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

Sera from C3H/HeHa mice immunized with syngeneic methylcholanthrene-induced sarcoma react with allogeneic thymus, lymphoma and leukemia cells. The presence on leukemia and lymphoma cells of H-2 specificities expressed on normal cells of other H-2 haplotypes from the one in which the tumor originates is described. It was observed that the reaction of antisera to H-2 specificities with lymphoma cells was blocked by anti-MCA sarcoma sera. The cross-reactivity between MC sarcomas, thymus, leukemia and lymphoma cells is considered to be due to antibodies against these "alien" allospecificities.
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PMID:Alien H-2 allospecificities in murine chemically-induced tumors. 9 37

Listeria monocytogenes-mediated tumor inhibition was studied in strain 13 guinea pigs by using a methylcholanthrene-induced fibrosarcoma (MCA-1). Mixtures of Listeria and tumor cells in ratios of 1:100, 1:200, or 1:400 (Listeria:MCA-1 cells) led to significant suppression of tumor growth. Intralesional injection of tumors on day 6 posttransplantation led to the regression of a highly significant number of tumors. Animals receiving injections of Listeria, either in a mixture with tumor cells or intralesionally, displayed enhanced skin test reactivity to a tumor extract. Tumor regressors were resistant for at least 2 to 3 months after the initial transplant to rechallenge with MCA-1 cells. Thus, with this particular tumor-host system, Listeria was successfully employed as an antitumor agent with no visibly detrimental side effects to the host.
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PMID:Antitumor activity of Listeria monocytogenes on a guinea pig fibrosarcoma. 10 6

A radio (51Cr) micro-tube leukocyte adherence inhibition assay is described. In this study, murine mononuclear cells were labeled with 51Cr, plated into tissue culture plates with different tumor extracts and counts/min (cpm) of the non-adherent cells were used as a parameter of adherence inhibition. This assay was used to measure anti-tumor immunity, in vitro, in 3 murine tumor systems: MCA-38 colon adenocarcinoma, L1210 lymphoma and P815 mastocytoma. Tumor immunity was detected using 3 doses (0.01-0.001 mg/ml) of tumor extract in the MCA-38 tumor model, and using 2 doses (0.1-0.05 mg/ml) of tumor extract in both the L1210 and P815 tumor models. It was observed that specific tumor-associated adherence inhibition could be measured in the MCA-38 tumor model between days 7 and 22 of tumor growth and in the L1210 and P815 tumor models between days 7 and 17 of tumor growth. The radio-LAI assay described is an easy, specific and reproducible way to measure tumor-associated adherence inhibition, in vitro.
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PMID:A radio (51Cr) micro-tube leukocyte adherence inhibition assay: specific tumor-associated immunity in 3 murine tumor systems. 11 17

The s.c. infection of DBF-1 mice with HSV-2 has a tumor enhancing effect on simultaneously i.m. implanted MCA-induced syngeneic spindle cell sarcoma. Thus with the dosage used here, the first palpable tumors appeared on day 6 in the virus treated group as compared to day 9 p.i. in the sham treated batch. Further, more tumors were formed: 75% among the infected and 40% among the sham injected. The tumor yield could be modulated: no difference between the 2 groups was found when the tumor cell dose was increased sufficiently to advance the first appearance of tumors to less than 6 days. The same result was obtained when the neoplastic cells were implanted 3 days ahead of injection of the virus. When the dose of the cells was decreased, no tumors were found in the sham treated batch, whereas there were some in the infected group. Previous in vitro mixing of the neoplastic cells with virus completely prevented tumor formation, probably due to their lysis by the virus. In fact, in tissue cultures, MCA cells become lytically infected with HSV-2. It is speculated that a similar situation occurs in acutely ill mice which die before the 13th day p.i., i.e., the tumor cells are destroyed by the virus. In fact, those animals, as a rule are free of neoplasmas. Thus it appears that an acute HSV-2 infection prevents MCA sarcoma whereas a latent infection promotes its growth. The possible reasons for this tumor enhancement caused by HSV-2 infection are discussed.
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PMID:The tumor enhancing property of herpes simplex virus type-2 (HSV-2). 19 79

The in situ localization of cytotoxic T-cells was examined in a methylcholanthrene-induced fibrosarcoma. The MCA 2 tumor was initiated in this laboratory and utilized before extensive in vivo passage. Tumor cell suspensions were separated by unit velocity sedimentation. The T cell-enriched tumor-derived fractions and spleen cells from MCA 2-bearing mice were cytotoxic for in vivo isolated MCA 2 and in vitro cultured MCA 2 tumor cells, but not for SAD2 tumor cells. The cytotoxic activity of effector cells isolated from MCA 2 tumors was abrogated by treatment with anti-theta serum plus complement. The significance of cytotoxic T cells with in a progressing tumor is discussed.
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PMID:In situ cytotoxic T cells in a methylcholanthrene-induced tumor. 30 17

Cells from the spleens and thymuses of BALB/c mice whose Moloney sarcoma virus (MSV)-induced, primary sarcomas have regressed 2-3 months earlier ("MSV regressors") or are in the process of regressing can, when adoptively transferred to syngeneic mice given MSV at the age of 20 days, prevent the natural regression of the MSV sarcomas in the recipient mice. The cells responsible for this tumor-enhancing effect express the Thy 1 marker. They are not demonstrable in the thymuses of normal untreated mice or in mice that have either been immunized against or are bearing methylcholanthrene-induced sarcomas. The tumor-enhancing cells are not destroyed after administration of 400 rads (1 rad = 1.00 x 10(-2) J/kg) of whole body radiation. However, the effect of the irradiated cells is seen only in the presence of a nonirradiated T-cell population, represented in the thymuses of normal control mice, with which we postulate that they interact. Studies on a transplantable, chemically induced, murine leukemia virus antigen-negative sarcoma, MCA-1460, further support the concept that relatively radioresistant thymus cells from immune mice can enhance tumor outgrowth by interacting with radiosensitive T cells that are present in nonimmune mice.
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PMID:Tumor-enhancing suppressor activator T cells in spleens and thymuses of tumor immune mice. 31 60

