Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility of passive immunotherapy was examined using syngeneic antitumor serum, which could lyse tumor cells in co-operation with immune or activated macrophages. Intraperitoneal injection of syngeneic antiserum into mice soon after inoculation of MM46 tumor cells clearly suppressed peritoneal or subcutaneous tumor growth. However, the antiserum did not suppress an established tumor. The tumor-specific synantibody responsible for the protection was shown by gel filtration to be in the IgG fraction, not the IgM fraction.
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PMID:Protective effect of syngeneic antitumor serum on mammary tumor in a syngeneic host. 59 Jun 80

Lymphokine-activated killer activity in vivo (endogenous LAK activity) was found to be augmented by combined administration of lentinan, a beta (1-3) glucan with beta-1,6 branches, and interleukin 2 (IL-2). In contrast, addition of lentinan during culture in vitro did not augment LAK activity induced by IL-2. Surface marker analysis of endogenous LAK cells revealed that endogenous LAK cells induced by a combined administration of lentinan and IL-2 were all NK-type LAK cells, which express asialo-GM1 and lack T3, Thy-1 and Lyt2, whereas LAK cells generated in vitro were composed of both NK-type LAK and T-type LAK cells, which express T3 and Thy-1, and lack asialo-GM1. Furthermore, combined administration of lentinan and IL-2 was found to augment the endogenous LAK activity even in the tumor bearer, and show a substantial inhibition of tumor growth and a significant increase in survival rate in the C3H/HeN/MM46 system. Results of the present investigation offer a possible clinical application of a combination of lentinan and IL-2 for immunotherapy against cancer without detrimental side effects.
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PMID:Induction of endogenous lymphokine-activated killer activity by combined administration of lentinan and interleukin 2. 227 26

We investigated the short-term effects of a single high-dose radiation upon transplanted MM46 tumor cells in mice by means of immunohistochemistry and electron microscopy. The irradiation induced: 1) giant cell formation from the 3rd day, 2) arrest of tumor cell mitosis in prophase and metaphase due to the disorganization of the mitotic spindles, 3) changes in immunoreactivity of laminin and cytoskeletons, and 4) multilayering of the vascular basal lamina and perivascular fibrosis. The above findings suggest a decrease in tumor cell compliance, growth and invasiveness and the potentiation of defensive host responses against vascular invasion after irradiation. The analysis of the temporal sequences of the events indicates that the time lapse between the optimal host response, tumor growth and invasion constitutes a critical period.
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PMID:The irradiation effects on the cytoskeletons of C3H/He mouse mammary tumor cells and vascular basement membrane in relation to vascular invasion: a model of intraoperative radiotherapy. 245 98

A new series of amphiphilic 1-octadecyl glycerolipids (eleven compounds, 1a-k) were designed and synthesized, in which the 3-phosphocholine portion of platelet-activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) was replaced by the 2-(2-trimethylammonioethoxy)ethyl group and congeneric groups having oligo(ethyleneoxy)ethyl bridges of various lengths at position 3, together with modification at position 2 (lower alkyl, acetonyl, acetoacetyl, carboxymethyl and pyrimidin-2-yl groups). These ether lipids, characterized by a nonphosphorus lysoglycerolipid structure, showed potent antitumor activity in vitro (human promyelocytic leukemia cells, HL-60, and human epidermoid carcinoma cells, KB) and in vivo (mouse sarcoma S180 and mouse mammary carcinoma MM46). Maximal in vitro potency was obtained with 1-O-octadecyl-2-O-(2-pyrimidinyl)-3-O-[2-(2-trimethylammonioethoxy )ethyl] glycerol (1g; IC50 values for both HL-60 and KB were 0.32 microgram/ml, indicating a higher activity than alkyl-lysophospholipid, ET18-OMe). Several appropriately 2-substituted 1-octadecylglycerolipids with the 3-[2-(2-trimethylammonioethoxy)ethyl] group (e.g., methyl, 1b; butyl, 1f; 2,2,2-trifluoroethyl, 1j; and acetonyl, 1k) showed a potent life-span-prolonging effect on mice with ascites sarcoma S180 and on those with mammary carcinoma MM46, when administered intraperitoneally at 16.5 and 12.5 mg/kg/d, respectively. Compounds 1b and 1k showed definite tumor growth inhibition against solid sarcoma S180 in mice, whether given p.o. or i.v. at 16.5 mg/kg/d. Studies on the structure-activity relationships indicate that the metabolic stability to phospholipase C or related enzymes is at least partly responsible for the potent antitumor activity of this series of ether lipids.
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PMID:Synthesis and antitumor activity of new amphiphilic alkylglycerolipids substituted with a polar head group, 2-(2-trimethylammonioethoxy)ethyl or a congeneric oligo(ethyleneoxy)ethyl group. 263 72

