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)

The effects of Krestin (PSK) on the generation of lymphokine-activated killer (LAK) cells were examined in tumor-bearing mice. BALB/c mice were inoculated subcutaneously with methylcholanthrene-induced fibrosarcoma (Meth A) cells, and PSK was administered intraperitoneally every other day. The reduced LAK activity in tumor-bearing mice was restored by the administration of PSK. Since involvement of the humoral immunosuppressive factor in the impairment of LAK activity has been suggested, the effect of PSK on the impaired LAK activity in the presence of an immunosuppressive factor isolated from the ascites of X5563 (plasmacytoma)-inoculated mice was examined. The activity reduced by the immunosuppressive factor in an in vitro induction of LAK was restored by incubation with PSK. The antimetastatic effect of IL-2 was also augmented by its combined use with PSK. The data provide a rational basis for using PSK in combination with recombinant IL-2 in cancer immunotherapy.
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PMID:Effect of Krestin (PSK) on the induction of IL-2 activated killer cells. 161 82

The antitumor activity of an extract of seeds from Aeginetia indica L., a parasitic plant, was investigated. BALB/c mice, inoculated i.p. 1 x 10(5) syngeneic Meth A tumor cells, were administered 2.5 mg/kg A. indica extract i.p. every 2 days from day 0. The untreated mice died of an ascitic form of tumor growth within 21 days, whereas all the treated mice completely recovered from tumor challenge without any side-effects. The extract did not exert direct cytotoxic activity against Meth A in vitro. Mice that survived after the first challenge as a result of A. indica treatment overcame the rechallenge with homologous Meth A without additional administration of the extract. On the other hand, those mice could not survive after rechallenge with Meth 1 tumor cells, which were also established in BALB/c mice but were different in antigenicity from Meth A, suggesting the development of antigen-specific concomitant immunity in the A. indica-cured mice. In the induction phase of antitumor resistance in this system, CD4+ T cells appeared to be the main contributors, since in vivo administration of anti-CD4 mAb completely abolished such resistance. In contrast, anti-CD8 mAb administration did not influence the effect of A. indica. The importance of CD4+ T cells in antitumor immunity was again clarified by Winn assay; that is, spleen and lymph node cells depleted of CD4+ T cells in vitro prior to assay abolished antitumor activity on co-grafted Meth A tumor cells in vivo.
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PMID:An extract of seeds from Aeginetia indica L., a parasitic plant, induces potent antigen-specific antitumor immunity in Meth A-bearing BALB/c mice. 163 54

We prepared a novel recombinant tumor necrosis factor-alpha (TNF) mutant (mutant 471), in which 7 N-terminal amino-acids were deleted and Pro8Ser9Asp10 was replaced by ArgLysArg, and compared its biological activity with that of wild-type recombinant TNF. Mutant 471 had a 7-fold higher anti-tumor activity against murine L-M cells in vitro, and a higher binding activity to TNF receptors on L-M cells, than wild-type TNF. Furthermore, mutant 471 showed a higher anti-tumor effect on murine Meth A-HM tumors transplanted into BALB/c mice, with complete regression of the tumors being observed in the animals. The possible cachectin activity of mutant 471 was almost the same as that of wild-type TNF. The acute lethal toxicity of mutant 471 in beta-D-galactosamine-sensitized C3H/HeJ mice was 18 times lower than that of wild-type TNF. These results suggest that mutant 471 might be a more promising anti-cancer agent than wild-type TNF.
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PMID:A novel recombinant tumor necrosis factor-alpha mutant with increased anti-tumor activity and lower toxicity. 164 39

