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)

A steroid, 6-chloro-17-hydroxypregna-1,4,6-triene-3,20-doine (CHP) that exhibits selective activity in several models of cellular immunity including an apparent inhibitory action on the elicitation of delayed hypersensitivity, was examined in a new, simple experimental model for assessing aspects of host-cell-mediated immunological competence. This model is based upon the capacity of the adult mouse to prevent the progressive growth of tumors induced by the Moloney sarcoma virus. Two steroids reported to have immunosuppressive activity in other assay systems, namely, cortisol and progesterone, were also studied. Control mice and those injected with CHP maintained their capacity to reject the tumor. In contrast, significant numbers of mice receiving a single large injection of cortisol or progesterone succumbed to progressive tumor growth under the experimental conditions used. The data indicate that CHP, while influencing selected parameters of cellular immunity, e.g., the elicitation of delayed hypersensitivity, does not decrease the capacity of the host to mount a defense against the progressive growth of the Moloney virus-induced sarcoma. The results indicate that CHP may be useful in modulating specific aspects of cellular immunity without altering others. In addition, the experimental model described provides a simple method of assessing the possible immunosuppressive effects of naturally occurring and synthetic agents on viral-induced tumor growth.
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PMID:Selective immunosuppressive activity of steroids in mice inoculated with the Moloney Sarcoma virus (38503). 4 58

A molecular hybridization technique has been used to quantitatively measure the nucleotide sequence relationships of selected mammalian RNA tumor viruses. Reciprocal cross-hybridization tests were done in which a given radioactively labeled, viral genomic RNA species was annealed with an excess of unlabeled, complementary DNA product synthesized in endogenously instructed reverse transcriptase reactions. Hybrid formation was measured with pancreatic RNase A. Three representative mammalian RNA tumor virus groups were examined: murine viruses, simian viruses, and feline viruses. The results of reciprocal cross-hybridization testing have revealed that the murine viruses consist of four distinctly related subgroups: (i) the Friend leukemia virus/Rauscher leukemia virus subgroup, (ii) the Gross leukemia virus subgroup, (iii) the Moloney sarcoma virus subgroup, and (iv) the Kirsten sarcoma virus subgroup. Simian sarcoma virus, the only simian virus examined, appeared to share limited interspecies sequence relationships with members of the other virus groups and in particular with Kirsten sarcoma virus. Of the two members of the feline virus group tested, Rickard feline sarcoma virus and RD-114, each was placed in a separate, unrelated subgroup. Rickard feline sarcoma virus exhibited limited sequence relatedness with members of the other virus groups, whereas RD-114 exhibited none.
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PMID:Quantitative nucleotide sequence relationships of mammalian RNA tumor viruses. 4 42

The biological properties of the HMV-1 virus, spontaneously released from a human X C57BL/6 mouse hybrid cell line, were similar to those of RadLV, the prototype B-tropic virus of C57BL/6 mice. Both viruses replicated on B-type mouse cells and in the wild mouse cell line SC-1. The plaque-forming abilities of the two viruses were relatively low, but gradually increased after passage in new host cells. Both viruses were neutralized by AKR antisera but not by FMR antisera. HMV-1 virus could rescue the defective sarcoma genome from S+H- mouse cells. The pseudotype sarcoma virus so produced was deficient in "helper virus" activity. Newborn mice inoculated with HMV-1 virus remained tumor-free over a 1-yr observation period.
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PMID:Biological properties of a type C virus isolated from a human X mouse hybrid cell line. 4 96

Type C virions were spontaneously released from cultures of a diploid human cell strain. The varions have properties of known type C RNA tumor viruses and share antigenic determinants with the major interspecies-specific antigen (p30) of simian sarcoma virus. Antiserum to reverse transcriptase of gibbon ape leukemia virus inhibits the reverse transcriptase of the putative human virions and that of simian sarcoma virus, but has no effect on the corresponding enzymes of avian or murine RNA tumor viruses.
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PMID:Isolation of type C virions from a normal human fibroblast strain. 4 27

