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

M0use alloantisera produced against different specificities of the K, I, and D regions of the H-2 gene complex reacted as immunogenetically anticipated with normal lymphoid target cells of different haplotypes in cytotoxicity and indirect immunofluorescence tests. These same alloantisera, however, produced anomalous positive reactions when tested on cultured MCA-induced sarcoma cells from B10 background H-2 congenic mice. Absorption experiments demonstrated that the anomalous activity in these sera was directed against a tumor membrane antigen(s) which was distinct from H-2 region specificities against which the reference alloantisera were produced, and which was shared in common by multiple cultured sarcoma lines. Similar anti-tumor antibody activity could be demonstrated in the serum of older (greater than 12 weeks) but not younger normal unimmunized mice of the strains used as recipients for alloantiserum production. It is suggested that the observed anamalous anti-tumor activity in these alloantisera may be due to the presence of antibodies reactive with envelope antigens of murine leukemia virus which are expressed on sarcoma cells maintained in culture.
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PMID:Anomalous reactions of mouse alloantisera with cultured tumor cells. I. Demonstration of widespread occurrence using reference typing sera. 5 86

Lymphoid leukosis (LL), a neoplasm of the bursa-dependent lymphoid cells of the chicken, was induced by Rous-associated virus-1 in susceptible chickens. Cyclophosphamide (CY), which destroyed the lymphoid elements of the bursa of Fabricius and abrogated humoral immunity, prevented LL. Concomitantly, osteopetorosis and other neoplasms increased. Transfer of bursa cells from chickens into CY-treated hatchmates restored immune competence. Birds whose B-cell functions were reconstituted died of LL and were less likely to die of osteopetrosis and other neoplasms than were CY-treated chicks. These results suggested that the bursa cell transferred into the CY-treated chicks were the target cells for lymphoid leukosis transformation.
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PMID:Lymphoid leukosis in chickens chemically bursectomized and subsequently inoculated with bursa cells. 5 19

The line-1 guinea pig hepatoma was used to study in vitro tumor cytotoxicity. Cytotoxicity was determined by measurement of the loss of tritiated thymidine-labeled target cells from culture vessels. With this technique, we demonstrated that significant tumor cytotoxicity was caused by lymphoid cells from tumor-immune guinea pigs, by cells from guinea pigs immunized against an antigen urelated to the tumor target, and by cell-free supernatants rich in lymphocyte mediators. Addition of normal peritoneal exudate cells enhanced the cytotoxic potential of a small number of highly purified immune lymphocytes, which suggested that recruitment of normal cells is an additional mechanism of tumor cell death in this system.
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PMID:Multiple in vitro mechanisms of tumor cytotoxicity demonstrated in the line-1 guinea pig hepatoma model. 5 20

Lymphoid cells of mice were sensitized in vivo either by H-2 strain-specific tumor allografts or by activation in lethally irradiated F1 hybrids and tested for cytotoxicity on 51Cr-labeled target cells. The release of 51Cr varied linearly with the logarithm to the proportion of effector lymphocytes to target cells and with the time of interaction. The release of 51Cr was immunologically specific and restricted to H-2 incompatibility. Spleen cells immune to public specificities of the target genotype were not cytotoxic. However, lymphoid cells immune to only one private specificity of a third-party target genotype were highly cytotoxic. The cytotoxicity of activated thymus cells on target cells sharing one private specificity with the genotype used for sensitization was significantly enhanced when the effector thymocytes were activated also against H-2 specificities not shared by the target strain. The results suggest that gene products that facilitate sensitization of effector cells may be determined both by the H-2K and the H-2D end of the H-2 complex. It remains to be shown whether the products of these loci, operating during sensitization in vivo, are body-wide correlated to the lymphocyte-defined specificities detectable during the mixed leukocyte culture interaction.
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PMID:Incompatibility at irrelevant H-2 specificities augments in vivo stimulation of alloaggressive cells. 5 89

