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

Secondary cell-mediated cytotoxicity generated in vivo against a syngeneic Gross virus-induced lymphoma [(C58NT)D] in WF rats was detected by the 4-hour 51Cr release assay. At 30 days or more following primary tumor cell inoculation, after the tumors had regressed, lymphoid cells had little or no detectable direct cytotoxic reactivity. At rechallenge with tumor cells, high levels of cytotoxicity were detected in the peritoneal exudate, peripheral blood, mesenteric lymph node, and spleen cells. The secondary cellular immune response after challenge developed earlier, reached higher levels, and lasted longer than the primary immune response. The secondary cytotoxic reactivity was shown to be immunologically specific by the use of various tumor cells both as target and inhibitor cells. Treatment of immune spleen cells with specific antiserum to rat T-cells and complement abolished their cytotoxic reactivity, whereas removal of complement receptor-bearing cells or phagocytic cells did not reduct the cytotoxicity. These data demonstrated that specific-memory T-cells persisted for long periods in the lymphoid organs of immune rats and could rapidly become cytotoxic from rechallenge with the tumor.
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PMID:Secondary cell-mediated cytotoxic response to challenge of rats with syngeneic Gross virus-induced lymphoma. 6 41

Partial biochemical characterization of several neural tissue specific antigens isolated from a murine glioblastoma cell line was accomplished by means of radioiodination of intact cells followed by immunoprecipitation of the cell lysate with a rabbit serum specific for neural tissue antigens. Polyacrylamide gel electrophoresis of the immunoprecipitate in sodium dodecyl sulfate resolved the labeled antigens into several major components: two proteins (or glycoproteins) having apparent m.w.'s of 84,000 and 120,000 and lipid associated components which may be heterogeneous. The protein and lipid associated components apparently possess independent antigenicity because after chloroformmethanol extraction the protein components can be immunoprecipitated from the aqueous phase and the lipid associated component can be immunoprecipitated from the organic phase. Despite their independent antigenicity it is not known whether the components may be noncovalently associated on the cell surface. Although some of these antigens can be isolated from brain or glioma cells (a related tumor), non can be demonstrated in lymphoid tissues or C1300 neuroblastoma cells using identical methods. Therefore, these studies confirm our previous findings concerning the specificity of the anti-NS-2 antiserum by using cytotoxicity tests.
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PMID:Partial characterization of nervous system-specific cell surface antigen(s) NS-2. 6 27

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.
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PMID:Uridine kinase activities in normal and neoplastic lymphoid cells. 6 93

Spleen, lymph node and thymus cells from normal C57BL/6 mice or mice given injections 6 to 20 days previously with syngeneic methylocholanthrene-induced fibrosarcoma (B6MCA) cells were tested for their ability to mediate growth stimulation and/or inhibition of B6MCA cells in vitro. At an effector cell to tumor cell ratio of 10:1,, nucleated spleen cells from mice bearing the tumor for 6 days enhanced tumor cell growth. Neither lymph node nor thymus cells from tumor-bearing mice were stimulatory. Tumor cell growth was inhibited by either spleen or lymph node cells only when a ratio of 1000:1 was exceeded. Thymocytes, however, were inhibitory at a ratio of 100:1,. Lymphoid cells from normal mice were not stimulatory at low ratios or inhibitory at any ratio tested. Both stimulatory and inhibitory activities disappeared by Day 20. Filtration of sensitized spleen cells through a glass wool column did not remove stimulatory or inhibitory activities. Subsequent passage through a nylon wool column resulted in a loss of stimulation, but not inhibition, of tumor cell growth. Stimulatory activity was completely abrogated by treatment with either anti-theta or rabbit anti-mouse gamma-globulin serum. A 1:1 mixture of spleen cells treated with either antisera did not restore stimulation. Spleen cells from T-cell- or B-cell-deficient mice bearing the tumor for 6 days were also not stimulatory. The results suggest that immunostimulation of tumor growth in vitro is mediated by a lymphoid cell that is distinct from the cytotoxic effector cell.
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PMID:In vitro stimulation and inhibition of tumor cell growth mediated by different lymphoid cell populations. 6 82

