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

We have investigated the pathogenesis of the polyclonal hypogammaglobulinemia associated with BALB/c plasmacytomas TEPC-183 and SPQC-11 to gain insight into the hypogammaglobulinemia observed in human myeloma. With pokeweed mitogen-driven IgM biosynthesis by mouse splenocytes as the indicator system for suppression, we found that a protein extract of asscites cells obtained from these tumor-bearing animals could suppress immunoglobulin production, whereas like extracts from a non-suppressing plasmacytoma, modified RPC-5, caused no suppression in vitro. Extracts of tumor ascites depleted of mononuclear phagocytes by iron carbonyl treatment showed little suppressor activity. The active extract was not cytotoxic and contained no mycoplasma or common murine viruses. Furthermore, the active suppressor factor appears to be a low m.w. protein that is not affected by treatment with ribonuclease. These results and others are consistent with the idea that the hypogammaglobulinemia of myeloma is due to the formation of immunoregulatory macrophage-like cells which synthesize a suppressor substance.
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PMID:Hypogammaglobulinemia in experimental myeloma: the role of suppressor factors from mononuclear phagocytes. 85 68

Spleen cell suspensions of methylcholanthrene-induced tumor-bearing mice were tested for their ability to inhibit tumor growth in vitro. The level of cytostasis was correlated with tumor growth and disappeared rapidly after surgical removal of the tumor. Pretreatment by anti-Thy 1-2 antiserum and complement, or by carbonyl iron and a magnet, showed that adherent, non-T-cells were the main effector cells of the cytostatic antitumor effect. Thymus cells suspensions from tubor-bearing mice were not effective in inhibiting tumor growth. This cytostatic effect was not tumor specific, inasmuch as the same spleen cell suspension inhibited growth of tumor cells of different origin.
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PMID:Cytostatic effect of spleen cells of tumor-bearing mice on syngenetic tumor cells. 87 Jan 85

The purpose of this study was to further clarify the pathophysiology of anemia in malignancy. To accomplish this end a total of 210 normal or splenectomized rats with or without the solid form of Walker 256 carcinosarcoma was studied. In vivo studies demonstrated that in stage I cancer (tumor weight less than 10% of body weight) a slightly shortened red cell survival resulted in a mild degree of anemia. With increasing tumor size, 51Cr red cells mass decreased further, in spite of extramedullary erythropoiesis and a slightly increased incorporation transferrin-bound iron into red cells. Splenectomized rats with stage II cancer developed a more profound degree of anemia associated with a significantly decreased incorporation of 59Fe into red cells. Marrow cell culture studies demonstrated that heme synthesis in response to erythropoietin in stage I cancer was not significantly different from normal, but in rats with stage II cancer (tumor weight greater than 10% of body weight) heme synthesis in response to erythropoietin was markedly decreased. In vitro studies demonstrated that plasma erythropoietin levels were appropriately increased in most rats with transplanted malignancy. These studies indicate that bone marrow heme synthesis in response to erythropoietin is impaired in rats with the anemia of advanced malignancy.
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PMID:Pathogenesis of anemia in rats with Walker 256 carcinosarcoma. 89 4

Peripheral blood lymphocytes from patients with all stages of untreated Hodgkin's disease and from normal healthy adults were shown to synthesize and release ferritin in vitro. Ferritin synthesis was confirmed by immunoelectrophoresis, double immunodiffusion and autoradiography. Hodgkin's disease lymphocytes synthesized ferritin 4.2 times faster and released it 2.4 times faster than did normal lymphocytes, whereas total protein synthesis was faster in normal lymphocytes. Patients with nodular sclerosis and perhaps those with absence of fever had the highest synthetic rates; however no relationship was observed between relative rates of lymphocyte ferritin synthesis and sex, age, anatomical stage and presence of splenic or hepatic involvement by tumor. Addition of iron to normal human lymphocytes produced little or no change in ferritin synthesis. These data indicate that part of the intracellular ferritin detected in peripheral blood lymphocytes from patients with Hodgkin's disease and from normal individuals resulted from de novo synthesis rather than from uptake and storage of serum ferritin, and suggests that elevated ferritin levels detected in the serum and tumor tissue of Hodgkin's disease patients originate from lymphocytes.
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PMID:Increased ferritin synthesis and release by Hodgkin's disease peripheral blood lymphocytes. 90 87

