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Results for “Mast-Cell Sarcoma”

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At least 73 records · Page 4Linked to original sources
PubMed1976

Effects of Tumor-like assay conditions, lonizing radiation, and hyperthermia on immune lysis of tumor cells by cytotoxic T-lymphocytes.

Cytotoxic T-lymphocytes (CTL's) harvested from mixed splenic lymphocyte cultures (DBA/2 + C57BL) were tested for their ability to lyse allogeneic P815 mastocytoma cells under various tumor-like assay conditions, with or without previous exposure to ionizing radiation or hyperthermia (43 degrees). There was little or no decrease of immune cytolysis when CTL's were assayed by 51Cr release under tumor-like conditions (plateau-phase target cells, low pH, or anoxia) or after irradiation, but cytolytic activity was greatly reduced when CTL's were exposed to heat; 45 min of hyperthermic treatment decreased activity by greater than or equal to 99% while reducing the apparent cell viability (as indicated by trypan blue exclusion) by only 30%. When the P815 target cells rather than the CTL's were exposed to heat their susceptibility to immune lysis was not affected even after treatment times that were lethal to the tumor cells. Despite the dissimilar heat sensitivities of CTL and P815 cells, the dose-response curves for inhibition of protein synthesis by heat, as indicated by [3H]leucine incorporation, were similar for both cell types: neither the depression of protein synthesis in heated CTL's nor the decreased cytolytic ability of these cells was reversed within 3 hr. When irradiated or heated P815 cells were incubated with CTL's, the resulting survival curves were always additive, indicating that neither irradiation nor heat treatment affected the susceptibility of the tumor cells to immune attack. The extreme heat sensitivity of cytotoxic T-lymphocytes raises important questions about the possible effects of hyperthermic treatment on the immune competence of cancer patients.

Animals↗
PubMed1977

Characterization of suppressor cells in mice bearing syngeneic mastocytoma.

Suppressor cells from syngeneic P815 mastocytoma-bearing DBA/2 mice that inhibit in vitro generation of specific anti-tumor cytotoxicity were characterized. Suppressive activity was almost completely eliminated by treating suppressive spleen cells with anti-theta serum and complement. Treatment with anti-mouse lg serum and complement or with carbonyl iron did not affect their suppressive activity. When suppressive thymocytes from P815 tumor-bearing DBA/2 mice were tested for their capacity to inhibit the generation of cytotoxicity against L1210 cells, a leukemia line in DBa/2 mice, they did not affect the activity, indicating that the supressor cells in the thymocytes of P815 tumor-bearing mice are specific to the tumor. When Ficoll-Hypaque density cell separation was carried out with cytotoxic spleen cells and suppressive spleen cells from 815 tumor-bearing mice, the dense fraction was enriched for kiler cells whereas the suppressive activitty was mainly recovered in the light fraction. Therefore, killer cells and suppressor cells in P815 tumor-bearing mice are thought to be distinct populations.

Animals↗
PubMed1977

Uridine kinase activities in normal and neoplastic lymphoid cells.

Both adult (I) and embryonic (II) forms of uridine kinase have been identified in the transplantable EL-4 leukemia of C57BL/6 mice and in the P815Y mastocytoma of DBA/2 mice. Only Species I is found in primary tumor cells of lymphoid orgin (virus-induced feline lymphosarcoma, human acute and chronic lymphocytic leukemia) and in normal calf thymocytes and porcine peripheral blood lymphocytes; Species I was induced 4-fold upon stimulation of the normal blood lymphocytes with phytohemagglutinin. The level of uridine kinase activity in the feline lymphosarcoma of thymus-dependent lymphocyte orgin and childhood lymphocytic leukemia of possible thymus-dependent lymphocyte or null-cell origin was similar to the induced level in phytohemagglutinin-stimulated normal lymphocytes, i.e., thymus-dependent lymphocytes. In contrast lymphocytes of a patient with chronic lymphocytic leukemia of thymus-independent lymphocyte origin had a level of uridine kinase activity comparable to that of the unstimulated normal lymphocytes or thymocytes. The uridine kinase activity in the EL-4 tumor cells was repressed by acute treatment of the mice with 5-azacytidine.

Animals↗
PubMed1977

Increased primary cell-mediated immunity in culture subsequent to adriamycin or daunorubicin treatment of spleen donor mice.