Spleen cells or thymocytes immune to one H-2 genotype are cytotoxic to allogeneic target cells of a third-party genotype, provided the target shares private specificities determined by either the H-2K or the H-2D locus of the H-2 complex with the H-2 genotype used for sensitization in vivo. The present results on elimination of cytotoxicity to specificities determined by one of the H-2 loci after adsorption of the immune lymphoid cells onto fibroblasts bearing this specificity suggest a state of diversity among effector lymphocytes reactive to the antigens determined by either the H-2K or the H-2D locus of the H-2 complex. Thymus cells activated in vivo were less specifically adsorbable than spleen cells of tumor-allografted mice.
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PMID:H-2 private specificity of in vivo-sensitized lymphocytes studied by adsorption on fibroblast monolayers. 5 90

The interactions which occur between antigenic tumor cells and normal or immune lymphoid cells in a 3-day in vitro culture, have been studied with a murine sarcoma virus (MSV)-induced tumor. The 3H-thymidine incorporation of lymphoma cells growing in suspension, and the radioactive-chromium release of freshly sampled lymphoma cells regularly added to the culture, have been compared to determine the part played by immune lymphoid cells in cytolysis and cytostasis of the tumor-cell population. The cytolytic activity increases in the culture from day 0 to day 3. It is due, predominantly, to T-cells, and remains specific to antigens shared by MSV tumors and related lymphomas. This activity would be difficult to detect unless freshly sampled ascitic cells were used as targets, since the lymphoma cells spontaneously lose a part of their sensitivity to immune cytolysis during in vitro culture. The method used in the present experiments is a secondary chromium release test (SCRT), which measures the invitro secondary stimulation of cytotoxic T-lymphocytes (CTL) by tumor cells. In the absence of stimulatory cells, the CTL activity would have rapidly fallen in vitro. The cytostatic activity also increases during the 3 days in vitro, in parallel to the cytolytic activity: it is due to non-T-cells and remains mainly non-specific. The significance of these data for the interpretation of invitro demonstrated cell-mediated anti-tumor immune reactions is briefly discussed, as well as their relevance in the in vivo role of immune CTL.
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PMID:Secondary specific immune response in vitro to MSV tumor cells. 5 10

Cell-mediated immune reactions appear to play an important role in resistance against growth of leukemia cells in mice. Possible mechanisms for in vivo protection in two tumor systems are discussed. These tumor models, which are a Friend leukemia virus-induced transplantable tumor, FBL-3, and primary murine sarcoma virus (MSV) -induced tumors, are strongly antigenic; under some conditions, tumors regress completely. In mice with regressing FBL-3 tumors, cell-mediated cytotoxicity was measured by release of [125I]iododeoxyuridine. The response was biphasic, with an initial peak at 10 days and a 2nd peak after 30 days. A boost in reactivity could be elicited by later challenge with tumor cells. All of the reactivity was dependent on T-cells, being eliminated by treatment with anti-theta plus complement. The specificity of the reactions was not completely defined, but it was consistent with Friend type-specific antigen plus broader, common antigens. In mice with regressing MSV tumors, strong cell-mediated cytotoxicity, measured mainly by release of 51Cr, was seen against RBL-5, a Rauscher virus-induced leukemia. A single peak of response occurred at about 14 days after virus inoculation. Upon later challenge with RBL-5 cells, a vigorous and rapid secondary response was elicited, mainly in the region of tumor challenge. This cytotoxic reactivity and in vivo resistance to leukemia.lso was completely dependent on T-cells. In addition, macrophage-mediated inhibition of leukemia cell growth in vitro was seen in this system at the time of peak tumor development. The 51Cr release cytotoxicity was specific and directed primarily against an antigen, MEV-SA1, associated with mouse endogenous C-type viruses. The macrophage-induced growth inhibition appeared to be nonspecific. In both the FBL-3 and MSV tumor systems, protection against tumor growth could be adoptively transferred by immune lymphoid cells. In addition to induction of cell-mediated immunity by tumor cell or virus inoculation, cell-mediated cytotoxic reactivity was found to occur naturally in most young mice. This natural killer activity was quite distinct from the experimentally elicited reactions, being mediated by N-cells, a subpopulation of lymphoid cells with no clearly identifiable cell surface markers. The natural cytotoxicity was also directed against antigenic specificities different from those recognized by the MSV-immune cells. The central issue in all of these studies has been to determine the relationships between the in vitro-detected cell-mediated reactivity and in vivo resistance to leukemia.
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PMID:Cell-mediated immunity to leukemia virus- and tumor-associated antigens in mice. 5 23

