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T Kataoka

Publications and source records attributed to T Kataoka.

At least 253 records · Page 14Linked to original sources
PubMed1984

Antitumor activity of deoxyribonucleic acid fraction from Mycobacterium bovis BCG. I. Isolation, physicochemical characterization, and antitumor activity.

A fraction extracted from Mycobacterium bovis strain BCG, which was composed of 70.0% DNA, 28.0% RNA, 1.3% protein, 0.20% glucose, and 0.1% lipid and of no detectable amounts of cell wall components such as alpha, epsilon-diaminopimelic acid and hexosamine, was found to possess strong antitumor activity. Repeated intralesional injection of this fraction, designated MY-1, without attachment to oil or a single intralesional injection of MY-1 emulsified in mineral oil caused the IMC carcinoma of CDF1 mice and line 10 tumor of strain 2 guinea pigs to regress and/or prevented metastasis very effectively. MY-1 after digestion with RNase, which contained 97.0% single-stranded DNA with a guanine-cytosine content of 69.8%, was more effective than undigested MY-1 against IMC and line 10 tumor, while MY-1 digested with DNase, which contained 97.0% RNA, had reduced activity, suggesting that the DNA from BCG possessed strong antitumor activity under certain conditions. Details of the extraction procedures and physicochemical characterization of MY-1 were also described.

Animals↗
PubMed1984

Relative contribution of antiproliferative and host immunity-associated activity of mouse interferon in murine tumor therapy.

Administration of mouse interferon (IFN; 0.5 to 1 X 10(7) reference units/mg protein) inhibited the growth of Meth A and Meth 1 fibrosarcomas, but to a lesser extent, if at all, the growth of Colon 26 adenocarcinoma in BALB/c mice. The in vitro IFN sensitivity of these three tumors was not consistent with the in vivo therapeutic response in mice bearing these tumors under the present experimental conditions; Colon 26, the most sensitive of the three tumors in the in vitro antiproliferation test, did not respond or responded most poorly to IFN therapy; furthermore, Meth A and Meth 1 tumors responded similarly well to IFN therapy, although there was about a 100-fold difference in their in vitro IFN sensitivity. These results as well as the kinetic analysis of IFN concentrations of the serum of Meth A- or Colon 26-bearing mice did not indicate that the antiproliferative activity of IFN was solely responsible for its in vivo therapeutic effect. In contrast, abrogation of T-cell immunity by alpha mouse thymocyte globulin completely nullified the IFN-dependent therapeutic effect in Meth A-bearing mice. Furthermore, the IFN-dependent therapeutic response in Meth A tumors was much weaker in T-cell-defective BALB/c (nu/nu) mice than that in immunologically competent BALB/c (+/+) mice and was marginal, if present at all, confirming that T-cell immunity was involved in the IFN-dependent therapeutic effect and suggesting that the antiproliferative activity of IFN may only be responsible to a small extent for the therapeutic effect.

Animals↗
PubMed1984

6-Mercaptopurine-induced potentiation of active immunotherapy in L1210-bearing mice treated with concanavalin A-bound leukemia cell vaccine.

While the combination of L1210 murine leukemia cell vaccine (L1210 vaccine) with 6-mercaptopurine (6-MP) or 6-thioguanine produces a therapeutic response greater than that induced by either of these agents alone, its combination with cyclophosphamide, N4-behenoyl-1-beta-D-arabinofuranosylcytosine, or 5-fluorouracil does not produce such a response. The administration of cyclophosphamide, N4-behenoyl-1-beta-D-arabinofuranosylcytosine, or 5-fluorouracil alone resulted in a response as great as, or greater than, that induced by 6-MP alone. This and the finding that the 6-MP-induced response was more pronounced upon its delayed rather than its early administration indicate that 6-MP-induced reduction of the tumor burden does not explain this augmentation. The combination of 6-MP and L1210 vaccine was not effective in mice bearing 6-MP-resistant L1210 leukemia; however, an augmented response occurred when the tumor burden was reduced by N4-behenoyl-1-beta-D-arabinofuranosylcytosine, indicating that reduction of the tumor burden by 6-MP was only partially associated with augmentation of the therapeutic response. Augmentation was associated with vaccine-induced antitumor immunity because it was induced by the combination of 6-MP and concanavalin A-bound, but not concanavalin A-free L1210 vaccine. This augmentation was dependent on the timing of the L1210 vaccine administration. The combination was not effective in mice bearing P388 leukemia, indicating the tumor specificity of the augmentation. These results show that 6-MP not only reduced the tumor burden but also potentiated the vaccine-dependent antitumor immunity, resulting in the induction of an augmented therapeutic response.

Animals↗
PubMed1984

Enhancement of antiproliferation activity of vincristine and adriamycin by interferon.