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

Short- and long-term co-cultures of 49 cases of human osteosarcoma cells with bone marrow or peripheral blood cells of patients with different types of leukemia were studied. Morphological changes were observed in 7 of 13 long-term co-cultures resembling those induced by RNA tumor viruses. The changes were accompanied by appearance of cytoplasmic antigen as shown by fixed immunofluorescence test with sera from patients with osteosarcoma, leukemia, and of some apparently normal blood donors. Absorption with Forssman-like substances, whole human embryo cells or osteosarcoma cells demonstrated the reaction to be due to tumor antigen(s) in co-culture cells showing morphological changes. Electron microscopy showed a few type C virus particles in one co-culture. Cell-free filtrates of fluid from the transformed co-cultures induced morphological changes in 1 of 4 human embryo cultures. Uninoculated embryo cultures or those inoculated with filtrates from parental sarcoma or leukemia cultures showed no morphological changes. Human embryo cell cultures treated with fluid from parental leukemic bone marrow but not from parental sarcoma cultures showed appearance of cytoplasmic antigen by immunofluorescence test with sera of osteosarcoma and leukemia patients and of some apparently normal blood donors. Transformed human co-cultures showed the cytoplasmic antigen with 28 of 48 sera of osteosarcoma and leukemia patients tested, after absorption with Forssman-like material, human embryo, and mycoplasma suspensions. Fourteen of 49 sera of normal donors were also positive with the transformed co-cultures. Similar results were obtained in an earlier series of experiments with human embryonic cultures transformed by fluid from different osteosarcoma-leukemia co-cultures when examined by fixed immunofluorescence tests with sera of patients with osteosarcoma and leukemia. In 2 whole human embryo cell cultures showing morphological changes high molecular weight RNA was found, similar to that of RNA animal tumor viruses and in one of the cultures transient reverse transcriptase was detected.
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PMID:Virus retrieval studies in human neoplasia. 5 29

BALB/c mice were rendered immune to syngeneic SV40-induced sarcoma by subcutaneous injection of mKSA-TU5 tissue-culture adapted cells. Spleen cells from immune mice were examined for tumor-cell neutralization in the Winn assay as well as in in vitro lymphocyte stimulation assays. A microculture (200 mul) lymphocyte stimulation (LS) assay utilizing immune spleen cells was employed with mixed lymphocyte/tumor-cell cultures (MLTC) and the papain crude soluble (CS) extracts from mKSA-TU5 cells. Specificity in the LS assay was determined using spleen cells from mice immune to other syngeneic tumors and by soluble antigenic preparation of normal BALB/c spleen cells. The Winn assay studies demonstrated that spleen cells from mKSA-sensitized mice neutralized mKSA tumor cells and this was corroborated by their resistance to direct tumor challenge. Positive lymphocyte transformation responses in MLTC were observed when mKSA-TU5-sensitized spleen cells were mixed with mitocycin-C-treated intact tumor cells or when papain-solubilized antigens of mKSA cells were employed, but not with non-immune spleen cells or with a soluble antigen from normal cells. Papain-solubilized antigen preparations employed in in vitro assays also immunized against challenge with mKSA tumor cells. Specificity of these lymphocyte transformation reactions was demonstrated with non-sensitized lymphoid cells or lymphoid cells from mice sensitized with a syngeneic Kirsten virus-induced respond. Thus, mKSA tumor surface antigens were recognized on intact tumor cells or with microgram quantities of papain-solubilized extracts from these tumor cells. We believe the lymphocyte stimulation assay affords a method for demonstrating the presence of tumor-specific antigen and for monitoring further purification procedures.
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PMID:Studies of lymphocyte stimulation by intact tumor-cell and solubilized tumor antigen. 5 34

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

Indium-111 as the chloride and chelated to bleomycin has been reported useful as a tumor-scanning agent. This report of the kinetics of these compounds compared in Yale-Swiss mice bearing a transplantable, in situ brain sarcoma. Indium-111-chloride, pH 1.5, gave a maximum tumor uptake of 18.5% dose per gram tumor, a maximum tumor-to-brain ratio of 17.0, and a maximum tumor-to-blood ratio of 4.4. Its renal blood clearance was a slow 0.0022 ml/min. Indium-111-bleomycin showed a maximum tumor uptake of 3.0% dose per gram tumor, a maximum tumor-to-brain ratio of 13.5, a maximum tumor-to-blood ratio of 6.8, and renal blood clearance of 0.254 ml/min. The labeling of bleomycin with 111In results in a tracer with localizing properties in this tumor model which are quite different from those obtained with 111In as chloride or that labeled to bleomycin would appear to have significant potential as agents for imaging tumors.
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PMID:Kinetics of 111In-bleomycin and 111 In-chlorides in mice. 5 22


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