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)

A method for the purification of a membrane-bound glycoprotein, gamma-glutamyltranspeptidase ((gamma-glutamyl)-peptide:amino-acid gamma-glutamyltransferase, EC 2.3.2.2), from a transplantable rat mammary tumor (13762 MT) is described. The properties of the tumor enzyme were compared with those of gamma-glutamyltranspeptidase similarly isolated from mammary tissue of nonpregnant multiparous rats. Evidence has been presented elsewhere that the mammary and tumor enzymes exist as groups of species differing in isoelectric point and that the tumor enzyme contains more of the those species with lower isoelectric points. In this study the normal and tumor enzyme preparations are found to be identical or very similar in regards to the effect of papain on molecular size, the ratios of the enzymatic activities as measured with various amino acids, the Km for gamma-glutamyl-p-nitroanilide, and the Ki for inhibition by glutathione. Neuraminidase treatment had no effect on these catalytic properties. The properties observed were generally similar to those previously reported for highly purified rat kidney preparations.
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PMID:Purification and comparison of several catalytic parameters of the gamma-glutamyltranspeptidase of rat mammary adenocarcinoma (13762) and of normal rat mammary gland. 3 3

Immunological and biochemical studies of spontaneously metastasizing and nonmetastasizing rat mammary carcinomas and their plasma membranes indicated that: (i) all spontaneously metastasizing tumors have little or no demonstrable glycocalyx, while all nonmetastasizing tumors have a thick glycocalyx; (ii) there is a direct relationship between the glycocalyx and immunogenicity, and an inverse relationship with the metastasizing capacity of tumor cells, properties which can be quantitated by levels of the plasma membrane marker enzyme 5'-nucleotidase (EC3.1.3.5;5'-ribonucleotide phosphohydrolase) activity; (iii) the absence of glycocalyx from the metastasizing tumor cell surface seems to result from its dissociation from plasma membranes, for solubilized cell surface antigen is readily found in the blood of metastasizing tumor bearing rats, while there was no detectable tumor cell surface antigen in the blood of the nonmetastasizing tumor hosts tested; (iv) both metastasizing and nonmetastasizing mammary tumors appear to have a common soluble cell surface antigen; (v) in addition to this common antigen, there is another membrane-bound antigen in the nonmetastasizing, immunogenic tumor cell surface which presumably is the tumor specific transplantation antigen; and (vi) this antigen is immunobiologically unique, but seems to be immunochemically related to the common soluble antigen. It is postulated that the lack of an immunogenic coat and/or the presence of solubilized tumor cell surface antigen in the blood may provide an immune escape mechanism for tumor cells by interfering with cell-mediated immune response of tumor hosts, leading to their dissemination.
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PMID:Immunological escape mechanism in spontaneously metastasizing mammary tumors. 4 47

Here we describe the 500-fold purification of an mRNA encoding an immunoglobulin lambda light chain derived from the mouse myeloma tumor, RPC-20. Purification involves the isolation of membrane-bound polysomes, oligo(dT)-cellulose chromatography, and sucrose gradient centrifugation under conditions favoring denaturation of polynucleotide complexes. The mRNA purified in this way directs the cell-free synthesis of a polypeptide which is five or six amino acids longer than the mature form of RPC-20 light chain. In addition to directing the synthesis of a precursor-like polypeptide, the mRNA migrates on electrophoresis as a band containing approximately 1150 nucleotides, about 500 more than required to encode the mature form of the light chain.
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PMID:Purification and translation of an immunoglobulin lambda chain messenger RNA from mouse myeloma. 5 5

The cellular events in the formation of melanotic tumors in the tu-W mutant larva of Drosophila melanogaster are described. The first step is the differentiation of spherical hemocytes to flattened cells, the lamellocyte variants. Subsequently, the surface of the caudal fat body undergoes changes to which the hemocytes respond by forming cellular capsules. The hemocytes utilize two mechanisms in this process: (1) phagocytosis of small particulate materials escaping from the adipose cells, (2) adhesion to form a multilayered wall of lamellocytes. Differentiating hemocytes in the vicinity of the tumor-forming site extrude membrane-bound vesicles that tend to adhere to the hemocyte surfaces. These vesicles are trapped between the lamellocytes as they pile in layers to form the capsule wall. It is suggested that the vesicles play a role in lamellocyte-to-lamellocyte adhesion during the initial stages of hemocyte aggregation at the tumor-forming site.
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PMID:Cell interactions in the differentiation of a melanotic tumor in Drosophila. 11 92

Two lymphoid neoplasms induced by simian virus 40 (SV40) in Syrian hamsters were analyzed for lymphocyte characteristics. The hymphocytes from both tumors contained membrane-bound Ig that was exclusively of 7Sgamma2 class. Furthermore, neither lymphoid tumor had a complement receptor. Thus both tumors oringinated from a particular B-cell population, which suggests that this B-cell type is associated with an SV40 receptor.
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PMID:B-cell origin of hamster lymphoid tumors induced by simian virus 40. 16 22