We have attempted to augment specifically the antiproliferative effect of recombinant human lymphotoxin (rhLT) on tumor cells in combined use with diethyldithiocarbamate (DDC) which is known to inactivate superoxide dismutase. For this purpose, anti-Meth A tumor cell antibody-DDC conjugates were used to confer the selectivity on the augmented antiproliferative effect in combined use of rhLT with DDC. Simultaneous addition of rhLT (1 u/ml to 100 u/ml) with the diluted conjugates to the target Meth A tumor cells induced the augmentation of the antiproliferative effect although antibody control was not effective. Similar augmentation of the antiproliferative effect was obtained when the target cells were treated with the conjugates prior to the addition of rhLT although the rate of inhibition was low. This approach seems to be useful because the antiproliferative effect of LT on target tumor cells could be augmented and side effects of LT could be avoided.
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PMID:Attempt to augment the anti-proliferative effect of recombinant human lymphotoxin in combined use with anti-tumor antibody-diethyldithiocarbamate conjugates. 165 45

The radiosensitizing effect of the nitroimidazole derivative RK28 and diethyldithiocarbamate (DDC), which is an inhibitor of superoxide dismutase activity, was examined in vitro by using Meth A tumor cells. The radiosensitizing effect of 0.5 mM RK28 was observed in both of 10 Gy and 15 Gy irradiated groups. The addition of 5 x 10(-7) M DDC also enhanced the radiation-induced proliferation inhibition. Marked enhancement of the antiproliferative effect was observed in combined use of 0.2 mM or 0.5 mM RK28 with 2 x 10(-7) M or 5 x 10(-7) M DDC. These results suggest that enhanced oxygen effect could be expected through combined use of the ionizing irradiation with both of these agents.
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PMID:Enhancement of radiosensitizing effect of the nitroimidazole derivative RK28 on the proliferation of MethA tumor cells in combined use with diethyldithiocarbamate. 165 11

By using two different syngeneic tumors, Meth A sarcoma and RL male 1 lymphoma of BALB/c origin, the present study was designed to investigate the subset(s) of T cells mediating in vivo antitumor immune responses and some of the effector mechanisms of in vivo protective immunity in BALB/c mice immunized against tumor or bearing tumor. Spleen cells from the mice immunized against Meth A tumor or bearing Meth A tumor inhibited the growth of Meth A tumor in the Winn assay. In the Meth A-immunized mice, L3T4+ (CD4+) cells played a major role in mediating the inhibitory activity against Meth A tumor growth, whereas in the Meth A-bearing mice, the antitumor protective immunity was mediated by both L3T4+ and Lyt-2+ (CD8+) cells. Spleen cells from the Meth A-immunized or Meth A-bearing mice were not able to generate cytotoxic T lymphocytes (CTL) directed against Meth A tumor after the in vitro restimulation of spleen cells with mitomycin C (MMC)-treated Meth A cells, while fresh spleen cells from the Meth A-immunized or Meth A-bearing mice were able to induce the strong delayed-type hypersensitivity (DTH) responses to Meth A tumor. The DTH response to Meth A tumor was mediated by L3T4+ cells in the Meth A-immunized mice and by both L3T4+ and Lyt-2+ cells in the Meth A-bearing mice. In the similar experiments performed in the RL male 1 lymphoma, the antitumor activity in spleen cells from the RL male 1-immunized or RL male 1-bearing mice depended on Lyt-2+ but not L3T4+ cells in the Winn assay. When spleen cells from the RL male 1-immunized or RL male 1-bearing mice were cultured with MMC-treated RL male 1 cells for 5 days, an appreciable CTL response to RL male 1 tumor was induced. These results suggest that the nature of tumor and/or tumor antigens determines which T cell subset is required to exhibit the protective immunity against tumor and thus the different effector mechanisms could be induced in the different tumor models. Furthermore, these data support the conclusion that antitumor T cell responses are affected by the immune state of host to tumor.
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PMID:Effector phenotypes and mechanisms of antitumor immune reactivity of tumor-immunized and tumor-bearing mice in two syngeneic tumors. 167 79

