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)

A significant tumor damaging effect (growth inhibition) on transplanted syngeneic sarcoma in mouse was obtained by means of pH-dependent activation of a transport form of a cancerostatic drug by an enzyme foreign to the organism. This effect was achieved by combined administration of 8-0-(alpha-L-arabinofuranosyl)beta-peltatin-A as a transport form of beta-peltatin-A and the exogenous enzyme alpha-L-arabinofuranosidase from Aspergillus niger and additional increase of the acidity of the tumor by injection of glucose. The combined application of the transport form plus enzyme showed a more favorable effect on selectivity than free peltatin when a quantitative comparison was made between the tumor growth inhibition and the damage to the blood picture.
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PMID:Experiments to increase the selectivity of tumor chemotherapy by means of in vivo activation of transport forms of cancerostatics by exogenous enzymes. 2 45

The inoculation of sarcoma-37 against the background of the ganglionary blockade, provided by the intraperitoneal injection of 1 ml of pentamine, is not associated with its less take rate, but there is a manifest suppression of the tumor growth during the period up to 63 days. A preliminary ganglionary blockade completely eliminates the stimulating effect of a trauma on the tumor growth.
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PMID:[Transplantability and growth of sarcoma 37 under a ganglionic blockade]. 3 50

A steroid, 6-chloro-17-hydroxypregna-1,4,6-triene-3,20-doine (CHP) that exhibits selective activity in several models of cellular immunity including an apparent inhibitory action on the elicitation of delayed hypersensitivity, was examined in a new, simple experimental model for assessing aspects of host-cell-mediated immunological competence. This model is based upon the capacity of the adult mouse to prevent the progressive growth of tumors induced by the Moloney sarcoma virus. Two steroids reported to have immunosuppressive activity in other assay systems, namely, cortisol and progesterone, were also studied. Control mice and those injected with CHP maintained their capacity to reject the tumor. In contrast, significant numbers of mice receiving a single large injection of cortisol or progesterone succumbed to progressive tumor growth under the experimental conditions used. The data indicate that CHP, while influencing selected parameters of cellular immunity, e.g., the elicitation of delayed hypersensitivity, does not decrease the capacity of the host to mount a defense against the progressive growth of the Moloney virus-induced sarcoma. The results indicate that CHP may be useful in modulating specific aspects of cellular immunity without altering others. In addition, the experimental model described provides a simple method of assessing the possible immunosuppressive effects of naturally occurring and synthetic agents on viral-induced tumor growth.
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PMID:Selective immunosuppressive activity of steroids in mice inoculated with the Moloney Sarcoma virus (38503). 4 58

The survival time of animals, inhibition of the incorporation of thymidine-[6-3H] (3H-TdR) into DNA, and histopathological observation were made after the injection of Mitomycin-C, Bleomycin, cyclophosphamide, Daunomycin, Actinomycin-D, or 5-fluorouracil into mice transplanted with sarcoma-180 to their liver, kidney, and lung. The most prolonged survival time was obtained by the injection with cyclophosphamide and a moderate prolonged survival by Bleomycin and Actinomycin-D. In the case of 5-fluorouracil and Daunomycin, there were extreme variations in the survival time depending on the site of tumor growth. Cyclophosphamide and 5-fluorouracil showed greater and longer lasting inhibition of the incorporation of 3H-TdR into DNA of the tumor tissue, whereas the remaining agents caused transient inhibition on the tumor tissue. Inhibitory ratio and duration of the incorporation of 3H-TdR into DNA of normal site of the tissue of tumor-bearing organ were found to be more increased or almost the same compared with those of the tumor tissue. The most rapid recovery of the incorporation of 3H-TdR into DNA was observed in the small intestine among various organs and tumor in any treatment groups. From the histopathological observation, the degree of tumor cell damage by the agent was almost in agreement with inhibition of the incorporation of 3H-TdR up to 72 hr after the treatment.
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PMID:Effect of antitumor agents on sarcoma-180 tumor cells transplanted to liver, kidney, and lung. 5 69

Cell-mediated immune reactions appear to play an important role in resistance against growth of leukemia cells in mice. Possible mechanisms for in vivo protection in two tumor systems are discussed. These tumor models, which are a Friend leukemia virus-induced transplantable tumor, FBL-3, and primary murine sarcoma virus (MSV) -induced tumors, are strongly antigenic; under some conditions, tumors regress completely. In mice with regressing FBL-3 tumors, cell-mediated cytotoxicity was measured by release of [125I]iododeoxyuridine. The response was biphasic, with an initial peak at 10 days and a 2nd peak after 30 days. A boost in reactivity could be elicited by later challenge with tumor cells. All of the reactivity was dependent on T-cells, being eliminated by treatment with anti-theta plus complement. The specificity of the reactions was not completely defined, but it was consistent with Friend type-specific antigen plus broader, common antigens. In mice with regressing MSV tumors, strong cell-mediated cytotoxicity, measured mainly by release of 51Cr, was seen against RBL-5, a Rauscher virus-induced leukemia. A single peak of response occurred at about 14 days after virus inoculation. Upon later challenge with RBL-5 cells, a vigorous and rapid secondary response was elicited, mainly in the region of tumor challenge. This cytotoxic reactivity and in vivo resistance to leukemia.lso was completely dependent on T-cells. In addition, macrophage-mediated inhibition of leukemia cell growth in vitro was seen in this system at the time of peak tumor development. The 51Cr release cytotoxicity was specific and directed primarily against an antigen, MEV-SA1, associated with mouse endogenous C-type viruses. The macrophage-induced growth inhibition appeared to be nonspecific. In both the FBL-3 and MSV tumor systems, protection against tumor growth could be adoptively transferred by immune lymphoid cells. In addition to induction of cell-mediated immunity by tumor cell or virus inoculation, cell-mediated cytotoxic reactivity was found to occur naturally in most young mice. This natural killer activity was quite distinct from the experimentally elicited reactions, being mediated by N-cells, a subpopulation of lymphoid cells with no clearly identifiable cell surface markers. The natural cytotoxicity was also directed against antigenic specificities different from those recognized by the MSV-immune cells. The central issue in all of these studies has been to determine the relationships between the in vitro-detected cell-mediated reactivity and in vivo resistance to leukemia.
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PMID:Cell-mediated immunity to leukemia virus- and tumor-associated antigens in mice. 5 23

