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Glycoprotein modifications of sarcoma L-1 tumor cells by tunicamycin, swainsonine, bromoconduritol or 1-desoxynojirimycin treatment inhibits their metastatic lung colonization in Balb/c-mice.

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Synthesis and expression of cell surface carbohydrates appear to be involved in recognition events associated with tumor invasion and metastasis. Thus, the potential of murine sarcoma L-1 cells to form experimental lung metastases after i.v. injection was assessed after inhibiting tumor cell protein

The mannosidase inhibitors 1-deoxymannojirimycin and swainsonine have no effect on the biosynthesis and infectivity of Rous sarcoma virus.

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The effects of inhibitors, which interfere with oligosaccharide trimming by blocking mannosidases, on the processing and export of the viral glycoproteins of Rous sarcoma virus (RSV), have been studied. 1-Deoxymannojirimycin (DIM) prevents removal of mannose residues from the Man9 (GlcNAc)2

Swainsonine inhibition of spontaneous metastasis.

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We have previously shown that swainsonine, administered systemically to C57BL/6 mice, inhibited the pulmonary metastasis of iv injected B16-F10 melanoma cells by a mechanism involving interleukin-2 production and augmentation of natural killer cell activity. From this finding, which uses an

Studies of an immunomodulator, swainsonine. II. Effect of swainsonine on mouse immunodeficient system and experimental murine tumor.

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We examined the effect of swainsonine on antibody response to sheep red blood cells (SRBC) in immunodeficient mice which were treated with immunosuppressive factor or antitumor drugs, or inoculated with sarcoma 180 ascites tumor. The administration of swainsonine restored the capacities of the

Studies of an immunomodulator, swainsonine. I. Enhancement of immune response by swainsonine in vitro.

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Swainsonine isolated from Metarhizium sp., was found to enhance the activities of the mouse immune system in vitro. Concanavalin A stimulated lymphocyte proliferation and proliferative response in mixed lymphocytes culture, which were suppressed by immunosuppressive factor obtained from serum of

Appropriate glycosylation of the fms gene product is a prerequisite for its transforming potency.

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Processing inhibitors of N-linked glycans were used to determine whether correct glycosylation of the oncogene product gp140v-fms, encoded by the McDonough strain of feline sarcoma virus (SM-FeSV), is required to maintain the oncogenic properties of v-fms. SM-FeSV-transformed cells treated with the

Transformation by the v-fms oncogene product: role of glycosylational processing and cell surface expression.

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The effect of glycosylational-processing inhibitors on the synthesis, cell surface expression, endocytosis, and transforming function of the v-fms oncogene protein (gp140fms) was examined in McDonough feline sarcoma virus-transformed Fischer rat embryo (SM-FRE) cells. Swainsonine (SW), a mannosidase

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