In studies of the mouse thymus, lymphocyte mitoses are seen to be most frequent in the thymus cortex. There is evidence from thymic grafts that a hypothetical factor, thymopoietin, may stimulate mitosis of thymic lymphocytes. It is a factor which is postulated to act in conjunction with the PAS-positive mesenchymal reticular cells and epithelial reticular cells of the cortex. The thymus medulla is necessary for the integrity of thymic grafts, and may also elaborate a secretion for maintaining the cellular functions of the gland. Thymectomy has been used as a gauge for judging normal thymic function and results, in the mouse, in lymphopenia, degeneration of spleen and lymph nodes, delayed rejection of skin allografts, reduced ability of spleen cells to mount the graft versus host reaction, and reduced primary immune response to certain antigens. Correction of these deficiencies offers a means of evaluating various thymic extracts and grafts. Lymphocytosis-stimulating hormone (LSH) is known to maintain the peripheral lymphoid organs and cause lymphocytosis in the thymectomized animal. Diffusion chamber studies of thymic grafts also show restored lymphoid tissue by a cell-free factor (CIF). These two factors may be the same and probably represent the basis of the highly purified lymphocyte-stimulating proteins, LSHr and LSHh, which restore the L/P ratio in thymectomized animals and may stimulate lymphopoiesis in spleen and lymph nodes. LSHr, unlike LSHh, increases the total lymphocyte count. LSHr has been found to increase the humoral antibody response in neonatal mice both by the PFC technique and by direct hemolysis of sheep erythrocytes. Homeostatic thymic hormone (HTH) is a thymic extract of small molecular weight and contains nucleic acid. In the thymectomized guinea pig it has been found to maintain normal levels of lymphocytes in the blood, spleen and lymph nodes, to restore antibody titers to typhoid H antigen and to restore the toxic allergic reaction. Thymic humoral factor (THF) is of smaller molecular weight (less than 1,000) and probably is not a protein. It also enhances lymphoid proliferation in neonatally thymectomized mice. There is evidence that THF participates in humoral antibody formation because it stimulates PFC formation from neonatally thymectomized mice after inoculation with sheep erythrocytes. Its effects on cell-mediated immunity are seen from findings that injection of THF restores the ability of thymectomized mice to reject skin allografts. THF enables spleen cells from thymectomized or neonatal animals to mount the graft versus host reaction, and causes maturation of bone marrow cells and spleen or lymph node cells so that they can participate in the graft versus host reaction. It has been reported to stimulate lymphocytes to kill isogeneic tumor cells in vitro. Thymosin is protein extracted from the thymus. It has been found to alleviate leukopenia slightly and provide some improvement in lymphoid histology in thymectomized mice...
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PMID:Some endocrine aspects of the thymus gland. 6 31

Experiments employing two new methods for the in vitro assessment of cell-mediated immunity against neoplastic target cells are indicated. Both methods offer the advantage of rapid and quantifiable determination of very early events in cell-cell confrontations. One technique measures the incorporation of precursors of proteins, RNA, and DNA synthesis by neoplastic cells incubated with effector cells during the first hours of contact. It was found that exposure of BALB/c plasmacytoma (PCT) cells to splenocytes from PCT-sensitized donors failed to bring about inactivation of the target cells or their release of 51Cr during several hours of interaction. However, inhibition of 3H-thymidine incorporation was almost instantaneous and pronounced. This observation suggests that cytostatic events may transpire in cell-cell interactions in the absence, or before the onset, of lethal changes. The second method assays the specific adherence of 51Cr-labeled lymphoid cells from Rous sarcoma (RS)-bearing chickens to RS target cells. This immunoadherence test revealed perferential, specific reactivity in autochthonous as compared with allogeneic interactions, which indicated recognition of individual-specific tumor-associated antigens against a background of strongly expressed group antigenicities.
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PMID:Recent studies on the assessment of cell-mediated cytotoxicity in vitro. 6 61

AFP is one of several oncofetal proteins synthesized in large amounts by the fetus. Although synthesis drops markedly shortly after birth, small amounts of AFP continue to be produced in the adult. The function of AFP is unknown, but recent studies suggest the possibility that it may have immunoregulatory properties and/or may influence cell proliferation and growth. The high affinity of AFP for estrogen could have important biological functions, although the significance of this binding has not yet been clearly defined. Elevated levels of AFP are seen in a variety of clinical situations, including pregnancy; hepatic disorders, especially chronic hepatitis; and various malignancies, particularly hepatomas, teratomas, and those of primitive gut origin. It is also produced in murine GVH reactions and in lymphomas, both in mice and humans. In human and murine lymphomas, and murine GVH reactions, the presence of AFP-positive cells and immune suppression are highly correlated, but the role of these in the pathogenesis of the diseases is as yet unclear. It appears, however, that AFP may be produced locally in lymphoid tissues involved in GVH and lymphomatous disease without elevations in serum AFP levels. It is speculated that the local production of AFP in these situations may result from blastogenesis of lymphoid cells directed against foreign tumor or viral antigens. AFP could promote the development of tumors either by suppressing immune surveillance and/or immunity to oncogenic viruses, although this is speculative. Finally, the AFP elevations in maternal serum and amniotic fluid are valuable diagnostically in the detection of fetal abnormalities, particularly neural-tube defects.
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PMID:Structure and function of alpha-fetoprotein. 6 21