Vincristine (VCR) combined with interferon (IFN)-beta suppressed H.Ep #2 cell proliferation more than additively, whereas 6-mercaptopurine combined with IFN-beta suppressed it less than additively. Factors associated with the more-than-additive effect were examined. The enhanced antiproliferation was achieved in HeLa cells as well as H.Ep #2 cells but not in Daudi or M-14 cells, indicating cell dependency of the enhancement. This enhancement was not dependent on the IFN species, including IFN-beta, IFN-alpha (leukocyte), and IFN-alpha (lymphoblastoid), although the cells were variably sensitive to these IFN species. In contrast, the enhance antiproliferation was critically dependent on the species of antineoplastic agents, and was selective to VCR and adriamycin among those tested under the present experimental conditions. The sequential exposure of H.Ep #2 cells to IFN and VCR induced the enhancement but exposure to VCR followed by IFN did not, suggesting that IFN-induced cell modification made the cells more sensitive to VCR. Either IFN or VCR was successfully replaced by colchicine, an antimicrotubule agent, but not by cytochalasin D, an antimicrofilament agent, suggesting the involvement of microtubule modification in the enhanced antiproliferation observed with IFN and VCR.

Cell Division↗
PubMed1983

Mechanism of the antitumor activity of 5,5'-bis(2'-tetrahydropyranyl) secalonic acid D against Meth-A.

The mechanism of the antitumor activity of 5,5'-bis(2'-tetrahydropyranyl) secalonic acid D (PSA) was examined in Balb/c mice bearing Meth-A fibrosarcoma. IP-injected PSA showed remarkable antitumor activity against IP-implanted Meth-A tumor. Antitumor activity of PSA was not abolished by treatment with silica as an antimacrophage agent or anti-asialo GM1 antiserum that selectively eliminates natural killer cells. Although it was significantly suppressed by treatment with antithymocyte globulin in Balb/c mice, PSA was effective against Meth-A tumors implanted in athymic Balb/c mice. PSA inhibited in vitro Meth-A proliferation as effectively as mitomycin C and was not effective against Meth-A tumor implanted SC at a site where direct contact of PSA and Meth-A cells was unlikely. These results suggest that the antitumor activity of PSA was mainly achieved by inhibiting Meth-A cell proliferation, although the host T cell-mediated immunity was partly involved in the eventual therapeutic efficacy of PSA.

Animals↗
PubMed1983

Effect of experimental anaemia on red cell GSH and enzyme activities in guinea-pig and rabbit.

1. The effect of experimental anaemia on red cell GSH and enzyme activities of GSH-Px, GSSG-R and G6PD was investigated in guinea-pig and rabbit. 2. The anaemia was induced by injection of PHH in guinea-pig and rabbit and also by bleeding in guinea-pig. 3. Red cell GSH increased from 115.5 to 141.8 mg/dl RBC in the guinea-pig and from 108.5 to 133.5 mg/dl RBC in the rabbit during anaemia. 4. There were significant rises in the level of all the three enzymes activities in both the species of animals. However, the changes in rabbit were more pronounced than in the guinea-pig.

Anemia↗
PubMed1983

Escherichia coli extract-catalyzed recombination in switch regions of mouse immunoglobulin genes.

We have shown that Escherichia coli extracts catalyze recombination between mouse immunoglobulin mu and alpha genes inserted separately in lambda phage vectors carrying different genetic markers. Most of the recombination sites in the inserts are located in the switch regions of the heavy chain genes, as previously found in the expressed genes of myeloma cells. The recombination took place at relatively high frequency (10(-4)). The recombinational system in E. coli or lambda phage seems to prefer short nucleotide sequences similar to those used in the class switch recombination.

Animals↗
PubMed1983

Absence of detectable cytotoxic lymphocytes in the spleens of guinea pigs immunized with allogeneic cells.

Using inbred guinea pigs of strains JY 1, JY 2, 2 and 13, whose major histocompatibility gene complexes are different from each other at the B region and/or the I region, the authors aimed to detect cytotoxic thymus-derived lymphocytes (CTL) against allogeneic target cells. Various in vivo and in vitro sensitization methods that have been described for murine CTL systems were used. For detection of CTL, Con A- or PHA-induced 51Cr-labeled lymphoblasts were incubated with sensitized spleen cells or lymph node cells for 4 hr, and 51Cr released into the supernatant was assayed. Under these conditions, no significant lysis of the target cells was observed. On the other hand, significant levels of both delayed-type hypersensitivity and humoral antibodies were detected in the animals sensitized by in vivo methods.

Animals↗
PubMed1983

[Preclinical analysis of antitumor activity of interferon].

The present study reviewed preclinical informations of antitumor activity of interferon and discussed on its possible mechanism. In the literature we found not much information of in vivo antitumor potency of interferon. This urged us to analyze and evaluate in vitro biological activities of interferon in association with possible in vivo antitumor activity. A number of in vitro studies showed immunomodulating potency of interferon. However, we did not find sound basis for claiming any of them involved in in vivo antitumor effect of interferon. Instead, direct interaction of interferon with tumor cells was considered more likely involved in interferon-induced in vivo antitumor effect by suppressing tumor cell proliferation.

Adjuvants, Immunologic↗