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Biomedical subjects

S Sone

Publications and source records attributed to S Sone.

At least 379 records · Page 21Linked to original sources
PubMed1986

[A phase II study of UFT in non-small cell lung cancer].

A phase II evaluation of UFT, a mixture of tegafur and uracil, was performed in 13 patients with non-small cell lung cancer (eight patients with adenocarcinoma and five patients with squamous cell carcinoma). UFT at a dose of 600 mg was given per os every day for more than four weeks. Among 12 evaluable patients, one patient with adenocarcinoma of the lung showed partial response. The response rate for UFT was 8.3%. Toxic effects included anorexia (31%), nausea (15%), liver disorder (15%), and pigmentation (8%).

Adenocarcinoma↗
PubMed1986

[Phase II study of bronchial artery infusion of mitomycin C in non-small cell lung cancer].

A phase II study of bronchial artery infusion of mitomycin C (MMC) was performed in 14 patients with non-small cell lung cancer (6 patients with adenocarcinoma, 6 patients with squamous cell carcinoma and 2 patients with large cell carcinoma). MMC at a dose of 20 mg was infused into the bronchial artery (total dose 20-60 mg, mean 27 mg). Among the 14 patients, one with adenocarcinoma of the lung showed partial response. The response rate for bronchial artery infusion of MMC was thus 7.1%. The toxic effects included anemia (35.7%), leukopenia (28.6%), thrombopenia (14.3%), elevation of GPT (14.3%), anorexia (14.3%), nausea (7.1%) and eruption (7.1%).

Adult↗
PubMed1986

[Induction of tumoricidal properties in human monocytes by synergism between interferon-gamma and liposome-entrapped muramyl tripeptide].

Human blood monocytes from healthy volunteers, separated by centrifugal elutriation, were not cytotoxic to allogeneic A 375 melanoma cells. The monocytes were rendered tumoricidal by incubation for 24 h with natural interferon-alpha and beta or recombinant interferon-alpha A and alpha A/D (more than 100 U/ml) or with interferon-gamma (more than 1 U/ml). Liposome-MTP-PE at concentrations of more than 50 nmol/ml also induced tumoricidal activity of monocytes. When a combination of subthreshold concentrations of these IFNs and liposome-MTP-PE were added to monocyte cultures, IFN-alpha and beta acted additively in monocyte activation, while IFN-gamma acted synergistically. The synergism for monocyte activation required that monocytes be incubated first with IFN-gamma and then with liposome-MTP-PE. These findings suggest that the synergistic effect of IFN-gamma and liposome-MTP-PE can decrease the necessary clinical doses of these agents for malignant diseases, and may have therapeutic availability in the treatment of metastatic cancer in humans.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1986

[Augmentation of natural killer (NK) cell activity in human blood lymphocytes by a new synthetic acyltripeptide (FK-565) and its derivatives].

Natural killer (NK) activities of human blood lymphocyte populations that were depleted of monocytes by centrifugal elutriation, were significantly augmented by in vitro treatment with synthetic acyltripeptide (FK-565) at concentrations ranging from 10 micrograms/ml to 100 micrograms/ml in medium. Of FK-565 and its eight derivatives, FR-39868 was the most effective in potentiating human NK cell activity, and caused NK cell-mediated cytotoxicity against K-562 target cells even at a minimal concentration of 1 microgram/ml. The significant levels of cytotoxicity, increased with increasing NK cell/target ratio. These results indicate that acyltripeptide and its derivatives should be useful in enhancing natural host defense against neoplasias in vivo.

Adjuvants, Immunologic↗
PubMed1986

Lack of production of interleukin 1 by human blood monocytes activated to the antitumor state by liposome-encapsulated muramyl tripeptide.

Previously human blood monocytes were shown to become tumoricidal when treated in vitro with lipopolysaccharide, muramyl dipeptide analogue, or liposomes containing muramyl dipeptide analogue. In this study the ability of human blood monocytes activated to the antitumor state by these macrophage activators to produce interleukin 1 (IL-1) was examined. Blood monocytes separated by centrifugal elutriation did not release IL-1 into the culture supernatant but elaborated IL-1 maximally within 24 h after treatment with lipopolysaccharide or desmethyl muramyl dipeptide. In contrast, they did not elaborate IL-1 when rendered tumoricidal by muramyl tripeptide phosphatidylethanolamine (MTP-PE) encapsulated in multilamellar vesicle liposomes composed of phosphatidylcholine and phosphatidylserine in a molar ratio of 7:3. IL-1 rich supernatants that induced thymocyte proliferation were not adsorbed or destroyed by the liposomes, and addition of supernatants from cultures of monocytes treated with liposome-MTP-PE to IL-1 rich supernatants did not inhibit thymocyte proliferation. MTP-PE in liposomes composed of phosphatidylserine or phosphatidylcholine or both in various molar ratios also did not induce IL-1 production by monocytes. These results indicate that MTP-PE encapsulated in liposomes may be useful in in situ activation of human blood monocytes to the antitumor state for destruction of clinical micrometastases because MTP-PE encapsulated in liposomes does not stimulate production of IL-1, which is responsible for undesirable side effects such as fever and granulomatous reactions.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1986

Augmentation of 1-beta-D-arabinofuranosylcytosine resistance in human KB epidermoid carcinoma cells upon induction of a second resistance to vincristine.

