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)

Growth of tumors was inhibited or enhanced in mice by a synthetic (pyran) or a biologic (corynebacterium parvum) immunopotentiator. Marked inhibition of leukemogenesis induced by Friend leukemia virus was produced by prophylactic intraperitoneal treatment with pyran, while intravenous treatment with pyran (in the same dose and regimen) significantly enhanced growth of tumor virus. Paradoxical effects were also seen with the biologic immunopotentiator C. parvum in solid tumor systems. Treatment with C. parvum either potentiated disease or had no effect on the life span of most mice bearing the Lewis lung carcinoma. In contrast, the same treatment could produce a high percentage of tumor regressions in mice bearing the MCA 2182 sarcoma, although the effect was somewhat variable. These data, which show that a change in route of drug administration or in the type of tumor treated may reverse the effect of treatment, emphasize that the mechanism of action of immunopotentiators must be elucidated before consistent beneficial treatment of tumor viruses or tumors can be achieved.
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PMID:Paradoxical effects of immunopotentiators on tumors and tumor viruses. 93 3

Transplantability of mouse tumors superinfected with various kinds of membrane viruses was investigated in syngeneic hosts. Methylcholanthrene-induced fibrosarcomas in BALB/c mice, Meth A, and in C57BL/6 mice, BMT-, superinfected with Friend lymphatic leukemia virus in mice given neonatal injection of the virus, grew more slowly than uninfected tumors. The retardation of growths was not observed in mice that had been given injections of the virus at birth. Similarly, Meth A and a hepatoma in C3H/He mice, MH134, superinfected with Moloney murine sarcoma virus in nu/nu mice, had reduced their transplantability in respective syngeneic mice. Further, Meth A and MH134 superinfected with endogenous rat leukemia virus and human measles virus, respectively, in nu/nu mice also showed reduced transplantability, and some of the former were actually rejected by normal syngeneic hosts. On the other hand, the reduced transplantability was not found in irradiated mice, suggesting that the phenomenon was due to immunological events. However, a myelogenous leukemia in C57BL/6 mice, C1498, superinfected with Moloney sarcoma virus in nu/nu mice grew like uninfected tumor and did not show reduced transplantability at all.
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PMID:Reduced transplantability of syngenic mouse tumors superinfected with membrane viruses in nu/nu mice. 100 77

The following evidence from our research has implicated the macrophage as an important effector cell in pyran and/or C. parvum induced host resistance to solid tumors: (1) Increased infiltration of tumors with histiocytes following systemic treatment with pyran;17 (2) activated peritoneal macrophages with tumoricidal activity have been recovered from the peritoneal cavity of normal or tumor bearing mice treated with pyran or C. parvum;17 (3) activated peritoneal macrophages mixed with tumor cells in vitro and transplanted into syngeneic recipients inhibited tumor growth; (4) trypan blue, an inhibitor of macrophage function, prevent C. parvum induced regression of methylcholanthrene tumors; and (5) direct intralesional injection of activated macrophages into the MCA 2182 tumor inhibited tumor growth and increased the MST.
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PMID:Macrophage mediated tumor cell cytotoxicity. 107 61

This report documents for the first time BCG-induced protection against a murine malignant melanoma. Adult Balb/C mice recieved 0.1-cm3 doses of BCG prior to intramuscular challenge with 1 x 10-6 S-91 melanoma cells. A 65% reduction in melanoma incidence was noted in BCG-pretreated mice. The possibility of specific protection induced by the BCG against the melanoma exists, since the BCG pretreatment did not protect against challenge with 1 x 10-5 mammary carcinoma cells or 1 x 10-4 MCA fibrosarcoma cells in the same strain of mice. Lack of immunogenicity was not a factor in the inability of the carcinoma and sarcoma to be inhibited by BCG. The strenght of the BCG-induced protection against the S-91 melanoma was demonstrated by significantly decreased tumor incidence following three different log challenge doses of the melanoma. However, reduction of the sarcoma challenge dose to as few as 10-2 cells administered to BCG pretreated mice did not result in decreased tumor incidence. It was further discovered that as few as two doses of 0.1 cm3 of BCG were sufficient to produce a 70% reduction in melanoma incidence compared with the incidence in control animals (P less than .001). Lymphocyte-mediated cytotoxicity studies paralleled the results of the in vivo experiments. Lymphocytes immune to each of the three tumors showed significant cytotoxicity against their respective tumor target cells (p less than .001), while the only tumor cells that lymphocytes from BCG-pretreated mice showed significant cytotoxicity against were S-91 target cells (p less than .01). Nonspecific cytotoxicity was not a factor in the effect of BCG-immune lymphocytes against S-91 target cells, since BCG-immune lymphocytes were not cytotoxic to Balb/C fibroblasts.
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PMID:BCG-induced protection against malignant melanoma: possible immunospecific effect in a murine system. 111 14