Spleen cell populations from mice treated with Adriamycin or daunorubicin were found to develop a greater complement-independent cellular cytotoxic immune response during culture with allogeneic tumor cells than spleen cells from untreated or cyclophosphamide-treated animals. A temporal and drug dose dependence of this effect was demonstrated. The changes in spleen cell population occurring in the donor mice consequent to drug treatment were evident in the nylon woll-adherent fraction of the spleen cells. The results are consistent with the possibility that the concentration of specific progenitor or accessory cells in the spleen is increased consequent to drug treatment.

Animals↗
PubMed1977

In vitro induction of polyclonal killer T cells with 2-mercaptoethanol and the essential role of macrophages in this process.

Killer T cells against allogeneic and syngeneic tumor cells were generated in vitro by the addition of 2-mercaptoethanol (2-ME) to the murine spleen cell culture in the absence of any antigenic stimulation. The maximum activity of T cell-mediated cytotoxicity (CMC) induced with 2-ME was observed on day 4 of culture and the induction of CMC was completely inhibited by the addition of inhibitor of DNA synthesis, hydroxyurea, or cytosin arabinoside. CMC induced with 2-ME was specifically inhibited by the addition of unlabeled target cells to the 51Cr-release assay system. These results indicated that killer T cells were generated in the presence of 2-ME as a result of nonspecific polyclonal activation of precursors into cytotoxic effector cells and that they recognized target cells with antigen-specific recognition receptors. Spleen cells deprived of adherent cells showed impaired induction of CMC with 2-ME. The addition of peritoneal exudate macrophages to splenic T cells restored this response. The result indicated that macrophages were essential for the induction of CMC with 2-ME. The possibility that the function of macrophages was mediated by soluble factor(s) released from macrophages was demonstrated by the separate culture of splenic T cells and macrophages in double-chambered, Marbrook-type vessels and by the addition of supernatants from macrophage cultures to splenic T cells. 2-ME and soluble factor(s) released from macrophages seemed to be required for the activation of precursors into killer cells.

Animals↗
PubMed1977

Specificity of rat xenogeneic cell-mediated cytolysis for the products of the K and D loci of the mouse H-2 complex.

Lewis rat lymph node (LN) cells, when cultured with irradiated mouse spleen cells, develop cytotoxic effectors that were shown to be specific for the sensitizing mouse strain. Alloantisera directed to the products of the K and D loci of the target inhibited cytolysis whereas an antiserum to the I region gene products did not inhibit cytolysis even though LPS-induced spleen blasts were used as targets. Thus, it appears that even when effector cells from another species are generated to mouse spleen cells, the gene products of the K and D loci continue to play a predominant role.

Animals↗
PubMed1977

Noncytotoxic IgE-mediated release of histamine and serotonin from murine mastocytoma cells.

Cultured murine mastocytoma (AB-CBF1-MCT-1) cells were stimulated to release endogenous or incorporated histamine or serotonin by an IgE-mediated mechanisms without loss of viability. Stimulation was achieved by incubation of the cells with rat IgE-anti-IgE, rat IgE-anti-light chain, fluoresceinated rat IgE-anti-fluorescein, IgE-enriched mouse anti-ovalbumin-ovalbumin, or covalently linked dimers of rat IgE, at doses similar to those optimal for normal peritoneal mast cells. Active cell metabolism and Ca++ were required to obtain release. Despite the latter, no dose of the calcium ionophore, A23187, could be found which caused release without concomitant cytotoxicity. Phosphatidylserine did not enhance release.

Animals↗
PubMed1976

Formation and properties of retinylphosphate galactose.

Crude cell membrane fractions from a number of tissues can form acidic glycolipids. The formation of acidic galactose lipid and mannose lipid was greatly reduced in vitamin A deficiency, primarily in tissues known to be mucus-producing. Mouse mastocytoma tissue was active in forming acidic galactose lipids with UDP-galactose as substrate. One of the products was identified as retinylphosphate galactose. The synthetase reaction producing this compound exhibited an apparent pH optimum at 6.3. The presence of detergent and retinol stimulated the synthetase reaction, which exhibited an absolute requirement for Mn2+ or Mg2+. The synthetase reaction was readily reversible. Incubation of particulate enzyme with retinylphosphate galactose and UDP yielded UDP-galactose and a compound tentatively identified as retinylphosphate. The galactose lipid was isolated by column chromatography on DEAE-cellulose and silica gel. The retinylphosphate galactose was homogeneous when examined by thin layer chromatography. Mild acid hydrolysis of labeled retinylphosphate galactose yields [14C]galactose, whereas alkaline hydrolysis and hydrogenolysis produced [14C]galactose 1-phosphate. Retinylphosphate galactose bound to vitamin A-depleted, retinol-binding protein.

