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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Macrophages were isolated from 22 human ascitic ovarian epithelial tumors and their growth-inhibitory capacity was tested using as targets the following in vitro tumor cell lines: murine TLX9 lymphoma and FS6 sarcoma; human myeloid K562 leukemia and human E cell line derived from an ovarian carcinoma. Macrophage preparations were heterogeneous in their interaction with tumor target cells, and assay conditions, such as the type of target cell, incubation time, and attacker to target cell (A:T) ratio critically affected the evaluation of the cytotoxic potential of tumor-associated macrophages. At an A:T ratio of 7:1 no cytostatic activity on TLX9 and K562 cells was ever observed, but in the presence of specific antibody 8 out of 12 macrophage preparations tested showed significant antibody-dependent cytotoxicity on TLX9 lymphoma cells. Macrophage preparations from two patients significantly inhibited growth of the FS6 sarcoma and a cytostatic activity on E cells was observed in five additional patients. Significant stimulation of the proliferative capacity of at least one of the target cell lines was observed in 11 subjects at an A:T ratio of 7:1. In 12 patients, macrophage cytostatic activity on E cells was also tested at an A:T ratio of 35:1; eight out of 12 preparations showed significant cytotoxicity under these conditions. When the same subject was repeatedly tested at short intervals the same pattern of inhibition or stimulation of tumor growth was observed.
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PMID:Effects on in vitro tumor growth of macrophages isolated from human ascitic ovarian tumors. 76 40

The antitumor effect of reserve polysaccharide, paramylon, from Euglena gracilis on the transplantable sarcoma-180 was examined in mice. This polysaccharide had an effect similar to that of lentinan. Paramylon, in a dose of 1 mug/g body weight, injected intraperitoneally 24 hr after tumor implantation had an inhibitory effect on the tumor growth, although without causing complete regression of the tumor. Alkaline-treated paramylon had a similar effect but at a smaller concentration than the native one. The inhibitory activity was not lost when the paramylon preparation was treated with pronase, DNase, or RNase. The antitumor effect might be a lymphocyte-mediated process. In tumors that were regressing after treatment, there was extensive outpouring of lymphoid cells with plasma cells and macrophages. A test conducted using paramylon ruled out the possibility of an interferon-mediated inhibiotry effect on tumor growth.
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PMID:Antitumor activity of paramylon on sarcoma-180 in mice. 82 42

Spleen cells taken from W/Fu rats 4 to 6 weeks after immunization with the syngeneic Gross virus-induced lymphoma, (C58NT)D cells, at a time when they lack detectable activity in a short-term 51Cr release assay, were previously shown to retain the capacity to generate cytotoxic activity upon reexposure to mitomycin C-treated lymphoma (C58NT)D cells in vitro. In the studies presented here, we evaluated whether in vitro sensitization of immune lymphoid cells before systemic transfer to a nonimmune recipient allows for more effective transfer of tumor immunity. The results show that the passive transfer of immune spleen cells after in vitro cocultivation with mitomycin-treated (C58NT)D cells allows for inhibition of growth of a subcutaneous inoculum of lymphoma cells. In contrast, spleen cells obtained 4 to 6 weeks after primary sensitization or after secondary in vivo sensitization did not effectively confer anti-tumor immunity. As few as 5 x 107 in vitro sensitized cells permitted complete inhibition of 106 (C58NT)D cells and also allowed for inhibition of the growth of 107 (C58NT)D-F cells, which was lethal to control animals. Immune cells sensitized with syngeneic thymocytes or normal spleen cells sensitized with (C58NT)D cells in vitro did not confer in vivo anti-tumor immunity. After systemic transfer of in vitro sensitized cells, delayed hypersensitivity occurred at the site of tumor inoculation and tumor growth was suppressed. Specificity of the passive immunity was shown by the failure to inhibit growth of a polyoma virus-induced sarcoma in rats which inhibited growth of the Gross virus-induced lymphoma cells. In vitro sensitized cells were more effective in the transfer of anti-tumor protection after 5 days, as compared to 2 days, of cocultivation with tumor. Results show that in vitro sensitized cells can effectively transfer systemic tumor immunity.
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PMID:Passive transfer of systemic tumor immunity with cells generated in vitro by a secondary immune response to a syngeneic rat gross virus-induced lymphoma. 83 Jul 44

The levels of natural cell-mediated cytotoxicity against tumor cells in young BALB/c and BALB/c nude mice could be augmented by inoculation of a variety of mouse tumor cells or of mouse thymocytes. In older mice with low levels of spontaneous cytotoxic reactivity, inoculation of tumor cells led to rapid appearance of cytotoxicity. This augmented cytotoxicity reached a peak 3 days after inoculation and then declined rapidly. The specificity of the augmented cytotoxicity appeared to be the same as that seen with natural cell-mediated cytotoxicity. The detected antigens were restricted to mouse tumor cells and thymocytes, and were absent on cells from other species. The effector cells after boosting also had the same cell surface characteristics as the natural cytotoxic effector cells, being non-adherent, non-phagocytic, and only weakly sensitive to treatment with anti-theta serum plus complement. In addition to this boosting by mouse tumor cells, marked increases in the levels of cytotoxicity were caused by a variety of murine viruses, including murine sarcoma virus and lymphocytic choriomeningitis virus. These effector cells also had the same properties as those seen with natural cytotoxic effector cells. The results indicate that the levels of natural cell-mediated cytotoxicity in conventional and athymic BALB/c mice can be consistently and rapidly boosted by inoculation with tumor cells or viruses. This should provide a valuable tool for better understanding of the mechanisms responsible for the expression of natural cytotoxicity and its relevance to in vivo resistance to tumor growth.
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PMID:Augmentation of natural cytotoxic reactivity of mouse lymphoid cells against syngeneic and allogeneic target cells. 84 21

