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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A human pancreatic beta cell tumor was maintained in monolayer cell culture for 80 days. The culture was terminated because of bacterial infection. Probably because extensive trypsin-collagenase dissociation was unnecessary, the dissociated cells attached much more quickly to the surface of the culture flask than do rat pancreatic cells obtained by enzymatic dissociation. Insulin release not only oscillated widely during the first 40 days of culture but also showed a decline from 380 mU the first week to about 50 mU/week the seventh week. For some unknown reason fibroblast overgrowth was not a major problem. Reduction of the medium glucose concentration from 16.5 mM to 5.5 mM did not alter insulin release rate. At glucose concentration of 16.5 mM, somatostatin 1.0 mug/ml reduced insulin release by 40%. From our previously reported studies on the effect of somatostatin on insulin release by monolayer cell cultures of rat endocrine pancreas, we conclude that the constant release of insulin by the tumor cells is relatively nonstimulated. We have confirmed that monolayer cultures of human pancreatic beta cell tumor do not represent a good model for normal human beta cell function because of the major shortcoming of an apparent inability to recognize glucose as a secretogogue.
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PMID:Monolayer cell culture of human pancreatic beta cell tumor: effect of glucose and somatostatin on insulin release. 17 3

The antigens of SV40-transformed BALB/3T3 cells measured by a radioisotopic footpad assay after removal by trypsin treatment regenerated in vitro in 3 to 6 hr. After X-irradiation with 3000 R, however, the antigens were regenerated to normal levels within 1 h. X-ray doses of between 1000 and 5000 R accelerated the regeneration of cell surface antigens, while X-irradiation with the larger dose of 8000 R did not. X-irradiation of nontrypsinized tumor cells was without effect. Possible mechanisms of this phenomenon are discussed.
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PMID:Accelerated regeneration of trypsin-treated surface antigens of simian virus 40-transformed BALB/3T3 cells induced by X-irradiation. 17 5

There is extensive physiological evidence implicating the cell surface as the key organelle which mediates the cell:cell interactions which underlie both normal and neoplastic growth. This information has now been supplemented with biochemical and biophysical data which indicates that surface macromolecules, in particular the heteroglycans of transformed cells, differ from those which lie at the periphery of normal cells. In the case of cells neoplastically transformed by most tumour viruses it is clear that the small virus genome (2-5 x 10(6) daltons) cannot carry the total genetic information to accomodate these various biochemical modifications, if indeed they are encoded in separate genes (1). To examine the part played in transformation by cellular genes coding for surface heteroglycan formation, we have turned to a study of SV-3T3 cells (ts H6-15) which are temperature-sensitive for expression of the transformed cell phenotype (2). The data show that cells grown under conditions permissive and non-permissive for such expression exhibit the same pattern of formation of glycolipids, and the majority of the polypeptides of the plasma membrane. There are, however, significant differences in the synthesis of some glycopeptides. A large molecular weight, trypsin-labile glycopeptide, present at the surface of untransformed fibroblasts but barely measurable in some of their virus-transformed derivatives (3), was detected, essentially at the same level, at the surface of ts H6-15 cells grown at the permissive and non-permissive temperatures. The signficance of these observations is discussed.
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PMID:A consideration of the role of cell surface macromolecules in the process of viral transformation. 17 54

Tubular inclusions were present in 13 out of 43 pituitary adenomas of acromegalic patients and in a single chromophobe pituitary adenoma. There were none in 76 other pituitary adenomas with differing endocrinological symptomatology. The arrays were usually located in the perinuclear cistern of capillary endothelial cells. The tubule diameter in osmium fixed material measured 19-26 nm and the light core averaged 6-11 nm. A longitudinal period of about 4.5 nm could be demonstrated with PTA block staining. Fixation with glutaraldehyde and block staining with ethidium bromide as well as permanganate fixation followed by RNAse treatment showed only the core of the tubules consisting of globular subunits. Several histochemical reactions (perchloric acid extraction, methenamine-silver staining, trypsin and DNAse digestion of frozen sections) suggested that the particles consist of a core of DNA coated with protein. No virus multiplication could be detected in cell cultures or in mice innoculated with fresh tumor material. No significant antibody titers against several virus antigens could be demonstrated.
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PMID:Ultrastructure of tubular inclusions in endothelial cells of pituitary tumors associated with acromegaly. 17 95

Mechanical and enzymatic methods of disaggregating tumors were studied with the goals of (1) minimizing cell losses while (2) maintaining functional and surface membrane markers needed to objectively identify inflammatory cells (IC)1 in resultant suspensions. Application of the principles and methods described makes accurate estimation of the percentage of each IC type present in neoplasms possible for the first time. Compared to purely mechanical means of disaggregating tumors, all enzyme mixtures tested markedly increased yields of viable cells/g neoplasm. Best results were obtained with a combination of collagenase and a protease of broader substrate range (alpha chymotrypsin, papain, pronase or trypsin). The combination of enzymes that gave the highest yields with the least effect on inflammatory cell markers was trypsin, collagenase and DNAse (TCD). Because mechanical injury appeared to be the greatest single cause of cell loss (the enzymes themselves had little direct effect), potential sources were identified and either eliminated or minimized. With TCD, depending on the tumor system, cell recovery (measured as DNA recovered in cell suspensions) was as high as 50% and yields were as much as 6.9 X 10(8) viable cells/g tumor. Complete disaggregation was not required to obtain representative IC populations from tumor fragments. Neutrophils, eosinophils and mast cells from disaggregated neoplasms were counted in Giemsa stained cytocentrifuge preparations based on their unique morphologic appearances. Macrophages were identified by their capacity to phagocytose zymosan, a function which proved highly resistant to the effect of enzymes. Flourescent microscopic identification of brain associated thymus antigen (BATA) allowed quantification of T lymphocytes, since this marker was virtually unchanged by enzyme exposure. Surface immunoglobulin (Ig) was stripped from B lymphocytes most rapidly by pronase and chymotrypsin, slowly by trypsin and papain, and not at all by collagenase. Ig positive cells therefore could be quantified in suspensions generated by collagenase or very short (20 min) exposure of fragments to trypsin.
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PMID:Inflammatory cells in solid murine neoplasms. I. Tumor disaggregation and identification of constituent inflammatory cells. 18 47