C57B1 mice bearing methylcholanthrene-induced fibrosarcomas (MCA-10) and receiving a single cryosurgical treatment to those tumors showed significantly greater humoral and lymphocyte-mediated cytotoxicity to MCA-10 target cells than did untreated tumor-bearing animals or mice which had undergone tumor amputation. Sera and lymphocytes from normal animals receiving crycosurgery demonstrated no immunity to the MCA-10 target cells. Specific immunity to the MCA-10 line following tumor cryosurgery was demonstrated since lymphocytes and sera from cryosurgically treated tumor-bearing mice were not cytotoxic to a different methylcholanthrene-induced sarcoma (MCAP) in C57 mice or a malignant melanoma (S91) being transferred in Balb/C mice. It can be concluded that cryosurgical treatment of the MCA-10 sarcoma does not produce heightened immunity to H-2 transplantation antigens, nor does it nonspecifically stimulate the immune system. Instead, the result of tumor cryosurgery appears to be a boosting of the immune response to the tumor-specific antigens of the sarcoma.
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PMID:In vitro demonstration of cryosurgical augmentation of tumor immunity. 112 99

Mice inoculated with MCA-10 sarcoma cells which had previously been incubated with Vibrio cholerae neuraminidase (VCN) demonstrated a significantly lower tumor incidence (9/26) than mice injected with untreated sarcoma cells (10/10) or sarcoma cells incubated with heat-inactivated neuraminidase (28/29) p less than .05. Rechallenge of nontumor-bearing mice from the VCN group with untreated sarcoma cells resulted in a low tumor incidence (4/11), indicating that these mice had developed systemic immunity following the initial injection of VCN-treated tumor cells. These mice also demonstrated significant lymphocytotoxicity against MCA-10 target cells compared with normal control mice (p less than .05). Subsequent cytotoxicity experiments, utilizing groin lymph node and splenic lymphocytes from mice five days following leg injection of VCN-treated, heat-inactivated VCN-treated or untreated MCA-10 cells, demonstrated that the mice injected with VCN-treated tumor cells demonstrated greater antitumor immunity both locally and systemically. This magnification of tumor immunity is postulated as the mechanism by which neuraminidase treated MCA-10 sarcoma cells grew less well in C57 mice than cells incubated with heat-inactivated VCN or cells left untreated.
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PMID:Antitumor immune response following injection of neuraminidase-treated sarcoma cells. 113 Aug 52

3-Methylcholanthrene (MC) in chloroform and trifluoroacetic acid-d1 yielded 3-methylcholanthrene-d4 (MC-d4), a compound selectively deuterated at the 1-, 5-, and 6-carbon atoms. In turn, the protodedeuteration of the labeled hydrocarbon at the 6-carbon atom led to 3-methylcholanthrene-d3 (MC-d3). A comparative test for carcinogenicity between MC and MC-d3 by repeated skin painting on female Swiss mice showed a significantly lower tumorigenic activity of the latter. The result implies that the 1-carbon atom of the hydrocarbon is a critical binding-site to cellular targets in the tumor-initiating process.
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PMID:Isotope effect on the carcinogenicity of 3-methylcholanthrene in mouse skin by selective deuteration of the 1-methylene group: biological evidence for a mechanism of tumor initiation. 115 89

Methylcholanthrene, in amount sufficient to induce tumors in 100% of treated animals failed to influence primary and secondary phases of antibody synthesis in mice immunized with sheep erythrocytes and human serum albumin. The early immune response in tumor bearing mice was also indistinguischable from that of normal animals, despite the presence of marked splenomegaly in the former group.
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PMID:[Correlation between chemical carcinogenesis and immune response]. 120 33

Benzene, toluene and acetone--frequently used as solvents of skin carcinogens--have different effects on the skin collagen of mice: Benzene and toluene lower the collagen content significantly whereas acetone does not. Methylcholanthrene solved in acetone causes a slower collagen decrease and a longer latency period of tumor development as can be observed, when solved in benzene or toluene. This leads to the conclusion, that benzene and toluene have a cocarcinogenic potency.
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PMID:[The effect of various solvents (benzene, toluene, acetone) used with carcinogens on the collagen content of the mouse dorsal skin]. 124 60

Systemic administration of the synthetic immunopotentiator pyran, was as effective as the use of the biologic immunopotentiator BCG in activating macrophages and in inhibiting the Lewis lung carcinoma and MCA 2182 sarcoma. Several other synthetic polyanions also activated macrophages and exhibited some anti-tumor activity, but none were as effective as pyran. Cell-wall fractions such as the Ribi vaccine and MER were considerably less effective than BCG. The anti-tumor activity of pyran against the virtually non-immunogenic Lewis lung carcinoma involved non-specifically activated macrophages, and both anti-tumor activity and macrophage activating ability persisted over a 100-fold range of drug from 0.5 mg/kg to 50 mg/kg. The ability of activated macrophages to destroy tumor cells was abrogated by treatment with trypan blue, an inhibitor of macrophage lysosomal enzymes. In addition, preincubation of tumor cells with activated peritoneal cells at effector-cell:target-cell ratios of 20:1 and 5:1 markedly decreased tumor incidence and mortality. Glycogen-stimulated or unstimulated peritoneal cells were completely inactive in inhibiting tumor growth in vivo or exhibiting cytotoxicity in vitro, demonstrating the requirement for activated macrophages selective for tumor-cell destruction.
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PMID:Macrophage activation and anti-tumor activity of biologic and synthetic agents. 124 2


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