Female C3H/He mice aged 14 weeks with transplanted MM46 tumor were used to investigate the effect of an immunomodulator, Z-100 (an arabinomannan lipid extracted from Mycobacterium tuberculosis strain Aoyama B) combined with local irradiation of 30 Gy (3,000 rad). Daily doses of 5 micrograms, 50 micrograms and 500 micrograms/kg of Z-100 were injected intramuscularly for 14 consecutive days after irradiation, and 2 times a week for 6 weeks thereafter. The antitumor effect was evaluated by the changes in tumor volume and survival curves. In groups administered 50 micrograms and 500 micrograms/kg of Z-100, tumor growth decreased significantly compared with the control group (radiotherapy group). Concerning survival rates of each group of mice, there were no marked differences between Z-100 administered groups and the control group. To clarify the mechanisms of action of Z-100, the changes in the lymphocyte subsets infiltrated into tumor tissue after Z-100 treatment were analysed immunohistochemically using monoclonal antibodies, anti-Thy 1.2, anti-Lyt-1, anti-Lyt-2, anti-L3T4, MAS034b and MAS053c and avidin-biotin-peroxidase complex method (ABC method). In the findings of immunohistochemical studies, differences were hardly observed between groups administered Z-100 and groups treated with radiation only. From these results, it was concluded that immunological effects of Z-100 resembled that of radiotherapy on the topical tumor tissue.
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PMID:[Experimental study of the antitumor effect of Z-100 in the treatment of MM46 tumor transplanted in C3H/He mice. 2. Effect of the combination therapy of radiation and long term administration of Z-100]. 273 40

Monoclonal antibodies were produced against MM46, an MM antigen-positive, ascitic mouse mammary tumor of C3H/He mice, and 14 clones were found to produce antibodies reactive with MM46, but not with an MM antigen-negative MM48 tumor. Among these 14 antibodies, 10 reacted also with lymph node cells of C3H.B6-Ly-6b, Ly-6.2 congenic mice. The antigen defined by the 10 antibodies was provisionally designated MM1, and the one defined by the other 4 was designated MM2. Further analysis of MM1 by antibody binding inhibition assay with 3H-labeled MM1-gamma 2b-1 antibody revealed that 8 of the 10 antibodies as well as monoclonal anti-Ly-6.2 showed significant inhibition. This result indicated that there were more than two antigenic determinants on MM1 antigen. The immunoglobulin class of eight antibodies detecting the same antigenic determinant on MM1 was examined and was found to cover major classes of mouse immunoglobulin (mu, gamma 1, gamma 2a, gamma 2b, gamma 3, and alpha). Therefore, the in vivo effect against MM46 tumor cells by these antibodies was studied by a serological tumor neutralization assay. Tumor cells (4 X 10(5)) were treated with antibodies and then injected s.c. into syngeneic C3H/He mice. Ten days later, the tumor was weighed. gamma 2a antibody showed significant suppression of tumor growth, and both gamma 2b and gamma 1 antibodies also revealed suppression. However, mu, gamma 3, and alpha antibodies did not show any significant effect on the tumor growth. To elucidate the mechanisms of tumor suppression by antibodies, the role of macrophages was studied by the antibody-dependent macrophage-mediated cytotoxicity test. In accordance with the in vivo tumor effects, gamma 2a antibody showed 40 to 60% cytotoxicity up to the concentration of 1 microgram/ml, and both gamma 2b and gamma 1 antibodies were also cytotoxic, although less so than gamma 2a. Neither mu nor alpha antibody showed any significant cytotoxicity. gamma 3 antibody showed very weak cytotoxicity against MM46 tumor cells. Thus, a good correlation was observed between the in vivo antitumor effects and in vitro antibody-dependent macrophage-mediated cytotoxicity activity with regard to each class of immunoglobulin, which suggested that macrophages may play an important role in the in vivo antitumor effect of the antibodies used.
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PMID:In vivo antitumor effects of monoclonal antibodies with different immunoglobulin classes. 619 9

A cytolytic factor partially purified from eggs of the sea hare Aplysia kurodai was examined for cytolytic activity against various target cells. All kinds of tumor cells tested were lysed in vitro by the cytolytic factor in the range of 10-100 ng protein/ml. In contrast, normal spleen cells were lysed by 10 micrograms/ml of this factor and red cells were not lysed even at this higher concentration. Tumor lysis was time-dependent and was complete within 10 hr. This factor inhibited DNA and RNA syntheses of tumor cells but not protein synthesis. The cytolytic activity was lost on heat-treatment (60 degrees) and at pH 2, and was partially inhibited by treatment with 8M urea and at pH 12, but the factor was resistant to treatments with trypsin, periodate and 2-mercaptoethanol. Neutralizing activity was observed in vivo on pretreatment of MM46 and L1210 cells with the factor. This cytolytic factor also inhibited the growth of solid-type MH134 tumor and ascitic-type MM46 tumor. These results indicate that Aplysia eggs contain a novel cytolytic factor that lyses tumor cells in vitro and inhibits tumor growth in vivo.
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PMID:Cytolytic factor in eggs of the sea hare Aplysia kurodai. 653 65

