Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1261473 (sarcoma)
 25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TA3Ha/MSWBS hybrid cells have been derived from the fusion of the TA3Ha ascites carcinoma (H-2a) and the methylcholanthrene-induced MSWBS ascites sarcoma (H-2s). MSWBS expresses a strong tumor-specific transplantation antigen (TSTA), capable of inducing a rejection reaction in the syngeneic A.SW host. The genetic determinants of the H-2 complex are known to be localized on chromosome No. 17. TA3Ha contributes two normal, telocentric chromosomes No. 17 to the hybrid. In contrast, both chromosomes No. 17 of MSWBS are localized on readily identifiable translocations (17/1 and 17/M1 ; see Wiener et al., 1974). We have previously shown that the chromosomes No. 17 of one parental strain, or the other (but not both) can be removed from the hybrid by selective passage in the opposite parental strain. The present paper examined the possibility, often suggested in the literature, that the MC-sarcoma-associated TSTA could be a modified form of H-2. MSWBS, unselected TA3Ha/MSWBS and YACIR/MSWBS hybrids were compared with TA3Ha/MSWBS-derived isoantigen loss variants, with regard to their immunogenicity in the TSTA test, i.e. their ability to induce rejection of MSWBS target cells in ASW mice. Whereas the unselected hybrids were as immunogenic as the parental MSWBS line itself, two strain A compatible and two strain A.SW compatible variants which had lost chromosome No. 17 of the opposite strain showed a residual, but clearly weakened immunogenicity. Since there was no systematic difference between the reciprocal types, it is concluded that the genetic determinant of TSTA is not localized on the chromosome No. 17 but that a proper balance of this chromosome is required for the full expression of immunogenicity in the TSTA system.
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PMID:Are methylcholanthrene-induced sarcoma-associated, rejection-inducing (TSTA) antigens, modified forms of H-2 or linked determinants? 5 Feb 91

A tumor specific transplantation antigen (TSTA) has been detected in a methylcholanthrene (MCA) induced guinea pig tumor. It was possible to induce resistance to rechallenge with the tumor by immunization with irradiated cells in CFA. In contrast, the same technique failed to detect TSTA in two viral (Kirsten strain mouse sarcoma virus, Ki-MSV) induced guinea pig tumors; these results are similar to observations made with mouse Ki-MSV-induced tumors. Transplantation studies with these tumors in both inbred and random-bred guinea pigs showed a complexity of growth and rejection patterns. The B alloantigen, a major serologically defined antigen of the guinea pig histocompatibility complex, seemed to play a central role in acting as a guniea pig transplantation antigen. In all cases studied, the absence of B antigens in the recipient led to tumor rejection and anti-B antibody protection.
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PMID:Antigenicity of carcinogen and viral induced sarcomas in inbred and random bred guinea pigs. 5 Mar 48

Tumor-specific transplantation antigen (TSTA) was solubilized from cell membranes of sarcoma Meth-A with non-ionic detergent Nonidet P40. Soluble TSTA was partially characterized by chromatographic separation and electrophoresis. The antigen responsible for tumor rejection activity had a molecular weight of approximately 70,000 daltons in the presence of detergent and an electrophoretic mobility of alpha-globulin. TSTA was well separated from mouse histocompatibility antigen H-2 by a sequence of procedures, including gel filtration, lectin affinity chromatography, column electrophoresis, and rechromatography on agarose, showed only three major bands on polyacrylamide gel electrophoresis. TSTA was specific for sarcoma Meth-A.
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PMID:Biological and biochemical properties of Nonidet P40-solubilized and partially purified tumor-specific antigens of the transplantation type from plasma membranes of a methylcholanthrene-induced sarcoma. 6 94

