The Experts below are selected from a list of 54225 Experts worldwide ranked by ideXlab platform
Roberto Tinoco - One of the best experts on this subject based on the ideXlab platform.
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Prebiotic-Induced Anti-Tumor Immunity Attenuates Tumor Growth
Cell reports, 2020Co-Authors: Lisa Elmén, Roberto Tinoco, Igor Segota, Yibo Xian, Yu Fujita, Yongmei Feng, Rafael R. Segura Munoz, Robert J. Schmaltz, Linda M. BradleyAbstract:Growing evidence supports the importance of gut microbiota in the control of Tumor growth and response to therapy. Here, we select prebiotics that can enrich bacterial taxa that promote anti-Tumor Immunity. Addition of the prebiotics inulin or mucin to the diet of C57BL/6 mice induces anti-Tumor immune responses and inhibition of BRAF mutant melanoma growth in a subcutaneously implanted syngeneic mouse model. Mucin fails to inhibit Tumor growth in germ-free mice, indicating that the gut microbiota is required for the activation of the anti-Tumor immune response. Inulin and mucin drive distinct changes in the microbiota, as inulin, but not mucin, limits Tumor growth in syngeneic mouse models of colon cancer and NRAS mutant melanoma and enhances the efficacy of a MEK inhibitor against melanoma while delaying the emergence of drug resistance. We highlight the importance of gut microbiota in anti-Tumor Immunity and the potential therapeutic role for prebiotics in this process.
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Gut microbiota dependent anti-Tumor Immunity restricts melanoma growth in Rnf5 −/− mice
Nature communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
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gut microbiota dependent anti Tumor Immunity restricts melanoma growth in rnf5 mice
Nature Communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
Yongmei Feng - One of the best experts on this subject based on the ideXlab platform.
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Prebiotic-Induced Anti-Tumor Immunity Attenuates Tumor Growth
Cell reports, 2020Co-Authors: Lisa Elmén, Roberto Tinoco, Igor Segota, Yibo Xian, Yu Fujita, Yongmei Feng, Rafael R. Segura Munoz, Robert J. Schmaltz, Linda M. BradleyAbstract:Growing evidence supports the importance of gut microbiota in the control of Tumor growth and response to therapy. Here, we select prebiotics that can enrich bacterial taxa that promote anti-Tumor Immunity. Addition of the prebiotics inulin or mucin to the diet of C57BL/6 mice induces anti-Tumor immune responses and inhibition of BRAF mutant melanoma growth in a subcutaneously implanted syngeneic mouse model. Mucin fails to inhibit Tumor growth in germ-free mice, indicating that the gut microbiota is required for the activation of the anti-Tumor immune response. Inulin and mucin drive distinct changes in the microbiota, as inulin, but not mucin, limits Tumor growth in syngeneic mouse models of colon cancer and NRAS mutant melanoma and enhances the efficacy of a MEK inhibitor against melanoma while delaying the emergence of drug resistance. We highlight the importance of gut microbiota in anti-Tumor Immunity and the potential therapeutic role for prebiotics in this process.
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Gut microbiota dependent anti-Tumor Immunity restricts melanoma growth in Rnf5 −/− mice
Nature communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
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gut microbiota dependent anti Tumor Immunity restricts melanoma growth in rnf5 mice
Nature Communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
Lisa Elmén - One of the best experts on this subject based on the ideXlab platform.
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Prebiotic-Induced Anti-Tumor Immunity Attenuates Tumor Growth
Cell reports, 2020Co-Authors: Lisa Elmén, Roberto Tinoco, Igor Segota, Yibo Xian, Yu Fujita, Yongmei Feng, Rafael R. Segura Munoz, Robert J. Schmaltz, Linda M. BradleyAbstract:Growing evidence supports the importance of gut microbiota in the control of Tumor growth and response to therapy. Here, we select prebiotics that can enrich bacterial taxa that promote anti-Tumor Immunity. Addition of the prebiotics inulin or mucin to the diet of C57BL/6 mice induces anti-Tumor immune responses and inhibition of BRAF mutant melanoma growth in a subcutaneously implanted syngeneic mouse model. Mucin fails to inhibit Tumor growth in germ-free mice, indicating that the gut microbiota is required for the activation of the anti-Tumor immune response. Inulin and mucin drive distinct changes in the microbiota, as inulin, but not mucin, limits Tumor growth in syngeneic mouse models of colon cancer and NRAS mutant melanoma and enhances the efficacy of a MEK inhibitor against melanoma while delaying the emergence of drug resistance. We highlight the importance of gut microbiota in anti-Tumor Immunity and the potential therapeutic role for prebiotics in this process.
