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

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

As background for a serological definition of the unique antigens of chemically induced sarcomas, we have typed a series of fibroblast and sarcoma cell lines of BALB/c and C57BL/6 origin by cytoxicity and absorption tests for murine leukemia virus (MuLV)-related cell surface antigens and known alloantigens. 7 of the 17 cultured lines expressed the range of cell surface antigens associated with MuLV (GIX, GCSA, gp70, p30), and this was invariably associated with MuLV production. In nonproducer lines of C57BL/6 (but not BALB/c) origin, a MuLV-gp70-like molecule was found on the surface of fibroblasts and sarcoma cells. The alloantigenic phenotype of these MuLV+ and MuLV- cell lines was H-2D+, H-2K+, Thy-1.2+ or -, PC.1+ or -, Lyt-1.2-, Lyt-2.2-, Ia.7-, and TL.2-. A unique antigen was defined on the BALB/c ascites sarcoma Meth A with antisera prepared in BALB/c or (BALB/c X C57BL/6)F1 mice. Tissue culture lines derived from this tumor were MuLV-, which facilitated serological study of the antigen. Absorption analysis indicated that the antigen was restricted to Meth A; it could not be detected in normal or fetal BALB/c tissue MuLV+ or MuLV- fibroblast lines, 12 syngeneic or allogeneic sarcomas, or normal lymphoid cells from 13 different inbred mouse strains.
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PMID:Cell surface antigens of chemically induced sarcomas of the mouse. I. Murine leukemia virus-related antigens and alloantigens on cultured fibroblasts and sarcoma cells: description of a unique antigen on BALB/c Meth A sarcoma. 19 92

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

We reported previously the partial purification of detergent-solubilized specific tumor rejection antigen of a chemically induced sarcoma, Meth-A. During the course of the study, rabbit antiserum against a partially purified specific tumor rejection antigen preparation was raised and rendered specific by in vivo absorption. In this report we show that an antigenic molecule defined by in vivo-absorbed rabbit antiserum, which we tentatively refer to as tumor-specific surface antigen, was solublized by detergent Nonidet P40, and extensive attempts at purification were carried out by a sequence of procedures including gel filtration, isotachophoresis, and polyacrylamide gel electrophoresis. The most highly purified tumor-specific surface antigen retained some specific tumor rejection antigen activity, suggesting an association of the two activities. Both antigens were shown to have a molecular weight of about 60,000 and an electrophoretic mobility of alpha-globulin.
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PMID:Immunochemical evidence of a tumor-specific surface antigen obtained by detergent solubilization of the membranes of a chemically induced sarcoma, meth-A. 34 27

Alkyl-lysophospholipids inhibit the growth of Meth A sarcoma cells in vitro. In contrast, murine bone marrow macrophages are not sensitive to the destructive effect of these substances. Since alkyl-lysophospholipids are antimetabolites in the synthesis of 3-sn-phosphatidylcholine, tumor cell destruction can be correlated with the disturbance of this metabolism. A decreased synthesis of 3-sn-phosphatidylcholine is accompanied by an increased degradation of cellular 3-sn-phosphatidylcholine in the presence of alkyl-lysophospholipids. As a consequence, endogeneously formed lysophospholipid accumulates, although the lysophospholipase is found to be stimulated. This accumulation of endogeneous lysophospholipids might be due to the fact that a high percentage of these compounds contain an alkyl bond which cannot be split by a lysophospholipase. On the other hand, the reacylation of the formed lysophospholipids is partially blocked as the lysophosphatidylcholine acyltransferase is inhibited by the added alkyllysophospholipids. An accumulation of potentially cytotoxic lysophospholipids in tumor cells might be an additional factor in the tumor cell destruction by alkyl-lysophospholipids.
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PMID:Disturbance of phospholipid metabolism during the selective destruction of tumor cells induced by alkyl-lysophospholipids. 49 95

Unspecific immunostimulation with or without specific tumor immunotherapy may well contribute to the control of minimal residual cancer. Corynebacterium parvum (C.p.) has been shown to raise the level of immunocompetence in tumor bearing animals. Experiments are reported, which aim at an evaluation of optimal conditions for an immunostimulation with C.p. prior to the transplantation of BALB/c Meth A ascitis. Using different dosages, routes of injection and schedules of vaccination it was found, that the highest non-toxic dose of C.p. per mouse yielded the optimal inhibition of tumor growth, the longest survival of tumor bearing hosts and the highest number of tumor rejections as compared to untreated controls. If the vaccine was distributed to at least 4 sites of injection, the s.c. route appeared superior to i.p. application. The intravenous route appeared to be most effective. The oral route seemed to inhibit tumor growth, if not less than 4 mg/mouse were fed daily for five days. The mechanism of action of C.p. in the model system used is discussed and correlated with an appropriate timing of both C.p. sensitization and tumor challenge.
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PMID:The effect of pretreatment with Corynebacterium parvum on the growth of a chemical induced transplanted murine tumor. 60 19