The mechanism of tumor regression by adoptive immunochemotherapy has been unknown. We examined tumor infiltrating lymphocytes (TILs) and cytokines, using immunohistochemical staining and the histo in situ hybridization (HISH) technique, on Meth A tumor in regression of BALB/c mice. In addition, we examined cytokine activity in the serum of mice with a tumor in regression. The result of immunohistochemical staining showed that the number of Thy-1+ cells, Lyt-1+ cells, OKIa1+ cells all increased in the tumors in regression compared to those in the tumors in non-regression. However, there were no these TILs in the necrotic part of tumor. This result suggested that TILs released substances which might include cytokines. A small number of each cytokine mRNA was observed, using HISH with cytokine DNA probes. TNF-alpha, and -beta mRNA were observed in both he tumors in regression and non-regression; while, IFN-beta and -gamma mRNA were observed only in the tumor in regression. TNF-alpha activity in the serum of tumor in regression group was higher than that of he tumor in non-regression group. IFN activity in the serum of the tumor in regression group started increasing after adoptive immunochemotherapy. These results show that cytokines as well as TILs have important roles in tumor regression.
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PMID:[Study on the mechanism of tumor regression by adoptive immunochemotherapy in mice]. 170 81

The effect of co-administration of granulocyte colony-stimulating factor (G-CSF), as an antineutropenia agent, on interferon therapy was examined in a mouse model, in anticipation of an enhancement of interferon efficacy, because neutrophils induced by G-CSF are thought to act as antitumor effectors. G-CSF was intraperitoneally co-administered with human interferon alpha A/D (IFN) on Day 6 to Day 10 after intradermal inoculation of Meth A fibrosarcoma. Although the co-administration of G-CSF could protect against neutropenia and leukopenia induced by IFN, it did not enhance the regression of tumor, and rather reduced the prolongation of survival time and the long-term survival incidence of IFN therapy. The subsequent in vitro study showed that the antiproliferative activity of peripheral blood leukocytes from Meth A-bearing mice given both IFN and G-CSF was much weaker than that of mice given IFN alone. Whether the observed nullifying effect of G-CSF on IFN therapy is also the case with tumors other than Meth A is open to further study.
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PMID:Effect of co-administration of granulocyte colony-stimulating factor on interferon therapy. 170 57

The intraperitoneal administration of human recombinant granulocyte colony-stimulating factor (G-CSF) enhanced the growth of intradermally inoculated tumor in mice; in a Meth A fibrosarcoma model, G-CSF administration significantly shortened the latency before tumor appearance, accelerated the increase of tumor size, shortened the survival time of tumor-bearing mice and increased the incidence of lethal tumor growth. A similar growth-enhancing effect of G-CSF was observed in models employing Meth 1 fibrosarcoma, colon carcinoma 26, and L1210 leukemia, although not all the effects were statistically significant. In vitro study showed that G-CSF did not enhance Meth A growth in suspension culture or in soft agar. These data suggest that G-CSF enhances the Meth A growth not directly but through the mediation of host factors. The accumulation of neutrophils was histologically observed in the tumor nodule, the blood, and the spleen in mice given G-CSF repeatedly. The spleen cells and the peripheral blood leukocytes of G-CSF-injected mice enhanced Meth A growth in vitro as compared with those of mice injected with physiological saline. These results suggest the possibility that the in vivo growth of tumor cells was enhanced by G-CSF-induced overproduction of cells including neutrophils.
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PMID:In vivo tumor growth enhancement by granulocyte colony-stimulating factor. 171 Jun 15

We previously reported that a 25-kDa Bacillus thuringiensis subsp. israelensis (BTI) toxin is cytotoxic to cultured tumor cells and can also potentiate the cytotoxic effect of some antitumor agents in vitro. In this study, we examined the in vivo effect of BTI toxin on the potentiation of antitumor activity of bleomycin (BLM) against solid tumor-bearing mice. Three tumor cell lines, Ehrlich carcinoma, B16 melanoma and Meth A fibrosarcoma, were employed. It was shown that dose of BTI toxin, ineffective alone, potentiated the antitumor activity of BLM when used in combination.
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PMID:Potentiation of antitumor activity of bleomycin towards solid tumors in mice by Bacillus thuringiensis subsp. israelensis toxin. 172 Sep 39


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