24 research outputs found

    Effects of thawing temperature on serum exosomal CEA values and quantity.

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    <p>A: Western blotting for CD63 of exosome from frozen serum samples from normal healthy subject that were thawed at 4, 25, and 37°C. B: Each color indicates the results obtained from exosome quantitation for frozen serum samples from the same patient that were thawed at 4, 25, and 37°C. C: Each color indicates exosomal CEA values measured using ELISA for frozen serum samples from the same patient that were thawed at 4, 25, and 37°C. The same colors in B and C correspond to the same patients. D: Exosomal CEA values for frozen serum samples from eight normal healthy subjects that were thawed at 4, 25, and 37°C.</p

    Relationships between exosomal CEA concentration and two solvents at different concentrations.

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    <p>The results obtained for samples dissolved in 250 μl of Milli-Q water (H<sub>2</sub>O) (1×), 50 μl of Milli-Q water (5×), 250 μl of 1% BSA (1×), or 50 μl of 1% BSA (5×) for the same patient.</p

    Serum exosomal CEA and serum CEA for diagnosis of distant metastasis in colorectal cancer patients.

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    <p>ROC curves for the presence of distant metastasis in colorectal cancer patients based on serum exosomal CEA samples thawed at 25°C and serum CEA from 116 patients with colorectal cancer; eCEA: serum exosomal CEA.</p

    ROC curves for the presence of distant metastasis of colorectal cancer for serum exosomal CEA samples thawed at 4, 25, or 37°C.

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    <p>Data represent samples from 48 patients. A: Serum exosomal CEA samples thawed at 25 (T25) or 4°C (T4). B: Serum exosomal CEA samples thawed at 25 or 37°C. C: Serum exosomal CEA samples thawed at 4 or 37°C.</p

    Inhibition of IL-17A in Tumor Microenvironment Augments Cytotoxicity of Tumor-Infiltrating Lymphocytes in Tumor-Bearing Mice

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    <div><p>It remains controversial whether IL-17A promotes or inhibits cancer progression. We hypothesized that IL-17A that is locally produced in the tumor microenvironment has an important role in angiogenesis and tumor immunity. We investigated the effect of inhibiting IL-17A at tumor sites on tumor growth and on local and systemic anti-tumor immunity. MC38 or B16 cells were inoculated subcutaneously into mice, and intratumoral injection of an adenovirus vector expressing siRNA against the mouse IL-17A gene (Ad-si-IL-17) significantly inhibited tumor growth in both tumor models compared with control mice. Inhibition of IL-17A at tumor sites significantly suppressed CD31, MMP9, and VEGF expression in tumor tissue. The cytotoxic activity of CD8<sup>+</sup> T cells from tumor-infiltrating lymphocytes in mice treated with Ad-si-IL-17 was significantly higher than in control mice; however, CD8<sup>+</sup> T cells from splenocytes had similar activity levels. Suppression of IL-17A at tumor sites led to a Th1-dominant environment, and moreover, eliminated myeloid-derived suppressor cells and regulatory T cells at tumor sites but not in splenocytes. In conclusion, blockade of IL-17A at tumor sites helped suppress tumor growth by inhibiting angiogenesis as well as cytotoxic T lymphocytes activation at tumor sites.</p> </div

    Inhibition of IL-17A in tumor sites increases Th1 cells in tumor microenvironment.

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    <p>Splenocytes and TILs were collected from spleens or tumor tissues of MC38 subcutaneous tumor model. Th1/Th2 cells were detected by intracellular staining assay of anti-IFN-γ mAb and anti-IL-4 mAb. Representative flow cytometry analysis profiles gated on anti-CD4 mAb. Ad-si-IL-17 treatment increased Th1 phenotype of TILs compared to control, but that of splenocytes was similar level in both treatments. Th2 phenotype was similar ratio of TILs and splenocytes in both treatment. Data are representative of two independent experiments (<i>n</i> = 5).</p
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