Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

The mechanism of enhancement of Bleomycin A5 antitumor activity by verapamil was explored by flow cytometry and tracing the radiolabelled bleomycin A5 in vivo. Verapamil was found to increase the G2 blocking effect of bleomycin A5 prominently in mouse S-180 and human HEP-2 cell lines. The distribution of 57Co-bleomycin A5 in mice bearing S-180 sarcoma was changed by verapamil and accumulation of the drug in tumor was increased. In contrast, the labelled drug in the lung was decreased. It seems that the effects of verapamil in enhancing the antitumor activity of bleomycin A5 are to increase the accumulation of the drug in tumor cells and enhance the G2 blocking effect of the drug in cell cycle.
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PMID:[Mechanism of enhancement of bleomycin A5 antitumor activity by verapamil]. 171 40

The aim of this work was to compare the distribution in organs of syngeneic mice sarcoma JWS and leukemia L-1210 cells previously labelled with sodium dichromate (Na2 51CrO4) and iododeoxyuridine (125IUDR) after i.v. transplantation. Also, the results obtained with both labels were compared. Both kinds of cells under study are trapped in lungs, but the number of trapped JWS cells is greater. L-1210 cells probably recirculate. The cells undergo extensive destruction during the first 3 days after transplantation. This kind of study requires the use of two markers: cytoplasmic and nuclear and careful analysis of radioactivity changes is also required to obtain proper conclusions.
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PMID:[Kinetics and distribution of transplanted sarcoma JWS and leukemia L1210 cells by intravenous route]. 182 78

The distribution of neoplastic--JWS sarcoma and lymphatic leukemia L-1210 cells after intravenous injection into allogeneic recipients is presented. Cells were labelled with two labels: cytoplasmic (sodium chromate-51CR) and nuclear (iododeoxyuridine-125IUDR). Radioactivity of blood, lungs, liver, spleen and kidneys was measured 90 minutes and 24 hours after cell transplantation. The pattern of cell trapping, destruction and elimination from the circulation was characteristic of cell line injected. Destruction and elimination processed faster in allogeneic system than in syngeneic one.
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PMID:[Distribution and elimination of transplanted sarcoma JWS and leukemia L1210 cells in allogeneic recipients--inbred C57BL mice by intravenous route]. 182 79

A panel of seven murine monoclonal antibodies reactive with human hepatocellular carcinoma (HCC) cell line, SK- HEP-1, resulted in the definition of four distinct antigen systems, designated HB4, HB5, HB1 and HJ2. HB4 antigen was found to be expressed specifically on HCC cell lines and fresh HCC specimens but not on normal liver. Immunoprecipitation tests suggest that the HB4 epitope may be a heat-stable carbohydrate determinant on a high molecular mass molecule. HB5 antigen was found to have less-restricted expression on a panel of normal adult tissues and on melanoma, astrocytoma, sarcoma, neuroblastoma and epithelial cancer cell lines. In fetal and adult liver, HB5 antigen localized to bile canaliculi and ducts. Under reducing conditions, three mAbs detected a Mr 140,000 glycoprotein using lysates of [125-I], [3-H]-glucosamine and [35-S]-methionine labeled SK-HEP-1 cells. Under non-reducing conditions an additional component of greater than Mr 200,000 was also detected. HB1 antigen was found on almost all monolayer cell lines and not on most cultured suspension cells. This antigen was also detected on cultured HCC cells inoculated into nu/nu mice. Immunoprecipitation experiments revealed that the HB1 antigen is a bimolecular complex with an Mr 170,000 alpha chain and Mr 130,000 beta chain under non-reducing conditions, and three subunits of Mr 140,000, Mr 30,000 and Mr 130,000 under reducing conditions. Two antibodies reacted with epitopes on the alpha chain. HJ2 antigenic determinant is a heat-stable component which could not be immunoprecipitated. This most widely expressed antigen was found in secreted form in many of the cells and tissues examined. These antibodies introduce new antigens which may serve as useful markers for the diagnosis, classification and investigation of HCC and other liver diseases.
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PMID:Serological analysis and biochemical characterization of monoclonal antibodies defining antigens of human hepatocellular carcinoma. 255 3