The presence of alien histocompatibility antigens on the cell surface of the 3-methylcholanthrene-induced BALB/c (H-2d) fibrosarcoma C-1, was investigated by serological and transplantation studied. Absorption experiments with monospecific alloantisera showed that C-1 cells expressed their original private (H-2.4 and 31) and public (H-2.3, 8, 28, and 35) specificities. C-1 cells were also able to absorb monospecific antisera directed to the private specificity H-2.23 of the H-2k haplotype, as well as antisera to the public specificities H-2.1, 5, 11 11 and 25 (H-2k and in part H-2q, H-2a and H-2b haplotypes), which are absent from H-2d normal cells. Conversely, other alien specificities (H-2.2, 17, 30, 32, and 33) were not detected on C-1 cells. The C-1 cells were also unable to absorb the activity of an anti-Ia serum (1-28) directed to 1a.1, 2 and 19 (lak) specificities. Transplantation studies showed that resistance against the challenge of C-1 cells could be induced in syngeneic BALB/c mice by preimmunization with normal tissues from C3Hf and AKR (H-2k), A (H-2a) and C57BL/6J (H-2b) strains (expressing all or some of the extra H-2 antigens of the tumor) whereas no protection was obtained with DBA/2 (H-2d) or with W/Fu rat tissues. The anti-tumor activity could be passively transferred by BALB/c lymphoid cells immune to normal C3Hf, AKR, A, and NIH (H-2q) tissues, but no protection was achieved with lymphoid cells immune to DBA/2 or to W/Fu normal rat tissues. These data indicate that foreign H-2 antigens are expressed on C-1 tumor and that they might function as tumor-associated transplantation antigen which was shown to be present and individually distinct on this sarcoma by appropriate in vivo tests.
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PMID:Expression of alien H-2 specificities of a chemically induced BALB/c fibrosarcoma. 7 Apr 14

A factor inhibiting tumour growth in syngeneic hosts was found in the sera of inbred Lewis rats carrying Rous sarcoma virus-induced tumour (RSL). The findings presented here suggest that the serum factor is a tumour-associated transplantation antigen (TATA) shed from the neoplasm into the circulation. All the tumour bearers' sera tested with RSL cells were negative in indirect membrane immunofluorescence;however, on passive transfer into syngeneic rats, they protected the animals against the growth of an RSL tumour inoculum. A similar protective effect was also observed after injection of TATA prepared from RSL cell membranes by solubilization with potassium cholate. When incorporated into Freund's adjuvant, tumour-bearers' sera immunized the animals against a subsequent RSL sarcoma graft. Sera collected from immunosuppressed rats bearing large sarcomas which presumably contain neither tumour-specific antibody nor antigen-antibody complexes, transferred inhibition of tumour growth to syngeneic hosts. Intact immunological reactivity of recipients was a necessary prerequisite for the protective effect of sera, since the passive transfer of an inhibitory serum to immunosuppressed rats did not inhibit tumour growth. We assume that the TATA present in tumour-bearers' serum is released from the growing neoplasm as a result of either cell death or membrane metabolic turnover.
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PMID:Tumour-associated transplantation antigen in sera of rats with large RSV-induced sarcomas. 17 Feb 16

Quantitative studies have been performed on the immunogenicity of a membrane-bound antigen of a simian virus 40 (SV40) -induced sarcoma in syngeneic BALB/c mice and of subcellular fractions derived from this tumor. The objectives of the investigation were: a) to develop a quantitative in vivo assay of the tumor-specific transplantation antigen (TSTA) and b) to compare the distribution of histocompatibility antigens, H-2, with that of the SV40 TSTA during several fractionation steps. The immunogenicity of the TSTA-containing fractions was assessed from dose-response curves relating tumor size and the amount of protein used for immunization. After digestion of the tumor cell membranes with a limited amount of papain, H-2 as well as TSTA were present in a soluble form. A single immunization with only 2 microng of the solubilized TSTA reduced the tumor size by 70% compared to that in nonimmunized control animals. The results of several fractionation steps suggest that H-2 and the TSTA are not tightly associated in the solubilized immunogenic material.
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PMID:Quantitative in vivo studies of soluble simian virus 40 tumor-specific transplantation antigens of the mouse. 19 45

Specific tumor rejection was obtained with the use of simian virus 40 (SV40)-transformed cells from several species including man, rat, ape, sheep, and hamster. Growth of the syngeneic sarcoma mKSA in BALB/c mice was strikingly inhibited following a single immunization with as few as 10(3) intact, viable cells. Non-SV40-transformed cells did not induce tumor rejection activity nor did SV40-transformed lines induce immunity against the 3-methylcholanthrene-induced sarcoma Meth A, syngeneic with BALB/c mice. A close relationship existed between the tumor rejection antigen, the tumor-specific transplantation antigen (TSTA) located on the plasma membrane, and the intranuclear tumor antigen (T-ag). Both were associated with the DNA sequence of the early region of the SV40 genome, and TSTA activity was found in the nucleus. However, we did not observe a close parallelism between T-ag activity and TSTA. Neverthesless, the results strongly suggested that TSTA, like T-ag, was encoded by the virus.
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PMID:Induction of simian virus 40 (SV40) transplantation immunity in mice by SV40-transformed cells of various species. 19 68