Animals↗
PubMed1979

The isolation of leukokinin-H and leukokininogen from human ascites fluid; their properties and role.

The leukokinin-leukokininogen system is a pathological kinin generating system which is catalyzed by acid proteases present in neoplastic cells, white cells and even normal tissues. The components of the human system including leukokinin-H and leukokininogen have now been isolated and characterized. Very specific protease inhibitors of the system such as pepstatin have been found and are now known to prevent "in vivo" the formation of pathological fluids such as neoplastic ascites. Strong evidence has been previously published and additional evidence has been presented here which indicates that pepstatin's actions are related to the inhibition of cathepsin-D in vivo and the inhibition of leukokinin formation. Both leukokinins and leukokininogens have been clearly defined and shown to differ from bradykinin and human bradykininogens. This clearly demonstrates the presence in pathological systems of a kinin-generating system which is separate and distinct from the bradykinin generating system. The importance of the leukokinin-leukokininogen system in disease would seem to be very great. The finding that pepstatin can inhibit the system in vivo opens the way for studies of pepstatin and related protease inhibitors as therapeutic agents in neoplastic disease and protease mediated inflammatory disorders.

Amino Acids↗
PubMed1978

Antibody-dependent lymphocytotoxicity: an analysis of effector cell-target cell interactions.

Antibody-dependent lymphocytotoxicity (ADL) was studied with human peripheral blood lymphocytes as effector cells and P815 mouse mastocytoma cells, sensitized with rabbit IgG antibodies, as target cells. Enzyme-substrate-like kinetics were used to describe ADL inhibition induced by two types of inhibitors. Human IgG, both native and heat-aggregated, proved to be a competitive inhibitor of ADL at the target cell level. Human peripheral blood monocytes inhibited ADL in an apparently irreversible fashion, without appreciable evidence for competition. The data obtained provide strong support for the validity of an enzyme-substrate-like mechanism of ADL. Moreover, our results indicate that in order to measure the lytic capacity properly, cell populations, well defined as to their composition, should be used. In the second part of the study, it was investigated whether the two types of cells capable of lysing sensitized target cells, i.e., null cells and T cells, differed with respect to their affinity for the target cells. Application of enzyme-like kinetics revealed considerable differences in maximal killing rate between the two subsets of K cells. However, the parameter related to the affinity toward the target cells was found to be of the same magnitude for the two types of effector cells.

Antibody-Dependent Cell Cytotoxicity↗
PubMedDate not supplied

[Solitary mastocytoma].

A case is reported of a four--month--old male infant with mastocytoma localized on antero--internal side of left leg. It was a single lesion seen since birth, of tumoral aspect, about 3.5 x 2 x 0.8 cms., light brown color. The pathologic study confirmed the diagnosis. The course was uneventful and disappeared spontaneouly in one year.

Humans↗
PubMed1978

Concurrent depression of tumor macrophage infiltration and systemic inflammation by progressive cancer growth.

Macrophage accumulation during the growth of a peritoneal ascites and three s.c. tumors in two animal species was analyzed and correlated with the capacity of the same tumor-bearing host to respond to inflammatory stimuli at sites distant to the tumor. Two of the three s.c. tumors induced systemic defects in macrophage accumulation; the tumor that did not (P-815 mastocytoma) did depress inflammation when transplanted to the peritoneal site. Macrophage accumulation within different tumors varied but, for a given tumor, it occurred in proportion to tumor growth when systemic inflammatory reactions were normal. However, the tumor to macrophage ratio increased dramatically and concurrently with onset of the generalized defect in macrophage inflammatory responsiveness. Accordingly, we concluded that macrophage mobility tested at remote sites is indicative of inflammatory events within the tumor. However, the antiinflammatory effect directed against macrophages is probably not a significant factor in tumor emergence since the required number of tumor cells was large and variable between not only tumors but also sites of transplantation.

Animals↗