N6,O2'-Dibutyryladenosine cyclic 3',5'-phosphate plus theophylline inhibited the growth of the mouse mast cell tumor line PY 815 both in vivo and in vitro. The inhibitory effect on growth in vitro was rapidly reversed following removal of the drugs. Growth inhibition was accompanied by reduced cell surface activity and increased cell-cell adhesion. The drug-treated cells accumulated distinct membrane-bound granules, which are characteristic of more mature mast cells. Treated cells also developed increased amounts of surface-associated acidic mucopolysaccharides. These results suggest that increased intracellular cyclic adenosine 3':5'-monophosphate causes mouse mastocytoma cells to decrease growth and elicits the expression of a more differentiated mast cell phenotype. The effect of the antileukemia drug, 4'-(9-acridinylamino)methanesulfon-m-anisidine, on cyclic adenosine 3':5'-monophosphate and adenosine 5'-triphosphate in mastocytoma cells is also reported.
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PMID:Regulation of growth of mouse mastocytoma cells. 16 78

Ultrastructural study of canine transmissible tumors in developing, mature, and regressing stages from 6 dogs revealed the presence of healthy and degenerating tumor cells in all neoplasms. The total number of neoplastic cells seemed to decrease, and the number of degenerating neoplastic cells seemed to increase in mature tumors. Macrophages, lymphocytes, and plasma cells infiltrated mature and regressing tumors. Alteratons in degenerating tumor cells consisted mainly of cytoplasmic changes in early stages and of both nuclear and cytoplasmic changes in cells in which degeneration was more advanced. Amounts of endoplasmic reticulum and ribosomes were decreased. There were swelling and vacuolation of mitochondria. Nuclear chromatin was clumped along the nuclear envelope, and the perinuclear space was widened. Degenerating cells often contained membrane-bound granules and clusters. Lamellar complexes were observed in tumor cells from 2 dogs. Virus particles were not seen.
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PMID:Ultrastructural characteristics of canine transmissible venereal tumor at various stages of growth and regression. 16 80

Nuclei of human neurilemoma cells exhibit deep and extensive invaginations of part of their surface. Such invaginations contain cytoplasmic matter. However, in areas of the nucleoplasm distant from the invaginations, small membrane-bound bodies, some of which contain a "nucleoid," occur either singly or grouped together and enclosed within a large membrane body. These small bodies are not considered virus-like. Degenerated nuclei from cultured tumor tissue contain spherical bodies, 130 to 230 nm in diameter, with spikes on their surface similar to those seen on envelopes of herpes-type viruses. Significance of these bodies in vivo and in vitro tumor tissues is not known.
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PMID:Ultrastructural characteristics of human neurilemoma cell nuclei. 16 42

Six biochemically differentiated clonal lines have been established from a transplantable glioma (tg26) of the C57BL/6 inbred mouse strain. Antibodies have been previously raised against G26 tumor cells, which define a cell surface component(s), NS-1 (nervous system antigen-1), found exclusively in the nervous system. NS-1 concentrations approximate the levels of the original G26 tumor when the clonal lines are grown as clonal tumors in vivo, but are reduced when the cells are grown in vitro. NS-1 concentrations are further reduced in vitro upon incubation of the cells with 1 mM dibutyryl 3:5-cyclic AMP. H-2 histocompatibility antigen concentration, in contrast, is unaffected by dibutyryl cAMP. In addition to expressing NS-1, the neuroectodermal origin of these cell lines is further confirmed by their synthesis of the nervous system specific acidic protein S-100 and by the high specific activity of the enzyme 2:3-cyclic nucleotide 3-phosphohydrolase. In addition, they respond to catecholamines by the elevation of intracellular 3:5-cyclic AMP levels. Whereas expression of S-100 protein is high under in vitro conditions but negligible after one passage in vivo, 2:3-cyclic nucleotide 3-phosphohydrolase is not detectable in vitro but becomes detectable again in vivo. The two membrane-bound constituents, NS-1 and 2:3-cyclic nucleotide 3-phosphohydrolase, therefore seem to be subjected to different regulatory mechanisms from that of the soluble, intracellular S-100 protein.
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PMID:Biochemically differentiated mouse glial lines carrying a nervous system specific cell surface antigen (NS-1). 16 83

Five cases of the type of mammary carcinoma that has been designated "signet-ring cell carcinoma" are presented. This tumor is characterized by the presence of numerous cells containing intracellular mucin, without large amounts of extracellular mucin as is seen in colloid (gelatinous, mucinous) carcinoma of the breast. Although such cells may be seen in many mammary carcinomas, they are never as frequent as in the variant described. Ultrastructurally, the most characteristic finding is the presence of numerous intracellular lumina containing material which appears to represent the mucin identified with the light microscope. This finding differs from that in colloid carcinoma, in which the scantier intracellular mucin occurs in the form of intracytoplasmic membrane-bound vesicles. The five tumors in the present series were all associated with either in situ lobular carcinoma or a "sinus catarrh"-like pattern of nodal metastases, or both. On the basis of these light and electron microscopic data, the signet-ring cell carcinoma is suggested as a variant of infiltrating lobular carcinoma, clinically and pathologically distinct from colloid carcinoma.
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PMID:Signet-ring cell carcinoma of the breast. The mucinous variant of infiltrating lobular carcinoma? 17 13


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