BALB/c mice immunized with Nonidet P-40 (NP-40) crude solubilized (CS) extracts of a syngenetic methylcholanthrene-induced BALB/c sarcoma (Meth A) were challenged with viable Meth A cells to determine the ability of the solubilized preparations to induce transplantation rejection. Animals resisting such challenge were then used in agarose microdroplet macrophage migration inhibition (MMI) and tumor cell neutralization (Winn) assays to evaluate the antigenic specificity of these CS extracts. Spleen cells from those animals that rejected Meth A after immunization with the NP-40-solubilized preparations effectively neutralized the tumor-producing capacity of Meth A tumor cells as determined in Winn assays. MMI assays were quite sensitive and detected migration inhibition of peritoneal exudate (PE) cells from immunized mice with extract concentrations as low as picogram quantities. Specificity studies demonstrated that Meth A expressed no antigenic cross-reactivity with similarly prepared extracts of an unrelated SV40-induced sarcoma (mKSA), nor with a mineral oil-induced plasmacytoma (ADJ-PC5) of BALB/c mice. Inhibition of PE cell migration was mediated by culture supernatants (presumably migration inhibition factor [MIF]) generated from a mixture of immune spleen cells and mitomycin C (MMC)-treated Meth A cells as assayed in an indirect MMI test.
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PMID:Cellular immunity to solubilized tumor antigens of a methylcholanthrene-induced sarcoma with a migration inhibition assay. 65 88

The response of the murine Meth-A fibrosarcoma (a methylcholanthrene-induced tumor) to single and fractionated doses of X-irradiation, actinomycin D chemotherapy, and/or concomitant local tumor hyperthermia was assayed with the use of an in situ method for estimating cell kill within a solid tumor. The cell survival assay was based on a standard curve plotting number of inoculated viable cells (10(1) to 10(7)) with and without radiation (10 kilorads)-inactivated homologous tumor cells (heavily irradiated) versus the time required for i.m. tumors to grow to 1.0 cu cm. The time for post-treatment tumors to grow to 1.0 cu cm was cross-referenced to the standard curve, and the number of surviving cells contributing to tumor regrowth was estimated. The resulting surviving fraction curves closely resemble those obtained with in vitro systems. The advantages and limitations of this technique are discussed as a method for evaluating treatment effectiveness.
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PMID:An in situ method for estimating cell survival in a solid tumor. 67 8

The objectives of this study were to quantitate the effects of local tumor hyperthermia (LTH) and concomitant x-irradiation (RAD) on a moderately radioresistant murine fibrosarcoma in situ. Comparisons were made to the combined treatment response on the Ridgway osteogenic sarcoma, a radio sensitive tumor previously used in this laboratory and to establish the Meth-A fibrosarcoma as a model system for combined modality studies. 1.0 cm3 tumors were exposed to single doses of RAD ranging from 0.5-3.5 krad alone or 0.5-2.3 krad in combination with LTH (water bath at 43.1 +/- .05 C for 20 minutes) applied immediately postirradiation. LTH significantly enhanced the action of radiation as measured by tumor volume analysis, mean survival time and cures. The ratio of radiation doses vs. RAD + LTH required to produce an equivalent response ranged from 1.4 to 2.5 depending upon the endpoints evaluated. These findings are consistent with single dose studies on the radiosensitive Ridgway osteogenic sarcoma and suggest that the tumoricidal effectiveness of combination radiation and hyperthermia cannot be predicted on the basis of the radiation alone responsiveness of tumor.
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PMID:Single dose X-irradiation and concomitant hyperthermia on a murine fibrosarcoma. 72 61

The dimensions of a BCG-potentiated antitumor response against the poorly immunogenic murine mastocytoma, P815 (MA), are described for a model in which the tumor immunogen is injected into subcutaneous sites previously infected with BCG; a distantly located tumor challenge is subsequently monitored for evidence of regression. A comparison of concomitant immunity and the immunity elicited by injection of varying doses of live MA into sites previously infected with BCG revealed similar antitumor effects. The subcutaneous site was the most effective route for immunization with BCG and irradiated tumor cells. Antitumor immunity was maximally expressed at intravascular sites and in the footpad. Complete tumor suppression was limited to footpadchallenge with 10-4-10-5 MA. Not only did the iv injection of BCG and immunogen fail to elicit immunity against subcutaneous challenge, but also systemically administered immunogens abrogated antitumor immunity elicited by subcutaneous immunization. These effects were reversed by prior splenectomy. Immunity was specific for the evoking tumor immunogen, but challenge with the specific tumor did not elicit nonspecific resistance against another 3-methylcholanthrene-induced tumor. In another strain of mice, immunity potentiated by BCG against the highly antigenic tumor, Meth A, was more effective than that potentiated against the poorly immunogenic MA.
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PMID:Immunopotentiation with BCG: dimensions of a specific antitumor response. 80 54


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