Localization of a radiopharmaceutical agent in a "tumor" is best conceptualized in terms of the altered regional physiology attendant to the presence of the "tumor". Such localization should be expected to occur in association with other disease states characterized by similar altered regional physiology. Neoplasms, areas of inflammation, and certain phases of infarct development are characterized by increased permeability of their capillary beds to macromolecules. This is largely due to neovascularization and the large intercapillary pores associated with new growth of capillary beds in these circumstances. Often, total perfusion to such lesions is increased in comparison to surrounding normal tissue. Thus, in all three clinical conditions, the entry of macro-molecules into the interstitial fluid space from the intravascular space is increased above that seen in normal tissue. Moreover, with neoplasms and inflammatory processes, there may be a delay in new lymphatic vessel growth adding to the residence time of the macromolecules in the interstitial fluid space. In all three conditions, the increased macrophage activity associated with tissue necrosis may result in ingestion of the labeled macromolecule by the macrophage. Pinocytosis may result in ingestion of the labeled macromolecule by other cells in the lesion, or there may be specific receptor sites on the cell membrane for the macromolecule, which may lead to fixation of the labeled macromolecule on the cell surface and possible intracellular translocation of the label itself. Radiolabeled macromolecules such as albumin, fibrinogen, or gamma globulins, and radionuclides that bind to macromolecules such as radiogallium, radioindium, and other radioelements, exhibit localizing behavior in tumors, inflammatory lesions, and during certain stages of infarcts. In the case of radiogallium and radioindium, the binding macromolecule is transferrin, and it is known that some cells have specific receptor sites for transferrin-bound iron on the cell membrane. It is possible that certain cells within these lesions have cell membrane receptor sites for radiogallium- and radioindium-labeled transferrin, and the cell erroneously accepts these radioelements from the transferrin in lieu of iron in attempting to engage in heme enzyme synthesis. Another mechanism that may be operative in the localization of agents in neoplasms, infarcts, and inflammatory lesions may be the altered cell permeability found in many cells of such lesions. It is known that many agents, such as supravital dyes, are excluded from entering normal cells by the selective permeability of normal cell membranes. When cell membrane permeability is altered, such as can be seen in traumatized, dying, or dead cells, the normally excluded agent may penetrate the abnormal cell membrane and bind, and consequently accumulate in intracellular constituents.
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PMID:Mechanisms for localization of radiopharmaceuticals in neoplasms. 98 76

A technique for induction of iron accumulation in hepatocytes of rats was used to identify early carcinogen-induced lesions by their histochemical absence of iron. Foci of iron-free altered hepatocytes produced by the feeding of N-2-fluorenylacetamide (FAA) for 3 weeks were composed of cells that were replicating when surrounding iron-containing hepatocytes were not, and that responded to a mitotic stimulus when surrounding hepatocytes were inhibited or showed a delayed response. Thus these lesions represented focal hyperplastic overgrowths. The iron-free hyperplastic foci developed into hyperplastic areas that progressed with longer feeding of FAA to form hyperplastic nodules. The lack of iron was a sensitive and reliable marker for hyperplastic lesions, which also permitted their identification in the fresh state. Both early hyperplastic lesions and nodules were often resistant to the necrogenic effects of dimethylnitrosamine, as well as to the antireplicative effect of FAA. The selection of such cells resistant to the toxic effects of carcinogens may be important in the pathogenesis of liver neoplasia.
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PMID:Nature of early appearing, carcinogen-induced liver lesions to iron accumulation. 100 98

The aim of the study was to determine which cell mediates adoptive immunotherapy and chemoimmunotherapy of a syngeneic transplantable Friend virus-induced leukemia (FBL-3). An adoptive immunotherapy model was developed in which adult C57BL/6 mice given a lethal dose (10(4)) of FBL-3 on day 0 were saved by treatment on day 1 with C57BL/6 spleen cells or peritoneal exudate cells (PEC) immune to FBL-3. Cells passed through a nylon wool column to remove B cells and macrophages or treated with carbonyl iron to remove phagocytic cells remained effective, whereas cells treated with anti-theta serum and complement were far less effective. For adoptive chemoimmunotherapy, mice inoculated with 10(7) FBL-3 were treated 5 days later with cyclophosphamide (CY) plus immune spleen cells. CY, with or without non-immune cells, prolonged survival but all mice died with leukemia, whereas mice given CY plus immune cells survived tumor-free. As an adjunct to CY, immune cells passed through nylon wool or treated with carbonyl iron remained quite effective whereas cells treated with anti-theta serum and complement were far less effective. Thus, immune thymus-derived lymphocytes were required for the adoptive immunotherapy of an early leukemia or chemoimmunotherapy of a disseminated leukemia.
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PMID:Syngeneic adoptive immunotherapy and chemoimmunotherapy of a Friend leukemia: requirement for T cells. 108 Jan 65