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Gut microbiota dependent anti-Tumor Immunity restricts melanoma growth in Rnf5 −/− mice
Nature communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
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gut microbiota dependent anti Tumor Immunity restricts melanoma growth in rnf5 mice
Nature Communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
Igor Segota - One of the best experts on this subject based on the ideXlab platform.
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Prebiotic-Induced Anti-Tumor Immunity Attenuates Tumor Growth
Cell reports, 2020Co-Authors: Lisa Elmén, Roberto Tinoco, Igor Segota, Yibo Xian, Yu Fujita, Yongmei Feng, Rafael R. Segura Munoz, Robert J. Schmaltz, Linda M. BradleyAbstract:Growing evidence supports the importance of gut microbiota in the control of Tumor growth and response to therapy. Here, we select prebiotics that can enrich bacterial taxa that promote anti-Tumor Immunity. Addition of the prebiotics inulin or mucin to the diet of C57BL/6 mice induces anti-Tumor immune responses and inhibition of BRAF mutant melanoma growth in a subcutaneously implanted syngeneic mouse model. Mucin fails to inhibit Tumor growth in germ-free mice, indicating that the gut microbiota is required for the activation of the anti-Tumor immune response. Inulin and mucin drive distinct changes in the microbiota, as inulin, but not mucin, limits Tumor growth in syngeneic mouse models of colon cancer and NRAS mutant melanoma and enhances the efficacy of a MEK inhibitor against melanoma while delaying the emergence of drug resistance. We highlight the importance of gut microbiota in anti-Tumor Immunity and the potential therapeutic role for prebiotics in this process.
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Gut microbiota dependent anti-Tumor Immunity restricts melanoma growth in Rnf5 −/− mice
Nature communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
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gut microbiota dependent anti Tumor Immunity restricts melanoma growth in rnf5 mice
Nature Communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
Yibo Xian - One of the best experts on this subject based on the ideXlab platform.
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Prebiotic-Induced Anti-Tumor Immunity Attenuates Tumor Growth
Cell reports, 2020Co-Authors: Lisa Elmén, Roberto Tinoco, Igor Segota, Yibo Xian, Yu Fujita, Yongmei Feng, Rafael R. Segura Munoz, Robert J. Schmaltz, Linda M. BradleyAbstract:Growing evidence supports the importance of gut microbiota in the control of Tumor growth and response to therapy. Here, we select prebiotics that can enrich bacterial taxa that promote anti-Tumor Immunity. Addition of the prebiotics inulin or mucin to the diet of C57BL/6 mice induces anti-Tumor immune responses and inhibition of BRAF mutant melanoma growth in a subcutaneously implanted syngeneic mouse model. Mucin fails to inhibit Tumor growth in germ-free mice, indicating that the gut microbiota is required for the activation of the anti-Tumor immune response. Inulin and mucin drive distinct changes in the microbiota, as inulin, but not mucin, limits Tumor growth in syngeneic mouse models of colon cancer and NRAS mutant melanoma and enhances the efficacy of a MEK inhibitor against melanoma while delaying the emergence of drug resistance. We highlight the importance of gut microbiota in anti-Tumor Immunity and the potential therapeutic role for prebiotics in this process.
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Gut microbiota dependent anti-Tumor Immunity restricts melanoma growth in Rnf5 −/− mice
Nature communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
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gut microbiota dependent anti Tumor Immunity restricts melanoma growth in rnf5 mice
Nature Communications, 2019Co-Authors: Roberto Tinoco, Lisa Elmén, Igor Segota, Yibo Xian, Yu Fujita, Avinash Das Sahu, Raphy Zarecki, Kerrie L. Marie, Yongmei FengAbstract:Accumulating evidence points to an important role for the gut microbiome in anti-Tumor Immunity. Here, we show that altered intestinal microbiota contributes to anti-Tumor Immunity, limiting Tumor expansion. Mice lacking the ubiquitin ligase RNF5 exhibit attenuated activation of the unfolded protein response (UPR) components, which coincides with increased expression of inflammasome components, recruitment and activation of dendritic cells and reduced expression of antimicrobial peptides in intestinal epithelial cells. Reduced UPR expression is also seen in murine and human melanoma Tumor specimens that responded to immune checkpoint therapy. Co-housing of Rnf5-/- and WT mice abolishes the anti-Tumor Immunity and Tumor inhibition phenotype, whereas transfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5-/- mice, establishes anti-Tumor Immunity and restricts melanoma growth in germ-free WT mice. Altered UPR signaling, exemplified in Rnf5-/- mice, coincides with altered gut microbiota composition and anti-Tumor Immunity to control melanoma growth.