A 45-year-old women had medullary tyroid carcinoma associated with Cushing's syndrome and galactorrhoea. Elevated plasma immunoreactive ACTH and cortisol were partially suppressed by intravenous dexamethasone, appreciably raised by lysine vasopressin, and urinary excretion of 17-oxogenic steroids slightly elevated by metyrapone. A large arterio-venous increase in plasma corticotrophin releasing factor-like activity across the thyroid gland was observed and tumour tissue contained corticotrophin releasing factor-like activity. Biologically active ACTH was not detected in tumour extracts before incubation with trypsin, but after trypsinization a value of 3.2 mU per gram was obtained. Arterial plasma contained biologically active ACTH (1.5 mU/100 ml) prior to trypsinization. Venous effluent from the thyroid gland contained biologically active (9.6 mU/100 ml) and immunoreactive ACTH (970 pg/ml) before trypsinization. Tumour extracts also contained prolactin production-stimulating activity. These findings can explain the Cushing's syndrome and the galactorrhoea both of which disappeared completely after thyroidectomy.
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PMID:Medullary thyroid carcinoma: ectopic production of peptides with ACTH-like, corticotrophin releasing factor-like and prolactin production-stimulating activities. 18 33

The effects of trypsin and EDTA on the cell coat of ascites tumor cells were studied by means of biochemical and electron microscopy techniques. EDTA seems to release, by chelation of the Ca2+-bridges, an outer layer of glycoproteins of presumably exogenous origin. On the contrary, trypsin produces a deeper enzymic cleavage which appears to affect the structural integrity of the bilayered cell membrane. The significance of the cell leakage in tumor cells and the effect of EDTA on the modification of this leakage by change of cell membrane permeability are discussed.
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PMID:Cell coat in tumor cells -- effects of trypsin and EDTA: a biochemical and morphological study. 18 64

The platelet aggregating principle of two mouse ascites tumors and of their cell-free supernatants released spontaneously has been studied. It was found that the principle disappeared from the cells after trypsin digestion and that part of it was recovered in the cell-free trypsinate. Digested cells regenerated the principle during subsequent incubation by a process requiring protein synthesis. The principle was found to be spontaneously released by intact cells into the medium and sensitive to proteolytic attack. The principle was not present in five varieties of nonneoplastic cells. Since previous work by the authors indicates that the principle is present in numerous other tumor cell lines, its study might reveal it to be an indicator of malignant transformation or malignant progression.
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PMID:Platelet aggregating material in mouse tumor cells. Removal and regeneration. 19 95

The Madison lung (M109) tumor cell line, initiated from a "spontaneous", anaplastic murine lung carcinoma, has been propagated continuously in vitro for more than 300 cell generations. Cytogenetic analysis revealed a mouse karyotype with a mode of 78 chromosomes (2n = 40). Three distinct marker chromosomes were identified by trypsin-giemsa banding. The cells piled up in culture and had a short generation time and high plating efficiency. Electron microscopy revealed highly undifferentiated cells with little rough endoplasmic reticulum, an abundance of free polysomes, the presence of few and often odd-shaped mitochondria, lipid bodies and phagocytic vacuoles. Virus particles of the C-type were found frequently. The subcutaneous transplantation of M109 cultured cells at a relatively low cell inoculum produced highly metastatic tumors in syngeneic BALG/c mice.
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PMID:Establishment and characterization of a cell line derived from a spontaneous murine lung carcinoma (M109). 19 26

Serum-free media of minced tissue cultures of VX-2 rabbit carcinoma contained a specific collagenolytic activity capable of releasing soluble radioactive peptides from [14C]-labeled collagen fibrils. It was also capable of reducing the viscosity of acid-soluble collagen solutions by cleaving the tropocollagen (TC) molecules primarily at one site to TCA (75%) and TCB (25%) fragments. Three chromatographic fractions were separated by gel filtration: F1, (MW 85-110,000) present in larger amounts in early cultures of younger tumor tissue; F2, (MW-35-40,000) the major component with maximum production in the day 3 media of younger and advanced tumor tissues; F3, (MW 18-22,000) the minor component. Early cultures of younger tumor tissue contained a latent collagenase and were subject to trypsin activation suggesting the presence of inactive enzyme precursors or an enzyme-inhibitor complex.
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PMID:Changes in the collagenolytic activity released by primary VX-2 carcinoma cultures as a function of tumor growth. 19 82


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