The leukocyte adherence inhibition (LAI) microassay detects tumor-associated antigen(s). Extracts of colon carcinoma (MCA-38 and B16 melanoma tumors, both syngeneic to the C57BL/6J mice) are recognized only by peritoneal cells from mice bearing the corresponding tumor. To ascertain whether this in vitro antigenic recognition correlates with the ability of the host to recognize and reject a tumor in vivo, serial LAI microassays were performed synchronously with experiments designed to test the ability of mice bearing tumors to reject live secondary tumor challenges. Concomitant tumor immunity was present in the MCA-38 tumor-bearing mice on 3 occasions from 5 to 15 days from primary inoculation. In the B16 system, concomitant immunity was present on one occasion 10 days after primary inoculation. These results in turn were paralleled with the specific in vitro recognition of tumor antigens as detected by the LAI microassays. Loss of immunity in the "eclipse" phase of tumor development, as detected by concomitant tumor immunity, was paralleled by nonreactivity of the indicator cells in the LAI microassay.
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PMID:Correlations between the leukocyte adherence inhibition microassay and in vivo tests of transplantation resistance. 36 84

To study the cellular basis for specific antigen-induced leukocyte adherence inhibition, enriched populations of B-cells, T-cells, and monocytes were prepared by a two-stage adherence separation procedure from spleen cells of normal C57BL/6J mice and mice bearing progressively growing MCA-38 tumors. The reactor cell undergoing specific antigen-induced adherence inhibition was identified as a monocyte (esterase positive, did not respond to mitogens, and did not bear Thy 1.2 antigen or surface immunoglobulin). Furthermore, an enriched population of MCA-38-sensitized B-cells could program normal monocytes to undergo specific antigen-induced adherence inhibition. In contrast, enriched populations of MCA-38-sensitized T-cells could not program normal nylon wool-adherent cells to undergo antigen-specific adherence inhibition. Programming of normal monocytes by MCA-38-sensitized B-cells occurs through a soluble mediator and not by direct cell contact. The soluble mediator appears to be immunoglobulin in nature and induced both adherence inhibition and the inhibition of adherence. Thus, in this murine tumor model, leukocyte adherence inhibition appears to be due to programming of monocytes by a secretory product of specifically sensitized B-cells.
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PMID:Cellular and humoral factors involved in the mechanism of the micro-leukocyte adherence inhibition reaction. 36 85

Antitumor activity induced by the oil-attached cell-wall skeleton of Nocardia rubra (N-CWS) was compared with that of the oil-attached cell-wall skeleton of Mycobacterium bovis BCG (BCG-CWS) in syngeneic BALB/c tumor-host systems. In normal BALB/c mice (+/+), N-CWS exhibited stronger suppressive effect on syngeneic Br-1 and MCA tumors than did BCG-CWS. In athymic nude mice (nu/nu), BCG-CWS was as effective as N-CWS for the suppression of growth of such tumors. Suppressive effect of N-CWS treatment appears to be stronger to some extent in +/+ mice than in nu/nu mice. Immune spleen cells obtained from +/+ mice after footpad inoculation of MCA tumor cells mixed with N-CWS were effective in suppressing the MCA tumor growth, although those obtained from mice after inoculation of MCA tumor cells mixed with BCG-CWS did not exhibit a suppressive effect. This antitumor activity of immune spleen cells may be attributed to tumor-specific killer T cells. The differences of antitumor activities induced by these agents were discussed with reference to T-cell dependency and independency.
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PMID:Comparative study on antitumor effect of cell-wall skeleton of Mycobacterium bovis BCG and Nocardia rubra, with reference to T-cell dependency and independency. 38 Oct 87

The morphologic characteristics of a scar may render it an "immunologically privileged site" providing fertile ground for tumor occurrence and growth. We sought to extend this concept and to determine the effect of different stages of wound healing on tumor occurrence. Syngeneic strain-2 guinea pigs and a methylcholanthrene-induced liposarcoma (MCA-2) were used. Incisional flank wounds were created at appropriate intervals such that at the time of tumor inoculation each group of animals had a sequentially aged wound which was a) acute, b) three weeks old, c) nine weeks old, d) 11 weeks old, e) created one week after tumor injection, or f) no wound. Wounds which were three, nine, or 11 weeks old consistently caused a significant increase in tumor growth rate following inoculation of a single cell tumor suspension (<.001). The delayed wounds, or those created following after tumor injection, and the acute wounds did not promote increased tumor growth. This study demonstrates that the ability of a wound to amplify or retard tumor growth may vary with its age. As a postulate we suggest that the relative paucity of lymphatic regeneration within scar tissue may render it an "immunologically privileged site" such that early recognition and destruction of tumor cells within the scar may be delayed long enough for the tumor to grow to a "critical size." Subsequent to this regardless of the host's immunocompetence the tumor can no longer be destroyed by an immune mechanism. The general lack of progressive growth of tumor cells placed in acute wounds suggests that they were not protected from immunocompetent cells and were destroyed by the ongoing inflammatory response to injury. Therefore, different biologic characteristics of a surgical scar are important in potentiating or retarding tumor growth. Variations in such factors may account for the local recurrence of cancer in operative wounds.
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PMID:Biologic determinants of tumor growth in healing wounds. 42 50


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