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

Immediate and delayed effects of nitrogen mustard (HN2) (0.1 mg/kg/day for 4 days) on the growth and cell proliferation patterns of the 3-methylcholanthrene-induced autogenous rat sarcoma were studied. Tumor cells were labeled continuously with 0.5 muCi tritiated thymidine/g for 24 hours. The labeling index fell from 36.4 to 14.0% and the mitotic index from 0.88 to 0.67% after two treatments with HN2. At that time, tumor growth stopped and remained arrested during HN2 administration. After four injections of HN2, the labeling index was reduced further to 0.73% and the mitotic index to 0.36%. After the drug was withdrawn, tumor growth resumed at the pretreatment rate, even though the labeling index on day 3 was only 15.5% (or 40% of the control). The percent labeled mitosis curves and DNA contents, before and 4 days after HN2 was given, were similar. It was concluded that a subpopulation of cells of predominantly short intermitotic times caused tumor growth before and after drug treatment.
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PMID:Growth and regrowth of an autogenous rat sarcoma: effects of nitrogen mustard. 115 48

Twenty-seven new derivatives of the 3-N,N-bis-(2-chlorethyl)-amino-4-methyl-benzoic-acid were synthesized and pharmacologically examined. The compounds showed to be highly active in the in vitro-vivo screening models (Crocker sarcoma 180, Sa-180; Friend virus leukemia, FVL) but less active in the in vivo screening models (leukemia L-1210; L-1210; Nemeth-Kellner lympho-sarcoma, NKL). The in vivo tumor growth inhibitions show that this class of compounds has possibilities for further improvement.
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PMID:[Aromatic N-mustard compounds. 1. Derivatives of 3-N, N-bis-(2-chlorethyl)amino-4-methylbenzoid acid]. 117 61

Levamisole and tetramisole had no antitumor effect against the following transplantable syngeneic murine tumors: L1210 leukemia, P388 leukemia, B16 melanoma, Madison 109 lung tumor, and Lewis lung carcinoma. In the Lewis lung carcinoma system there was no effect on primary tumor growth, metastasis, or survival. Tetramisole had a variable effect on the growth of rhabdomyosarcomas and the survival of BALB/c mice following intramuscular inoculation of Moloney sarcoma virus. In two experiments treatment with tetramisole either prior to or following inoculation of Moloney sarcoma virus increased the number of mice with tumor regression as opposed to progressive tumor growth, incrneased the number of long-term survivors, and prolonged the lifespan of mice that died of tumor. In two further tests neither levamisole nor tetramisole had an effect in this system. In mice immunosuppressed with cyclophosphamide prior to virus inoculation, there was not effect of treatment with levamisole or tetramisole.
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PMID:Effects of levamisole (NSC-177023) and tetramisole (NSC-102063) in experimental tumor systems. 117 64

The experimental treatment of a rat sarcoma (McFiFi 2) by intratumoral injection of BCG2 is described. Tumors which have a mean diameter of less than 10 mm at the beginning of treatment are fully susceptible to BCG, although spontaneous regression is not observed at this stage. The effective dose of living BCG ranges from two injections of 0.1 mg to two injections of 1 mg, given IT at an interval of 7 days. The permanent cure of a proporation of the tumors may also be induced by IT injection of a similar dose of heat-killed BCG or of MER, or of 10(9) heat-killed C. parvum, according to the same schedule. Preimmunization of the rats with living BCG does not improve the efficiency of heat-killed BCG. Direct contact between the therapeutic material and the tumor cells is critical. If rats are grafted with two pieces of the same tumor in widely separated sites, the intratumoral treatment of only one of these tumors with living BCG is sufficient to induce regression of both tumors in 50% of the animals. The effect of BCG is counteracted by injection of silica or by ingestion of polaramine. The same intratumoral treatment with living BCG was applied to different rat and mouse tumors. Only McFiFi 2 tumors were cured by intralesional BCG. C3H mouse plasmocytoma 5563 was not cured by intratumoral BCG but its growth could be prevented by mixing BCG and tumor cells at the time of grafting; this tumor was considered to be of medium susceptibility. However, until there is definite proof that the two mechanisms are identical, one should consider the regression and cure of a growing tumor, and the prevention of tumor growth, as two different phenomena. The clinical treatment of human tumors resembles the first experimental procedure more closely than the second.
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PMID:Therapeutic effect of intratumoral injection of bcg and other substances in rats and mice. 117 5