Sonicated liposomes containing actinomycin D in the membranes were chemically coated with the subunits of monoclonal immunoglobulin M (IgM) antibody against a mouse mammary tumor-associated antigen (MM antigen) and examined for their in vitro and in vivo antitumor effects against MM46 (MM+) and MM48 (MM-) tumors of C3H/He mouse origin. The antibody-bearing, actinomycin D-containing liposomes (chemoimmunoliposomes) were selectively bound to MM+ tumor cells and showed much more in vitro cytotoxicity against the tumor cells than that shown by free actinomycin D. The in vivo antitumor effect of the chemoimmunoliposomes was tested on the mammary tumor cells (5 X 10(4) to 5 X 10(6) transplanted i.p. into syngeneic mice. A single i.p. injection of the chemoimmunoliposomes containing 0.3, 0.5, or 1 microgram of actinomycin D into MM46 tumor-bearing mice resulted in the cure of some mice and a prolonged survival time in the rest of the mice as compared to results in controls. In this test, free actinomycin D, anti-MM IgM antibody, and bovine serum albumin-coated liposomes containing actinomycin D were marginally effective or ineffective. To examine a systemic antitumor effect of chemoimmunoliposomes, mice were inoculated with MM46 tumor cells and then treated with a single i.v. injection of liposomes 4 days later. If the mice were pretreated with an i.v. injection of unmodified multilamellar liposomes, an injection of the chemoimmunoliposomes containing 1 microgram of actinomycin D resulted in a significant inhibition of tumor growth. Both free actinomycin D and bovine serum albumin-coated liposomes containing actinomycin D were ineffective against the s.c. tumor. These results indicate that an antitumor drug entrapped in the membranes of small sonicated liposomes bearing antitumor monoclonal antibodies can be delivered to antigenic tumor cells and exert more efficient antitumor activity than does the free drug.
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PMID:Antitumor effect of actinomycin D entrapped in liposomes bearing subunits of tumor-specific monoclonal immunoglobulin M antibody. 661 68

Female C3H/He mice aged 10 weeks with transplanted MM46 tumor were used in an investigation of the timing of administration of immunomodulators, such as PSK (a protein-bound polysaccharide prepared from Coriolus versicolor), OK-432 (streptococcal preparation), bestatin (inhibitor of aminopeptidase B) combined with two fractionated local irradiation with the total dose of 3,000 rad. The daily dose of 250 mg/kg of PSK, 1.0 KE/mouse of OK-432, or 300 micrograms/mouse of bestatin were injected intraperitoneally for 4 consecutive days before or after irradiation. The antitumor effect was evaluated by the changes of tumor volume and survival curves. When PSK or OK-432 was administered after irradiation, tumor growth was decreased and 60-day survival rate and survival curve were significantly elongated compared with the control group and the group to which PSK or OK-432 were administered before irradiation (p less than 0.025, p less than 0.05, respectively). As for bestatin, no remarkable difference was observed irrespective of the timing of administration. These results suggested that some immunomodulators show different antitumor activity depending on the combined timing relative to radiotherapy.
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PMID:Combination therapy of radiation and immunomodulators in the treatment of MM46 tumor transplanted in C3H/He mice. 682 88

The antitumor effect of cyclophosphamide (CY) on a syngeneic mouse mammary tumor, MM46, was found to be due to selective elimination of host lymphoid cell populations as well as a direct cytotoxic effect of CY on tumor cells. marked inhibition of tumor growth after a single ip injection of CY on day 12 lasted for more than 3 weeks, unless the host was infused iv with spleen cells from tumor-bearing mice. The tumor-enhancing activity of spleen cells from tumor-bearing mice appeared to be mainly due to Thy 1.2 positive T lymphocytes and was no longer seen after CY treatment on day 12. The extent of tumor growth inhibition achieved with CY was critically dependent on the time of drug administration. CY had no antitumor effect when given before tumor inoculation. Associated with the antitumor effect of CY, augmentation of the antitumor delayed hypersensitivity reaction, or the cellular immune response, was observed. In contrast, the titer of antitumor antibody in the blood, or the humoral immune response, decreased. Cell transfer experiments showed that suppressor T cells for antitumor delayed hypersensitivity reaction specifically induced by the tumor inoculum were eliminated after CY treatment on day 12.
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PMID:Elimination of tumor-enhancing cells by cyclophosphamide and its relevance to cyclophosphamide therapy of the murine mammary tumor. 732 73


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