Cell lines were established from 2 primary hepatocellular carcinomas (HC's) and 3 sarcomas produced in Syrian golden hamsters inoculated as newborns with chicken embryo lethal orphan (CELO) virus. Cell lines from 2 sarcomas (COT, CMT) and 1 HC (CEHEP) produced CELO virus-specific T-antigen. The antigen was not detected in cells of the third sarcoma line (RCT) until they had undergone more than 34 passages in vitro. Although 5-10% of cells in the second HC line (CILT/2) contained T-antigen during early passages, it was not demonstrable after the fifth subculture. Nevertheless, cells of both HC lines possessed CELO virus tumor-specific transplantation antigen. All 5 cell lines also contained hamster type R particles, and both HC lines had type C and intracytoplasmic type A particles. The percentage of carcinoma cells producing type R particles increased during cultivation in vitro, whereas the number of cells with type A particles decreased. Treatment with dibutyryl cyclic AMP and theophylline enhanced the number of cells producing type C particles in 1 HC line and type R particles in 2 sarcoma lines.
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PMID:Virus-specific markers and virus-like particles in cell lines of tumors produced by CELO virus in Syrian golden hamsters. 20

Two phenotypically distinct T-lymphocyte populations infiltrating the peritoneal site of active tumor rejection were found to have specific reactivity against methylcolanthrene (MCA)-induced sarcoma(s) in two separate biological assays. One, expressing a Lyt 1+2- phenotype, mediates specific delayed type hypersensitivity (DTH) reaction to the immunizing MCA tumor transplantation antigen, and the other, expressing a Lyt 1+2+ phenotype, transfers in vivo protection against the MCA tumor in Winn assay. This latter antitumor immunity was specific for individually distinct transplantation antigens of each MCA sarcoma line. In contrast, standard transplantation tests by direct (whole animal) challenge demonstrated considerable tumor cross-reactivity. These findings and the relative contributions of the two T-cell populations are discussed in terms of effector mechanism.
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PMID:The roles of two peritoneal T-lymphocyte populations in the in vivo rejection of methylcolanthrene-induced sarcoma. 257 28

Fusion products of spleen cells of W/FuDp rats immunized with a methylcholanthrene-induced BALB/c sarcoma, CA-2, and mouse myeloma cells were screened in an attempt to identify a monoclonal antibody defining the individually distinct tumor-specific transplantation antigen of CA-2. A hybridoma, MP/69/04, was isolated which produces an IgG2a monoclonal antibody that recognized a tumor-restricted antigen of CA-2. In direct binding assay, MP/69/04 reacted only with 2 of 15 methylcholanthrene induced BALB/c sarcomas tested. Thymus, spleen, lymph nodes, bone marrow, brain, adult lung fibroblasts, newborn muscle fibroblasts and 3T3 cells were negative. Absorption tests revealed, however, expression of the MP/69/04 determinant on 8 of the 12 murine leukemia virus (MuLV) producer BALB/c sarcoma tested. The antigen was not detected on any of the three non-producer sarcomas tested nor on a wide range of normal tissues and cell lines. An N-dualtropic MuLV was isolated from CA-2, and cell lines susceptible to infection by this virus were shown to express the MP/69/04 epitope. By Western blotting, the MP/69/04 epitope was identified as being expressed on the MuLV structural protein with a molecular weight of 12,000, present in CA-2 cells and in the purified CA-2 MuLV. These results indicate the MP/69/04 antigen is not a unique tumor-specific transplantation antigen but is a gag product of a recombinant retrovirus which is expressed on the cell surface of many MuLV + methylcholanthrene-induced BALB/c fibrosarcomas.
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PMID:Cell surface antigens of chemically induced fibrosarcomas: detection by a monoclonal antibody of a tumor-restricted Mr 12,000 protein gag antigen encoded by a dual-tropic murine leukemia virus. 299 69


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