PS-K, a protein-bound polysaccharide from a basidiomycetes, was found to suppress tumor growth after grafting of sarcoma-180 or Ehrlich tumor in ICR mice. In the present study, effect of PS-K on antibody-forming capacities was examined in tumor-bearing mice and normal controls. 1) PS-K did not enhance the capacities of normal mice to produce antibodies against sheep erythrocytes (SRBC), hamster erythrocytes (HRBC), and trinitrophenyl group (TNP). 2) The capacities of mice to produce IgG antibody against SRBC, IgM antibody aganist HRBC, and IgG antibody against TNP were depressed after grafting of sarcoma-180. Intraperitoneal injection of PS-K restored these capacities to the normal levels. 3) Oral as well as intraperitoneal administration of PS-K restored the capacity of the mice bearing sarcoma-180 to produce IgG antibody against SRBC. 4) The capacity to produce IgG antibody against SRBC was depressed after grafting of Ehrlick tumor and it recovered to the normal level after intraperitoneal injection of PS-K. These results showed that antibody-fforming capacity of mice was depressed after tumor grafing and recovered after administration of PS-K.
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PMID:Restoration of antibody-forming capacities by PS-K in tumor-bearing mice. 118 73

Lymphokines such as migration inhibitory factor and type II interferon were released into the circulation of tuberculin-sensitive mice after iv injection of old tuberculin. Daily administration of such sera into the tumor sites of mice given implants of sarcoma MC-36 markedly suppressed tumor growth.
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PMID:Tumor suppression by a lymphokine released into the circulation of mice with delayed hypersensitivity. 120 52

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

Spleen cells from mice bearing primary tumours induced by Moloney strain of murine sarcoma virus (M-MuSV) strongly inhibited the in vitro generation of specific secondary cell-mediated cytotoxic response of spleen cells from M-MusV regressor mice. These suppressor cells were resistant to treatment with anti-theta serum and complement or to X-irradiation. It appeared that suppressor cells may have had a role in limiting the host's immune response against tumor growth.
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PMID:Inhibition of cell-mediated cytotoxicity against tumor-associated antigens by suppressor cells from tumor-bearing mice. 125 3

A bioassay is described for the quantitation of tumor cells in blood specimens in a syngeneic mouse tumor system (Sarcoma 1 in A/J mice). The procedure involved i.m. injection of blood containing tumor cells into each thigh of normal recipient mice and, 14 days later, examination of the sites of injection for evidence of tumor growth. For each specimen, a tumor index was calculated based on the number of tumor takes and the size of the tumors. The number of tumor cells was determined by comparison with tumor indices from standard specimens with known number of tumor cells. Optimal conditions for this assay were investigated. We have used this bioassay to quantitate tumor cells in the venous blood of tumor-bearing animals under various treatments and manipulations. At the same time, the incidence of regional node metastasis was obtained by direct histological examination. Surgical removal of a well-established primary tumor enhanced the dissemination of the tumor, as evidenced by an increased incidence in regional node metastasis and an increase in the number of tumor cells reaching the venous circulation. Similar results were obtained when the tumor-bearing feet were ligated to produce ischemia of the primary tumor. Repeated physical trauma to the primary tumor resulted in increased dissemination of tumor cells into the venous circulation, but it did not increase the incidence of regional node metastasis. Immunosuppression of the tumor-bearing animals increased the dissemination of tumor cells, whereas immunostimulation decreased the dissemination.
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PMID:Bioassay for quantitating circulating tumor cells in a syngeneic mouse tumor system. 126 58

Studies of peculiarities of acetylation with the use of sulfadimidine showed the distribution of female white non-bred mice into two groups - with high and low activity. In C3H/He mice a relatively high activity of sulfadimidine acetylation was observed, while in C57BL/He mice a low activity of acetylation was noted. The growth of transplanted melanoma B-16 in C57BL/He mice and sarcoma 37 and sarcoma 180 in non-bred mice resulted in an increased activity of sulfadimidine acetylation. The use of w-sodium methylpantothenate (an antagonist of pantothenic acid) failed to show an increased activity of sulfadimidine acetylation and inhibited the tumor growth.
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PMID:[Acetylation reaction in mice in the normal state and in tumors]. 127 65


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