Human KB epidermoid carcinoma cells (KB/p) and their variant cells (KB/ara-C) resistant to 1-beta-D-arabinofuranosylcytosine (ara-C) that were not cross-resistant to vincristine (VCR) were exposed to increasing concentrations of VCR to establish VCR resistant cells (KB/VCR) and doubly resistant variant cells (KB/ara-C/VCR). KB/VCR and KB/ara-C/VCR cells showed a similar increase in resistance to VCR (about 337- to 460-fold) over that of the parent KB/p cells. KB/ara-C showed a 911-fold increase in resistance to ara-C, while KB/ara-C/VCR showed a 60,837-fold increase in resistance to ara-C compared with the parent cells. The concentration of ara-C required for 50% inhibition of KB/ara-C/VCR cells was much higher (67-fold) than that for KB/ara-C cells, although the concentration of ara-C required for 50% inhibition of KB/VCR cells was 12-fold that for KB/p cells. Thus the acquisition of resistance to a second drug by these human KB cells augmented their resistance to the first drug. Induction of resistance to ara-C or VCR resulted in marked decrease in cellular uptake of the respective drugs, but there was no difference in cellular uptakes of ara-C by KB/ara-C and KB/ara-C/VCR or of VCR by KB/VCR and KB/ara-C/VCR. KB/VCR and KB/ara-C/VCR cells were cross-resistant to vinblastine, colchicine, vindesine, etoposide, mitomycin C, and Adriamycin. Cells of the two groups (KB/p and KB/ara-C; KB/VCR and KB/ara-C/VCR) differed in sizes and doubling times. In the absence of ara-C, the resistance of KB/ara-C cells to ara-C was stable for at least 1 year, whereas in the absence of VCR resistance to VCR was almost completely lost within 1 month.

Antineoplastic Agents↗
PubMed1986

Schwannoma of the trachea.

We recently encountered a tracheal schwannoma presenting as a polypoid mass. Computed tomography (CT) was very effective in evaluation of the size, shape and site of this rare tumour. Furthermore, CT images in the prone position made it easy to exclude tumour extension into the mediastinum.

Humans↗
PubMed1986

CT of intrathoracic neurogenic tumours.

Fifteen patients with primary intrathoracic neurogenic tumours were evaluated using computed tomography (CT) scans. Schwannomas were demonstrated as homogeneous or slightly inhomogeneous densities on plain CT images; 4 of 5 schwannomas showed rim enhancement with some enhancement in the central portion of the tumour on post-enhancement CT images. Neurofibromas and ganglioneuromas were visualized as homogeneous densities on plain CT images. Three of 5 ganglioneuromas revealed homogeneous contrast enhancement of post-contrast CT images. A ganglioneuroblastoma and 2 neuroblastomas manifested slightly inhomogeneous tumour density on plain CT images. The inhomogeneity of the tumours was accentuated on contrast enhancement CT images.

Adolescent↗
PubMed1985

Induction of human monocyte-mediated tumor cell killing by a plant lectin, wheat germ agglutinin.

Human peripheral blood monocytes from healthy donors were separated by discontinuous gradient centrifugation and adherence to yield highly purified adherent cell populations (greater than 99% monocytes). Five different plant lectins were tested for ability to induce lectin-dependent monocyte-mediated cytotoxicity (LDMC). Only one lectin, wheat germ agglutinin (WGA), induced significant and reproducible LDMC activity. All the tumor target cells tested were sensitive to variable extents to cytotoxicity mediated by WGA-treated monocytes. Pretreatment of monocytes with WGA did not result in development of LDMC. N-Acetylglucosamine, which specifically binds WGA, inhibited WGA-dependent monocyte-mediated cytotoxicity. Treatment of adherent monocyte-rich monolayers with monoclonal anti-natural killer cell antibody (anti-Leu-11b) and complement did not affect the LDMC activity induced by WGA. These results indicate that the plant lectin WGA, which binds specifically to both human monocytes and tumor cells, renders human blood monocytes cytotoxic to human tumor cells.

Acetylglucosamine↗
PubMed1985

Kinetics and function of tumor cytotoxic factor(s) produced by human blood monocytes activated to the tumoricidal state.

Human monocytes obtained from healthy volunteers and isolated by centrifugal elutriation were not cytotoxic to allogeneic tumorigenic cells. These freshly isolated monocytes were rendered tumoricidal following interaction in vitro for 24 hours with greater than 0.01 micrograms lipopolysaccharide (LPS)/ml or over 1 microgram nor-muramyl dipeptide/ml. Monocytes activated by this procedure produced a soluble factor that lysed tumor cells. Full expression of tumor cell lysis required a minimum of 18 hours' exposure of tumor cells to the factor. The degree of tumor cytotoxic factor (TCF) production was closely related to the intensity of monocyte activation to become tumoricidal. Significant production of TCF by monocytes was detected in the supernatants after treatment for 3 hours with LPS. TCF was also released by activated monocytes when cocultivated with tumorigenic cells. Similarly, the level of TCF production correlated with the monocyte density. TCF destroyed human allogeneic tumor cell lines (melanoma, glioblastoma, colon carcinoma, prostatic carcinoma, and breast carcinoma), but it did not affect nontumorigenic cell lines (lung and skin fibroblasts). TCF activity was not blocked by superoxide dismutase, catalase, or protease inhibitors; it was destroyed by being heated at 100 degrees C for 2 minutes. The ability of activated monocytes to release TCF could enhance host defense against cancer.

Cell Communication↗