Three of 42 (7%) monkeys given aflatoxin B1 (AFB1) for longer than 2 years have developed primary malignant neoplasms of the liver. Liver biopsies performed at intervals during aflatoxin administration revealed that neoplasia was preceded by pathologic lesions of the liver, including toxic hepatitis, proliferation of pseudotubules, and hyperplastic nodules. Serum alpha-fetoprotein levels, monitored in one of the monkeys by radioimmunoassay, paralleled tumor growth and recurrence of the hepatocellular carcinoma. Normal serum alpha-fetoprotein levels were noted for a monkey with hemangioendothelial sarcoma. Our results implicate AFB1 as a liver carcinogen in monkeys and add additional support to the hypothesis that humans exposed to this substance may be at risk of developing liver cancer.
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PMID:Carcinogenicity of aflatoxin B1 in rhesus monkeys: two additional cases of primary liver cancer. 6 57

In vivo immunogenicity and in vitro species-specific membrane antigens in tumor cells treated or untreated with glutaraldehyde (GA) were studied. Two different syngeneic Syrian hamster transplantable tumor cell lines (spontaneous liver cancer and SV40-induced sarcoma) not only lost immunogenicity after GA treatment but were responsible for enhancement of test-tumor growth in immunized animals. In vitro mixed hemadsorption test used for determination of species-specific membrane antigens in Syrian hamster, green monkey and interspecies hybrid cells revealed drastic alteration of antigens on the membrane of cells treated with GA.
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PMID:Sensitivity of TSTA and species-specific cell membrane antigens of tumor cells to glutaraldehyde treatment. 9 20

The tubulin-binding affinities of podophyllotoxin and 12 related compounds have been compared with the effectiveness of these drugs in three assays of antitumor activity: (1) The mastocytoma assay of inhibited tumor cell growth in vitro; (2) the 37 sarcoma assay of tumor remission in vivo; and (3) the Stentor regeneration inhibition assay which detects a requirement for microtubule polymerization. The results indicate that there is a positive Spearman rank correlation coefficient between the inhibition constant for the binding of colchicine to tubulin in the presence of these compounds and the effectiveness of the compounds in the three assays of tumor growth inhibition. It is suggested that tubulin-binding assays may be a useful step in the screening of podophyllotoxin-like compounds suspected of disrupting mitosis by binding to microtubule protein.
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PMID:Correlation of tubulin-binding and antitumor activities of podophyllotoxin analogs. 10 3

Effect of PS-K on tumor growth and antibody production was studied in inbred C57BL/6, SL, C3H/He, and AKR mice, and in colony-bred ICR mice. (1) PS-K exhibited antitumor activity on sarcoma-180 in ICR mice, but not in AKR mice. Growth of sarcoma-180 was suppressed to the intermediate extent in other strains. (2) In ICR strain, antibody production against trinitrophenyl was depressed in mice bearing sarcoma-180 and restored by PS-K. In AKR mice, on the other hand, antibody production was not depressed in tumor-bearing state and was not augmented by PS-K. Other strains showed intermediate degrees of suppression of antibody-producing capacity by sarcoma-180 and its restoration by PS-K.CR strain, the growth of Ehrlich tumor as the challenge tumor was enhanced in mice bearing sarcoma-180 as compared to that in controls. After the treatment with PS-K in this strain, however, not only the growth of sarcoma-180 but also of Ehrlich tumor was inhibited completely. On the other hand, the growth of Ehrlich tumor in AKR strain was neither enhanced in mice bearing sarcoma-180 nor inhibited by PS-K.
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PMID:Mouse strain difference in the expression of antitumor activity of PS-K. 13 29

N-Methyl-N-beta-chloroethyl-hydrazine and its benzaldehydhydrazone are two new cytostatic methylhydrazines. Administered intraperitoneally, they are more effective in inhibiting the ascites tumor growth (Ehrlich's carcinoma in mice and Yoshida sarcoma in rats) than procarbazine in vitro as well as in vivo. The intraperitoneal administration of hydrazone shows a minor effect on the solid tumor. This may be explained by a different pharmacocinetical behaviour. Hydrazone is less toxic than procarbazine.
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PMID:[On the cytosic action of N-methyl-N-beta-chloraethyl-hydrazine and its benzaldehydhydrazone (author's transl)]. 13 85


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