Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific cell-mediated immunity to SV40 tumor-specific transplantation antigen (TSTA) in BALB/c mice undergoing progressive tumorigenesis by syngeneic SV40-transformed cells (VLM) was investigated in vivo using a tumor-cell neutralization test. Specific cellular reactivity to SV40 TSTA was not detected in BALB/c mice bearing large tumors (10-15 mm mean diameter) but was demonstrable after tumor excision. Specific cytotoxic reactivity against syngeneic SV40-transformed cells in vivo could be restored to lymphoid cells from VLM tumor-bearing mice either by culturing the lymphoid cells in vitro or by treating them with papain or trypsin. Enzyme-treated lymphoid cells from MCA tumor-bearing BALB/c mice had no cytotoxic reactivity against VLM cells. These studies suggest that tumor-bearing hosts possess lymphocytes which are sensitized to the TSTA of the tumor but that the reactivity of these lymphocytes is blocked.
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PMID:Restoration of specific immunity against SV40 tumor-specific transplantation antigen to lymphoid cells from tumor-bearing mice. 5 Oct 12

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

In vitro transformation of BHK 21/13 cells by chemical carcinogens is reported. The hamster cells were treated with MCA, BP, 4-NQO and 5-azaCR at various concentration and duration of treatment. The morphological, karyological and growth characteristics of cell lines were investigated. Search for RNA tumor viruses in transformed cells using 3H-uridine labeling, detection of DNA polymerases, electron microscopy investigations failed to detect presence of C-type virus particles.
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PMID:Transformation of BHK 21/13 cells by chemical carcinogens and mutagens. 5 82

Serologic cross-reactivity has been demonstrated among three MCA-induced sarcomas in C57BL/6N female mice (MCA-2, MCA-3, and MCA-12) with a microcytotoxicity assay. Serum from mice bearing MCA-3 tumor was cytotoxic to both MCA-2 and MCA-3 tumor cells at a titer of 1:8. Sequential absorptions of this serum with syngeneic embryo cells completely eliminate cytotoxicity against MCA-2 cells without affecting the cytotoxic titer against MCA-3 cells. Serum hyperimmune to the MCA-3 tumor reacted with MCA-3, MCA-2, and MCA-12 tumors. Absorption of this serum with embryo cells eliminated cytotoxicity against MCA-2 and MCA-12 cells, but was incapable of lowering the titer against MCA-3 cells below 1:40. Similarly, serum hyperimmune to MCA-2 tumor was lytic to MCA-2, MCA-3, and MCA-12 before absorption, but was lytic only to MCA-2 cells after absorption with sygeneic embryo cells. Thus, the in vitro cross-reactivity between MCA-induced sarcomas is due to a common fetal antigen(s), which is distinct from the individual tumor-specific antigens of each tumor. Since these tumors do not exhibit cross-reactivity in in vivo challenge experiments, it appears that this fetal antigen is not responsible for in vivo immune protection.
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PMID:Cross-reacting antigens in chemically induced sarcomas are fetal determinants. 6 42

The humoral immune response to two transplanted chemically induced murine sarcomas (MCA-2 and MCA-3) was studied in C57BL/6N mice. These tumors were immunogenic as evidenced by tumor amputation and rechallenge experiments, and no cross-reactivity between them was observed in in vivo challenge experiments. Utilizing a complement-dependent microcytotoxicity assay, we detected antibody to both MCA-2 and MCA-3 in the sera of animals bearing MCA-3 as well as after tumor removal. The sera of animals hyperimmunized to MCA-3 (MCA-3HI) was also cytotoxic in high titer to both MCA-2 and MCA-3 (50% cytotoxicity titers of 1:80 and 1:320, respectively). Sequential absorptions of sera from animals bearing MCA-3 and MCA-3HI sera with fresh MCA-2 cells completely removed activity against MCA-2 but retained reactivity to MCA-3. Sequential absorptions with fresh MCA-3 cells produced stepwise reductions of activity against both tumors, whereas absorption with normal cells produced no loss of activity against either tumor. Thus both specific and cross-reactive antigens were expressed on the surfaces of MCA-3 cells. Only the specific tumor antigen appeared to be involved in in vivo protection against tumor challenge.
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PMID:Serologic identification of multiple tumor-associated antigens on murine sarcomas. 6 11