The interaction between cellular factors and polyoma virus (Py) DNA was investigated by using a gel retention assay. Nuclear extracts from various cell lines (NIH 3T3, NIH 3T6, LTK-, F9) contained proteins that formed specific and distinct complexes with Py B enhancer fragments of either wild-type or F9-1 mutant origin. The presence of an excess amount of other well-characterized DNA sequences, including the Py A enhancer, the murine sarcoma virus enhancer, and the simian virus 40 enhancer-promoter region, did not interfere with this protein-DNA interaction. However, a fragment previously defined as containing the lymphotropic papovavirus enhancer shares the binding of some common factor. This observation, in combination with the results of retention gel assays at different Mg2+ concentrations, indicates the interaction of several nuclear factors and Py DNA. The assay systems that were used allowed a distinction between some factors on the basis of their different biochemical and sequence requirements. The contact sites of these complexes were mapped to the B enhancer region of Py with Bal 31-derived mutant restriction fragments and ExoIII nuclease and are compatible with the functional domains determined in vivo.
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PMID:Interaction of distinct nuclear proteins with sequences controlling the expression of polyomavirus early genes. 302 89

C-type particles produced by a tissue culture-adapted BALB/c myeloma were characterized. It was determined that although the particles were morphologically and antigenically similar to murine leukemia and sarcoma virus, the size of their RNA was different, they lacked RNA-dependent DNA polymerase, they were unstable in NET buffer, sucrose and citrate but were stable in glycerol and Earle balanced salt solution, and they behaved differently from oncornaviruses when treated with ether and detergent.
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PMID:Characterization of C-type particles produced by a tissue culture-adapted murine myeloma. 412 86

Harvey and Kirsten murine sarcoma viruses have previously been shown to transform fibroblastic cells in culture, and type C virus pseudotypes of these viruses cause erythroleukemia in susceptible mice. We report a cell culture assay for quantitating the growth-promoting effect of Harvey and Kirsten viruses on erythroid cells. Murine hemopoietic cells were infected in vitro with Harvey or Kirsten sarcoma virus, and then cultured in methylcellulose in the presence of relatively low concentrations of erythropoietin. Under these conditions, large colonies of erythroid cells form in the semi-solid culture media 6 to 8 days after infection. The induction of erythroid bursts was not caused by the murine type C helper viruses used to pseudotype either Ha-MuSV or Ki-MuSV, or by media from cells carrying the Ki-MuSV and Ha-MuSV genomes. Induction of the erythroid colonies is under genetic control at the Fv1 susceptibility locus, but not at the Fv2 susceptibility locus. A striking feature of the erythroid colonies induced by the Harvey and Kirsten viruses was that they not only proliferated to large size but also differentiated along the erythroid lineage and synthesized hemoglobin. The results indicate that Ha-MuSV and Ki-MuSV can induce proliferation of erythroid precursor cells apparently without interfering with the differentiation program of the cells. The relation between the growth-promotion effect of these viruses on erythroid precursor cells and their ability to induce erythroleukemia is discussed.
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PMID:Harvey and Kirsten sarcoma viruses promote the growth and differentiation of erythroid precursor cells in vitro. 627 11

Several angiogenic preparations that have been shown to stimulate plasminogen activator (PA) and collagenase production by cultured bovine capillary endothelial (BCE) cells were tested for their ability to stimulate BCE cell motility in the phagokinetic track assay. Bovine retinal extract, medium conditioned by 3T3-F442A differentiated mouse adipocytes, SK HEP-1 human hepatoma cell lysate, mouse sarcoma 180 cell lysate, and medium conditioned by mouse sarcoma 180 cells stimulated motility 68.7%, 48.5%, 140.9%, 56.5%, and 102.1%, respectively, relative to untreated cells. The motility-stimulating activity of these preparations was dose dependent and linear over the 16-h assay period. Several hormones and growth factors were tested for BCE cell motility-stimulating activity, including insulin, vasopressin, fibroblast growth factor, and a partially purified preparation of sarcoma growth factor, and were found to be ineffective. 12-0-tetradecanoyl-phorbol-acetate (TPA), a potent stimulator of both PA and collagenase activities in BCE cells, also did not stimulate motility, indicating that protease production is not sufficient to stimulate BCE cell motility in this assay. Neither SK HEP-1 hepatoma cell lysate nor TPA was effective in stimulating motility in bovine aortic endothelial (BAE) cells. The inability of SK HEP-1 hepatoma cell lysate to stimulate movement in BAE cells is consistent with the observation that angiogenesis occurs by sprouting of capillaries, not large vessels.
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PMID:Stimulation of motility in cultured bovine capillary endothelial cells by angiogenic preparations. 632 76


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