interactions with macrophages.
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PMID:Inflammatory cells in solid murine neoplasms. II. Cell types found throughout the course of Moloney sarcoma regression or progression. 108 89

A clone of Cloudman S91 murine melanoma was fused in vitro with non-malignant hamster cheek pouch cells by means of lysolecithin, and the putative hybrid progeny cells, HCP-MM, were found to be highly malignant in hamster, but not in appropriate mice. A malignant clone of HCP-MM cells was shown to have hamster species-specific surface antigens (as demonstrated by immunofluorescence and the cytotoxic antibody) and hamster-like lactate dehydrogenase and NAD-dependent malate dehydrogenase isoenzyme profiles. Nevertheless, chromosomes similar to those of both murine and hamster parental cells could be distinguished in cells of this malignant clone and in hamster tumor grafts by the method of trypsin-Giemsa banding. A majority of the murine chromosomes, however, appeared to be lost. This study indicates that a murine melanoma previously found untransplantable in hamsters could produce a highly malignant and lethal tumor for hamsters after being mixed in vitro with non-malignant hamster cells, in the presence of a fusing chemical. It is not as yet certain whether the production of transformed cells in vitro and of highly malignant tumors in the hamster (both with predominantly hamster properties) required heterosynkarion formation between the murine melanoma and hamster cheek pouch cells. Nevertheless, our results suggest that the presence of the murine melanoma, and possibly the interaction of its genome with non-malignant hamster cells, was implicated in this process.
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PMID:Oncogenesis by interspecific interaction of malignant murine and non-malignant hamster cells in vitro. 109 20

The effect on tumor progression produced by the injection of VCN-treated tumor cells in dogs with spontaneous mammary tumors was investigated. Untreated dogs of different races and different ages with at least two palpable spontaneous mammary tumors were selected. One of the tumors was left in the animal for further clinical examination whereas the other tumor(s) was (were) excised for preparation of a single-cell suspension by mechanical disintegration and enzymatic digestion with collagenase and trypsin. (1) In the first group, each animal was infected with 2 times 10-7 similarly prepared autologous, mitomycin-treated tumor cells; in 8 out of 12 dogs of this group the tumors progressed while so far 1 dog has died of metastasis. (2) In the second group, each animal received the same number of 2 times 10-7 tumor cells, which were mitomycin- and VCN-treated: 13 out of 15 dogs had a significant regression of their tumors to less than 10% of the original volume; in 1 dog the tumor remained unchanged and in 1 dog it progressed. (3) In the third group, 8 dogs received 1 times 10-8 mitomycin- and VCN-treated tumor cells: the application of this cell dose resulted in an accelerated tumor progression in all 8 dogs, 3 of which have already died of metastasis. The significance of these findings, with respect to potentiation and abrogation of the immunological response and with regard to immunotherapy in man, is discussed.
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PMID:Regression of spontaneous mammary tumors in dogs after injection of neuraminidase-treated tumor cells. 114 Aug 60


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