This communication describes an automated micro-adherence inhibition assay. Tumor-specific immunity was demonstrated with B16 melanoma and MCA-38 colon adenocarcinoma, both of which are syngeneic to the same strain of mouse (C57B16/J). Abrogation of the leukocyte adherence inhibition (LAI) response of sensitized leukocytes has been demonstrated in the MCA-38 tumor system by the addition of serum from mice bearing MCA-38 progressively growing tumors, a property not present in normal serum. The sensitivity of the system has also been demonstrated by showing that LAI will change prior to a tumor becoming palpable. This microassay has the advantage of being simple, rapid and reproducible, and involves the use of minimal quantities of antigenic preparations and leukocytes, and in addition is amenable to rigorous statistical analysis.
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PMID:Leukocyte adherence inhibition: an automated microassay demonstrating specific antigen recognition and blocking activity in two murine tumor systems. 7 30

Methylcholanthrene-induced sarcomas of BALB/c mice express unique tumor specific transplantation antigens (TSTA), and weaker, common TSTA. Antigens of endogenous murine leukemia virus (MuLV) expressed by some of these tumors cannot completely account for these common TSTA. However, MuLV antigens on the immunizing tumor appear to increase the immunogenicity of the common TSTA.
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PMID:Unique and common tumor-specific transplantation antigens of chemically induced mouse sarcomas. 7 55

The relationship between tumor resistance and the antitumor delayed hypersensitivity reaction (TDHR) after resection of the tumor was studied by using the syngeneic 3-methylcholanthrene-induced murine tumor, MCA-DDD. MCA-DDD was inoculated subcutaneously into the tail of DDD mice and 4 weeks later the tumor-bearing tail was resected. The tumor resistances of the mice were then determined from the diameters of the tumor that developed 14 days after subcutaneous challenge of the mice with tumor cells in the flank. It was found that the mice showed a specific resistance to the tumor until 30 days after tumor resection. In parallel with tests on tumor resistance, TDHR of the mice after tumor resection was examined by the footpad test. The cell-free fraction of sonicated MCA-DDD tumor cells was used as the preparation of tumor antigens. TDHR of the mice appeared soon after tumor resection, reached a maximum on day 7, and then decreased slowly until day 29. Mice that acquired tumor resistance showed rapid increase of TDHR after challenge with fresh tumor cells. TDHR was high on day 4 after the challenge and its level was well correlated with tumor resistance of the mice.
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PMID:Antitumor immunity after surgical removal of 3-methylcholanthrene-induced murine tumors: correlation between resistance and delayed hypersensitivity reaction. 7 67

A rabbit antiserum raised by repeated immunization with BALB/c fetuses obtained at 10-14 days of gestation was used to search for oncofetal antigens (OFA) in murine sarcomas which had previously been characterized for the expression of endogenous murine leukemia virus (MuLV). Iodinated protein A from staphylococcus aureus (IPA) was used to quantitate binding of the antiserum to cultured tumor or fetal cells or to saline extracts of tumors and fetuses. Use of the "antigen" extracts facilitated the assay: the extracts bound to plastic and served as targets for the binding assay, eliminating the need to establish tumors in culture. After absorbtion in vitro and in vivo with adult tissues the rabbit antiserum bound to day 10-14 fetal cells and extract but not to endogenous MuLV (BALB virus 1). The antiserum bound equally well to MuLV-negative and MuLV-positive sublines of MCA-induced sarcomas 1420 and 1414 but not to Moloney sarcoma cells and MCA-induced sarcoma 1386. Thus, the absorbed antiserum detects a class of common cross-reacting antigens which are serologically distinct from MuLV-associated antigens.
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PMID:Expression of oncofetal antigens on murine sarcomas characterized for expression of endogenous MuLV. 8 Nov 87

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. This programming could be abolished by pretreatment of the MCA-38 sensitized B cells with anti-immunoglobulin and complement (indirect cytotoxicity method). In contrast, enriched populations of MCA-38 sensitized T cells could not program normal nylon wool adherent cells to undergo antigen-specific adherence inhibition; and anti-Thy 1.2 serum and complement had no effect on specific antigen-induced adherence inhibition. Thus, in this murine tumor model, leukocyte adherence inhibition appears to be due to the programming of monocytes by sensitized B cells.
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PMID:Micro-leukocyte adherence inhibition. I. Cellular basis of the mechanism of reactivity. 8 56


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