The main findings of the present study are: (a) highly reactive cytotoxic lymphocytes (CTL) against syngeneic and allogeneic murine leukemia cells were generated in vitro in macro 'one-way' mixed leukocyte-tumor cultures (MLTC). Cultures set up in large tissue culture flasks contained up to 400 X 10(6) normal spleen cells (responder cells) and 20--40 X (10(6) mitomycin C-treated leukemia cells (stimulator cells). Successful sensitization in macrocultures was greatly dependent upon the responder cell density and the responder/stimulator cell ratio. Cytotoxic activity, as measured by the 51Cr-release assay, peaked on day 5--7. (b) Sensitized 'memory' lymphocytes produced in primary MLTC could be restimulated with the original tumor cells to give a more rapid and stronger secondary cytotoxic response. (c) lymphocytes sensitized to allogeneic leukemia cells reacted equally well with sensitizing leukemia cells and with the corresponding normal lymphoid target cells, whereas lymphocytes sensitized to syngeneic leukemia cells did not react with the homologous normal lymphocytes. (d) Cryopreserved normal splenocytes and leukemia cells were as efficient as fresh cells in generating allogeneic and syngeneic CTL. (e) Using a Winn-type tumor neutralization assay, it was shown that both allogeneic and syngeneic splenocytes sensitized in vitro to EL4 leukemia (of C57BL/6 mice) and to YAC leukemia (of A mice) were capable of preventing tumor growth in the syngeneic host, whereas cultured normal splenocytes frequently showed a tumor-enhancing effect. Long-term survivors, remaining after inoculation of leukemia cells and sensitized lymphocytes, also became resistant to a tumor challenge that was up to 10,000 greater than the minimum lethal dose.
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PMID:In vitro induction of cell-mediated immunity to murine leukemia cells. II. cytotoxic activity in vitro and tumor-neutralizing capacity in vivo of anti-leukemia cytotoxic lymphocytes generated in macrocultures. 6 86

Lymphocyte mediated immune reactions play a major role in the immunological defense against antigenic tumor cells. Serum factors (antigens, antigen-antibody complexes) can thwart these reactions, perhaps by interfering with a lymphocyte "activation" process. Blocking factors can be eluted from lymphoid cells harvested from tumor-bearing animals. One way of increasing cell-mediated reactivity to tumor antigens appears to be to sensitize (or "activate") lymphocytes against tumor antigens in vitro. Another way may be to inoculate animals with sera containing lymphocyte-dependent and unblocking antibodies. Preliminary evidence is presented that inoculation of such sera from rabbits immunized with mouse embryonie cells and extensively absorbed may delay the appearance of primary, methyleholanthrene-induced sarcomas in BALB/c mice; the mechanisms responsible for this delay remain unknown.
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PMID:Cell-mediated immunity to mouse tumors: some recent findings. 6 97

Cytogenetic observations were made on 6 cell lines (MOB-1, MOB-2, MOB-3, MSB-1, HPRS Line 1, HPRS Line2) originating from Marek's disease lymphomas and 2 clones (1104-B, 1104-X-5) of a cell line established from an avian lymphoid leukosis tumor. The modal chromosome number was within the diploid range in all the lines except HPRS Line 1 and HPRS Line 2, both of which had a mode at about 60. Karyotypes were grossly abnormal in 4 cell lines: trisomy for No. 1 in MOB-2; the heteromorphic No. 1 pair in MSB-1, and marker chromosomes derived from rearrangements involving No. 3 or No. 5 and unidentified elements in HPRS Lines 1 and 2. The MOB-1 line which had been characterized by cells with an apparently normal karyotype was completely taken over by cells with a heteromorphic No. 1 pair morphologically similar to the one found in MSB-1 by the 95th day of continuous growth in vitro. BUdR-acridine orange differential staining technique revealed, however, different banding patterns in these abnormal chromosomes.
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PMID:Chromosomal characteristics of six cultured lymphoblastoid cell lines originating from Marek's disease lymphomas. 6 31


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