Studies were performed to characterize the effector cells responsible for natural cytotoxicity of mouse lymphoid cells against a variety of syngeneic and allogeneic tumor lines. Since spleen cells from normal nude mice were found to be highly cytotoxic, they were used for most of these experiments. Only a small proportion of the reactivity was affected by treatment with anti-theta serum plus complement. Macrophages dis not appear to be responsible for the reactivity, since treatment with carbonyl iron/magnet or carrageenan did not affect the levels of cytotoxicity. The effector cells were non-adherent, since passage over nylon columns resulted in a considerable increase in activity. The active cells did not have receptors for immunoglobulin or complement, since removal of cells with these receptors by columns or monolayers containing sheep erythrocyte-antibody (EA) complexes or EA-complement complexes did not remove activity. Antibody-dependent cell-mediated cytotoxicity appeared to be ruled out as the mechanism for natural cytotoxicity, since aggregated gamma globulin and a potent anti-immunoglobulin reagent did not inhibit reactivity, and since no role for humoral factors could be demonstrated. The natural effector cell was found to be quite labile at 37 degrees C, losing much of its activity after 4 h. Since no surface markers could be detected on the effector cells, and the mechanism for cytotoxicity appeared distince from others previously described, it is proposed that the natural cytotoxicity against mouse tumor cells is mediated by a unique subpopulation of lymphoid cells, which are tentatively designated N-cells.
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PMID:Natural cytotoxic reactivity of mouse lymphoid cells against syngeneic and allogeneic tumors. II. Characterization of effector cells. 108 Apr 80

During studies that showed the presence of fetal antigens on the surface of human malignant melanoma tumor cells, polyvalent antisera specific for human fetal tissues of varying ages were developed. These reagents demonstrated varying patterns of expression of fetal antigens at different ages in various tissues of the human fetus. The possibility that nonneoplastic adult cells showing either maturation arrest or excessive proliferation also might express fetal antigens led to studies of human bone marrow. Although normal bone marrow cells expressed low levels of fetal antigens, large amounts were seen on bone marrow cells of patients with anemias due to iron, B12, or folic acid deficiencies, as well as on those with leukemia. Moreover, normal adult tissues adapted to long-term culture also expressed fetal antigens. After 3 weeks in organ culture adult human skin showed morphological changes similar to those seen in fetal periderm and strongly expressed fetal antigens. In addition, lymphoblasts in long-term cultured human lymphoid cell lines established from normal donors also carried surface fetal antigens. These latter antigens were shared with neoplastic B-cells (chronic lymphocytic leukemia) but not with T-cells. Their expression varied with the cell cycle. The reexpression of fetal antigens on malignant cells is thought to signal a basic derangement in the control of differentiation which is considered to be peculiar to neoplasia. However, these studies indicate that normal adult cells also may reexpress fetal antigens under circumstances unrelated to neoplasia but associated with either maturation arrest or rapid and excessive proliferation.
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PMID:Fetal antigens in nonneoplastic conditions. 108 33

Suppressor cells were demonstrated in the spleens of C3H/He mice carrying 3-methylcholantrene-induced fibrosarcomas. These cells inhibited the in vitro reactivity of normal lymphocytes to T- and B-cell mitogens. They disappeared within a few days after the tumor was surgically removed. Pretreatment of spleen cells (ScC) from tumor-bearing (TB) mice with either iron and a nagnet, antiserum against Thy 1.2 antigen plus complement, or antiserum against immunoglobulin plus complement demonstrated that the suppressor cells were adherent, non-T-cells bearing immunoglobulin at their surfaces. The suppressive effect could still be demonstrated by addition of SpC from TB mice 24 or 48 hours after phytohemagglutinin stimulation of normal SpC, SpC from TB C3H/He mice inhibited mitogen-induced stimulation of both C3H/He and DBA/2 lymphocytes. In T-cell-deprived TB C3H/He mice, suppressor cells were also observed and had the same characteristics as those in non-T-cell-deprived mice. In nude mice, however, although suppressor cells were active, they were not adherent and did not bear immunoglobulin at their surfaces. The existence of these suppressor cells may be one reason why the immune system of TB animals is unable to reject the tumor.
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PMID:Evidence for splenic suppressor cells in C3H/He, T-cell-deprived C3H/He, and nude mice bearing a 3-methylcholanthrene-induced fibrosarcoma. 108 53


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