Transplantation of splenic cells from CBA mice bearing primary sarcoma SA7(C8) together with autologous sarcoma cells (in the ratio 1 : 1 and 10 : 1) into syngeneic recipients, irradiated with 600 rad, resulted in a marked decrease of the latent period of tumor development. Syngeneic splenocytes of normal mice would enhance the tumor growth with the ratio 10 : 1. Preliminary treatment of tumor-bearing and normal mice with hydrocortisone in the dosage of 6 mg per 100 g of weight fails to reduce the capacity of splenic cells to induce immunostimulation of tumor growth.
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PMID:[Immunostimulation of the growth of a syngeneic sarcoma primarily induced in mice by simian adenovirus SA7(C8)]. 90 8

Experiments were designed to assess 1) relative immunity after adoptive transfer of spleen cells or serum from tumor-bearing mice to untreated syngeneic mice, and 2) the degree of tumor-specific transplantation immunity imparted by cells or serum relative to tumor size and the presence of metastases in the donor at the time of spleen cell or serum transfer or after in situ necrosis of the primary tumor by cryosurgery in a CDF1-sarcoma system. Viable lymphoid spleen cells or serum from normal mice had no effect on tumor growth. Serum from mice that had large tumors and gross metastases induced a protective effect similar to that found after cryosurgery of the primary tumor. Serum from mice with small tumors and spleen cells from animals bearing either small or large tumors failed to induce immunity consistently. In no instance did serum from tumor-bearing mice induce enhancement of tumor growth.
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PMID:Transfer of tumor-specific immunity with syngeneic spleen cells and serum from mice that have large tumors and metastases. 90 74

Simultaneous measurement of cardiac output distribution with 86Rubidium and 57Cobalt-tagged microspheres in rats implanted with liver tumors by intraportal injection of sarcoma cells enables quantitation of arterial and portal tumor circulation. The portal circulation was found to be increased in small tumors as compared to the liver, but as the tumor grew there was a decrease in the portal tumor circulation. When the tumor growth became massive even the total liver circulation was reduced, as measured with 133Xenon wash-out. All the tumors had increased arterial circulation. This arterial hyperperfusion was changed into ischemia when the liver artery was occluded through embolization with degradable microspheres.
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PMID:The circulation in liver tissue and experimental liver metastases before and after embolization of the liver artery. 91 87

Three in vivo techniques were used to establish the specificity of tumor immunity induced after sensitization of F344 rats to syngeneic MCA-induced sarcomas: (1) post-excision resistance to tumor challenge, (2) passive tumor neutralization (the Winn test), and (3) concomitant immunity. In general, these assays revealed unique non-cross-reactive antigens associated with each of three sarcomas, FMF1, FMM2, and FMM3. However, spleen cells from tumor-sensitized rats did not demonstrate cell-mediated cytotoxicity in vitro corresponding to the specificity of tumor resistance in vivo. In the (3H)-proline cytotoxicity assay, spleen cells from FMM3 tumor-bearing rats or from FMM3 tumor-immune rats were not selectively cytotoxic for cultured FMM3 target cells. Parallel analysis of spleen cells from normal or FMM3-sensitized rats using the Winn assay and the (3H)-proline assay revealed that (1) spleen cell cytotoxicity in vitro did not correlate with effective tumor protection in vivo; and (2) normal spleen cells were cytotoxic against cultured sarcoma target cells in vitro and inhibited tumor growth in vivo. Thus, passive tumor protection by normal spleen cells in vivo corresponded with the demonstration of natural cytotoxicity in vitro, but induced specific anti-tumor reactivity was observed only in vivo.
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PMID:Immunity to MCA-induced rat sarcomas: analysis of in vivo and in vitro results. 92 92

Lentinan, an antitumor polysaccharide from Lentinus edodes, was degraded to seven fractions by treatment with formic acid. The low molecular-weight fractions (I and II) showed no antitumor activity against sarcoma-180 solid-type tumor and the absorption maximum of Congo Red did not shift in their presence in 0.1M sodium hydroxide. The medium molecular-weight fraction III, which required the increase of doses (5 or 10 mg/kg) for inhibition of tumor growth, caused a little shift. On the other hand, the absorption maximum of Congo Red shifted largely by the presence of high molecular-weight fractions (IV approximately VII) which showed the inhibition ratio of over 95% in a dose of 1 mg/kg. Participation of molecular weight in the antitumor activity of polysaccharides which contain (1 leads to 3)-beta-D-glucan main chain was discussed.
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PMID:Antitumor activity of degraded products of lentinan: its correlation with molecular weight. 96 51

In both isogeneic (Sarcoma 1 in A/JAX mice) and allogeneic (Sarcoma 180 in C57BL/6 mice) mouse tumor systems, treatment of the tumor-bearing mice with niridazole, an antiprarasitic drug, known to be a potent suppressor of cell mediated but not humoral immunity caused enhancement of metastases to regional popliteal nodes. Niridazole also inhibited tumor growth in vivo, as manifested by a significant decrease in the weight of the primary tumors. The enhancement of metastases is attributed to the suppression of cell-mediated immunity by the drug, but the mechanism of tumor-growth inhibition is not yet clear.
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PMID:Effects of the immunosuppressive drug niridazole in isogeneic and allogeneic mouse tumor systems in vivo. 97 80


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