With the aid of an assay measuring complement-dependent cytotoxocity mediated by syngeneic antibodies, we performed a serological analysis of surface antigens of a polyoma-virus-induced murine tumor (SEYF-a). In vivo propagated SEYF-a ascites tumor cells expressed a specific membrane antigen in addition to various other cross-reacting antigens. Among these we could identify at least four separate specificities. Two of these were present on MuLV-induced lymphoma cells, the first on Moloney-virus-induced YAC cells and the second on Gross-virus-induced GHA cells. The third cross-reacting antigen was detected on EL-4 cells. At least one additional specificity was present on two methylcholantthrene-induced murine sarcomas. Normal syngeneic lymphoid cells were insensitive to cytotoxicity mediated by the anti-tumor antisera. Quantitative and perhaps also qualitative differences between that antigenic expression of in vivo propagated on cultured SEYF-a cells were indicated. These studies show that hyperimmune sera produced in syngeneic mice against transplanted tumors may contain a considerable number of antibody specificities, only some of which are specific for the tumor. Furthermore, the results also suggest that polyoma-virus-induced tumors may possess individually distinct antigenic specificities, over and above the known cross-reacting TSTA or TSSA type antigen.
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PMID:Serologically detectable specific and cross-reactive antigens on the membrane of a polyoma virus-induced murine tumor. 6 Feb 89

Spleen lymphoid cells from A/J mice recognize specific antigenic differences on the surface membranes of syngeneic C1300 neuroblastoma cells and incorporate 3H-thymidine into DNA in unidirectional mixed cell cultures in the absence of isologous serum. The response requires an optimal ratio of responder to stimulator cells, and is detectable after 24 h. It is specifically blocked by the presence of a papain-solubilized crude membrane extract from the same neuroblastoma cells, the extent of inhibition being dependent on the concentration of the extract and the time when it is added to the cultures. Spleen cells from mice bearing the neuroblastoma respond earlier and incorporate more 3H-thymidine than cells from unsensitized mice. The enhanced response of the primed spleen cells to the stimulator cells is similar to a secondary immune response and can be induced by soluble crude tumor extracts in the absence of stimulator cells.
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PMID:In vitro stimulation of mouse lymphoid cells by C1300 neuroblastoma cells or tumor membrane extracts. 6 46

With the in vivo tumor neutralization test (Winn test), growth of a transplanted (KMT-17) from Wistar-King-Aptekman rats was inhibited by allogeneic tumor (AH-66 from Donryu rats)-sensitized syngeneic lymphoid cells admixed with mitomycin C (MMC)-treated AH-66 cells. The observed tumor inhibition may be immunologically nonspecific, since no cross-antigens were detected by membrane immunofluorescence on the surfaces of KMT-17 and AH-66 cells. Close contact among KMT-17, AH-66-sensitized lymphoid cells and MMC-treated AH-66 cells was required for the inhibition of KMT-17 growth. AH-66 cells pretreated with formalin or ultrasonication lost tumor inhibitory activity when they were admixed with AH-66-sensitized lymphoid cells, and only MMC-treatment effectively preserved the tumor inhibitory activity of AH-66 cells. The sensitized spleen cells, draining lymph node, or peripheral blood cells inhibited tumor growth when they were admixed with MMC-treated AH-66 cells, whereas nucleated cells from bone marrow, thymus, or distal lymph node did not. Growths of KMT-17 were inhibited by admixed sensitized spleen cells and MMC-treated AH-66 even when pre-irradiated rats were used as recipients.
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PMID:Nonspecific inhibition of tumor growth in vivo by admixed allogeneic tumor-sensitized lymphoid cells and identical inactivated allogeneic tumor cells. 6 98


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