The Experts below are selected from a list of 8862 Experts worldwide ranked by ideXlab platform
Steven M Albelda - One of the best experts on this subject based on the ideXlab platform.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
Mark Bloomston - One of the best experts on this subject based on the ideXlab platform.
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distinct Myeloid Suppressor Cell subsets correlate with plasma il 6 and il 10 and reduced interferon alpha signaling in cd4 t Cells from patients with gi malignancy
Cancer Immunology Immunotherapy, 2011Co-Authors: Gregory S Young, Todd M Bauer, Elaine Binkley, Mark Bloomston, Bethany L MundybosseAbstract:Interferon-alpha (IFN-α) promotes anti-tumor immunity through its actions on immune Cells. We hypothesized that elevated percentages of Myeloid-derived Suppressor Cells (MDSC) and increased pro-inflammatory cytokines in peripheral blood would be associated with impaired response to IFN-α in patients with gastrointestinal (GI) malignancies. This study evaluated relationships between plasma IL-6, IL-10, circulating MDSC subsets, and IFN-α-induced signal transduction in 40 patients with GI malignancies. Plasma IL-6 and IL-10 were significantly higher in patients versus normal donors. CD33+HLADR−CD11b+CD15+ and CD33+HLADR−/lowCD14+ MDSC subsets were also elevated in patients versus normal donors (P < 0.0001). Plasma IL-6 was correlated with CD33+HLADR−CD15+ MDSC (P = 0.008) and IL-10 with CD33+HLADR−CD15− MDSC (P = 0.002). The percentage of CD15+ and CD15− but not CD14+ MDSC subsets were inversely correlated with IFN-α-induced STAT1 phosphorylation in CD4+ T Cells, while co-culture with in vitro generated MDSC led to reduced IFN-α responsiveness in both PBMC and the CD4+ subset of T Cells from normal donors. Exploratory multivariable Cox proportional hazards models revealed that an increased percentage of the CD33+HLADR−CD15− MDSC subset was associated with reduced overall survival (P = 0.049), while an increased percentage of the CD33+HLADR−/lowCD14+ subset was associated with greater overall survival (P = 0.033). These data provide evidence for a unique relationship between specific cytokines, MDSC subsets, and IFN-α responsiveness in patients with GI malignancies.
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abstract 5517 distinct Myeloid Suppressor Cell subsets correlate with plasma il 6 and il 10 and reduced interferon α signal transduction in cd4 t Cells from patients with gastrointestinal malignancy
Cancer Research, 2011Co-Authors: Bethany L Mundy, Gregory S Young, Todd M Bauer, Elaine Binkley, Mark Bloomston, Matthew A Bill, Tanios Bekaiisaab, William E Carson, Gregory B LesinskiAbstract:Interferon-alpha (IFNα) can promote anti-tumor immunity through its actions on immune Cells. We have shown in murine models that a class of immune Suppressor Cells known as Myeloid-derived Suppressor Cells (MDSC) have inhibitory effects on IFN signal transduction and gene regulation. Interleukin (IL)-6 and IL-10 are produced by tumor Cells in cancer patients and can regulate the survival and function of MDSC. This study evaluated relationships between plasma IL-6, IL-10, circulating MDSC subsets and IFNα-induced signal transduction in 40 patients with gastrointestinal (GI) malignancies. Plasma IL-6 and IL-10 levels were significantly higher in patients versus normal donors. CD33 + HLADR − CD11b + CD15 + and CD33 + HLADR −/low CD14 + MDSC were also elevated in patients versus normal donors (p + ) and monocytic (CD15 − ) subsets. Therefore relationships between CD15 expression on MDSC and cytokines elevated in GI patients were examined. A significant correlation between plasma IL-6 with CD33 + HLADRCD15 + MDSC (p=0.008) and IL10 with CD33 + HLADR − CD15 − MDSC (p=0.002) was observed. The level of CD15 + and CD15 − but not CD14 + MDSC subsets were inversely correlated with IFNα-induced STAT1 phosphorylation in CD4 + T Cells, while co-culture with in vitro generated MDSC led to reduced IFNα-responsiveness in PBMC from normal donors. In a multivariable Cox proportional hazards model, an increased percentage of the CD33 + HLADR − CD15 − MDSC subset was associated with reduced overall survival (hazard ratio = 1.43; p = 0.049) while an increased percentage of the CD33 + HLADR −/low CD14 + subset was associated with greater overall survival (hazard ratio = 0.69, p=0.033). These data provide evidence for a unique relationship between specific cytokines, MDSC subsets and IFNα responsiveness in patients with GI malignancies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5517. doi:10.1158/1538-7445.AM2011-5517
Eiji Suzuki - One of the best experts on this subject based on the ideXlab platform.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
Larry R Kaiser - One of the best experts on this subject based on the ideXlab platform.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
Arminder S Jassar - One of the best experts on this subject based on the ideXlab platform.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
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gemcitabine selectively eliminates splenic gr 1 cd11b Myeloid Suppressor Cells in tumor bearing animals and enhances antitumor immune activity
Clinical Cancer Research, 2005Co-Authors: Eiji Suzuki, Veena Kapoor, Arminder S Jassar, Larry R Kaiser, Steven M AlbeldaAbstract:Purpose: Myeloid Suppressor (Gr-1+/CD11b+) Cells accumulate in the spleens of tumor-bearing mice where they contribute to immunosuppression by inhibiting the function of CD8+ T Cells and by promoting tumor angiogenesis. Elimination of these Myeloid Suppressor Cells may thus significantly improve antitumor responses and enhance effects of cancer immunotherapy, although to date few practical options exist. Experimental Design: The effect of the chemotherapy drug gemcitabine on the number of (Gr-1+/CD11b+) Cells in the spleens of animals bearing large tumors derived from five cancer lines grown in both C57Bl/6 and BALB/c mice was analyzed. Suppressive activity of splenocytes from gemcitabine-treated and control animals was measured in natural killer (NK) Cell lysis and Winn assays. The impact of Myeloid Suppressor Cell activity was determined in an immunogene therapy model using an adenovirus expressing IFN-β. Results: This study shows that the chemotherapeutic drug gemcitabine, given at a dose similar to the equivalent dose used in patients, was able to dramatically and specifically reduce the number of Myeloid Suppressor Cells found in the spleens of animals bearing large tumors with no significant reductions in CD4+ T Cells, CD8+ T Cells, NK Cells, macrophages, or B Cells. The loss of Myeloid Suppressor Cells was accompanied by an increase in the antitumor activity of CD8+ T Cells and activated NK Cells. Combining gemcitabine with cytokine immunogene therapy using IFN-β markedly enhanced antitumor efficacy. Conclusions: These results suggest that gemcitabine may be a practical strategy for the reduction of Myeloid Suppressor Cells and should be evaluated in conjunction with a variety of immunotherapy approaches.
