1,721,054 research outputs found
Humoral and cellular immunoresponse of mice treated with pyrazole-carboxamide-4-amino (PCA).
[The pharmacologic activity of 1(2-(p-chloro-alpha-phenylbenzyloxy)ethyl)piperidine (cloperastine)]
Adoptive immunotherapy in BALB-c times DBA-2 Cr F1 mice bearing an immunogenic subline of L1210 leukemia
That treatment with 5 (3,3 dimethyl 1 triazeno) imidazole 4 carboxamide (DIC) in vivo may have induced new antigen(s) on L1210/Ha leukemic cells is supported by the finding of spleen cells in sensitized mice that are specifically immune to the DIC treated L1210/Ha leukemia (L1210/Ha/DIC). An infusion of immune spleen cells 'cured' immunosuppressed BALB/c x DBA/2 Cr F1 mice bearing the L1210/Ha/DIC leukemia and did not exhibit any therapeutic activity in mice bearing 106 cells of the parental L1210/Ha leukemia. Spleen cells that are immune to syngeneic or allogeneic tumor cells did not protect the mice challenged with 106 L1210/Ha/DIC cells. The therapeutic activity of immune spleen cells is increased as the number of cells is increased. The extent of activity was influenced by the size of the tumor inoculum, the time of lymphocyte transfusion following inoculation of viable leukemia, and the amount of sensitizing antigen. Adoptive immunotherapy using L1210/Ha cells with increased immunogenicity resulting from in vivo DIC treatment provides a potential approach for experimental cancer therapy
Immunological and cytogenetic characterization of lymphocitic mouse leukemias after treatment with antineoplastic drugs
New antigenic specificities, not detectable on parental cells and transmissible after the drug withdrawal, have been induced in mouse lymphomas by a treatment with antineoplastic agents. Some surface properties and chromosome analysis of drug-altered cells have been studied
Adoptive immunity in mice challenged with L1210/DTIC clones
New antigenic specificities, not detectable on parental cells, have been induced by many investigators in mouse lymphomas by treatment with the antitumor agent 5(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC). The antigens are transmissible, after withdrawal of the drug treatment, as an inheritable character. The mechanism of induction, the molecular nature, and the number of the new antigenic specificities have not been completely elucidated. Four clones from murine leukemia L1210 isolated and expanded in vitro were treated in vivo with DTIC and the new sublines were studied in detail. The four drug-treated sublines studied exhibited strong immunogenicity since they were rejected by syngeneic animals. Immunosuppressed animals challenged with 10(7) A/DTIC or P/DTIC cells were reciprocally protected by the adoptive transfer of spleen cells from donors that had rejected a lethal challenge of A/DTIC or P/DTIC clone. In a similar fashion, the adoptive transfer of spleen cells obtained from animals that had rejected the Q/DTIC or the R/DTIC clones protected immunosuppressed mice challenged with Q/DTIC or R/DTIC cells. No antitumor activity was observed in cross-protective schedules other than those indicated. It was been concluded that (a) the L1210 leukemia line does not have antigenic cells, (b) four DTIC-treated clone sublines were rejected by compatible hosts, and (c) two mutually exclusive sets of antigens were expressed in four antigenic clone sublines
Macrophage antitumor activity induced by the antigenic lymphoma L5178Y/DTIC subline
Murine leukemic cells, after in vivo treatment with antineoplastic drugs, have been shown to express new antigenic specificities that were not detectable on parental cells and that were heritable after the withdrawal of drug treatment. A study was conducted of macrophage antitumor activity triggered by LY/DTIC cells, a subline of LY murine lymphoma, antigenically altered by the drug DTIC. In vitro non-specific inhibition of tumor cell growth was exhibited by spleen and peritoneal macrophages from mice previously challenged with viable LY/DTIC. Peritoneal macrophages from LY/DTIC immune animals showed moderate, although significant lytic activity against unrelated tumor target cells. Supernatants from mixed lymphocyte-tumor cell cultures, in which LY/DTIC immune lymphocytes and LY/DTIC tumor cells had been cultured, rendered normal macrophages non-specifically growth inhibitory for tumor cells
Time-resolved fluorescence spectroscopy of hematoporphyrin derivatives and disulfonated aluminum phthalocyanine incorporated in vivo in a murine ascitic tumor
Evaluation of growth fractions with monoclonal antibodies to human alpha-DNA polymerase.
We have established and partially characterized a panel of monoclonal antibodies against alpha-DNA polymerase. One of the hybridomas, clone 5F, has been exploited for cell kinetic studies on three colon cancer cell lines, LOVO, SW 620, and SW 403, which are endowed with different growth patterns and differentiation status. By an immunoperoxidase method, we could demonstrate the specific intranuclear localization of alpha-DNA polymerase during the exponential phase of in vitro growth and contrast it with the diffuse distribution of the enzyme throughout the cytoplasm during the resting state. The percentage of intranuclear staining positive cells, evaluated at successive time points of in vitro growth, changed from 75 to 95\% (assayed on Days 3 and 7) to 15 to 25\% in confluent and resting populations assayed on Days 12 to 14. In agreement with the assumption that the enzyme moves from nucleus to cytoplasm after entering quiescence, alpha-DNA polymerase was still present in the cytoplasm or in the cytoplasmic perinuclear area of cells in resting phase cultures. Comparisons between traditional kinetic parameters (thymidine labeling index and primer-dependent alpha-DNA polymerase) and proliferative state determined by the monoclonal antibody supported the feasibility of this approach to define the proportion of actively proliferating elements in a tumor cell population. Moreover, parallel flow cytometric analysis performed on Days 5 and 14 of continuous culture showed fluctuations of alpha-DNA polymerase content in relation to exponential and steady-state phases, with a significant increase in the amount of alpha-DNA polymerase in actively proliferating populations and a progressive reduction of the enzyme as the cultures entered the resting stage
Chemotherapy and immunotherapy of L1210 leukemic mice with antigenic tumor sublines
Tumor cells, treated in vivo with anticancer compounds, may acquire new antigenic specificities in addition to any original antigens associated with parental tumors. Treatment of mice carrying the parental leukemias L1210 Ha or L1210 Cr with leukemia cells antigenically altered by treatment with 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (L1210 Ha/DTIC and L1210 Cr/DTIC, respectively) was essentially ineffective in prolonging the life span of the animals. However, synergic therapeutic activity was exhibited by administration of L1210 Ha/DTIC cells plus 1,3-bis(2-chloroethyl)-1-nitrosourea in the treatment of the moderately immunogenic L1210 Ha leukemia and by the combination of L1210 Cr/DTIC cells and lymphocytes immune to L1210 Cr/DTIC administered with 1,3-lymphocytes immune to L1210 Cr/DTIC administered with 1,3-bis(2-chloroethyl)-1-nitrosourea in the treatment of the low immunogenic L1210 Cr leukemia. Early and advanced L1210 Cr-bearing mice showed marked increases in survival time and a significant number of tumor-free survivors on treatment with cyclophosphamide followed by transfer of lymphocytes immune to L1210 Cr/DTIC cells. When parental tumor cells were used as the immunogen, the therapeutic effect was diminished. Thus, in the current investigation, although immunotherapy per se was essentially ineffective, the immunochemotherapeutic modalities used were successful in markedly increasing the survival time of leukemic animals and resulted in an incidence of cures
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