The Experts below are selected from a list of 297 Experts worldwide ranked by ideXlab platform
Muriel Moser - One of the best experts on this subject based on the ideXlab platform.
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murine dendritic cells pulsed in vitro with Tumor antigen induce Tumor Resistance in vivo
European Journal of Immunology, 1994Co-Authors: Veronique Flamand, Thierry Sornasse, Kris Thielemans, Christian Demanet, Marleen Bakkus, Herve Bazin, Francoise Tielemans, Jacques Urbain, Muriel MoserAbstract:The aim of this work is to induce Tumor Resistance to a B cell lymphoma in BALB/c mice using elements of the immune system. It has indeed been shown by us and by others that antigen-presenting cells (APC) like dendritic cells can induce efficient immune responses and can even substitute for Freund's adjuvant. Here we show that mice immunized with syngeneic dendritic cells pulsed in vitro with Tumor antigen (BCL1 idiotype expressed by lymphoma cells) are protected against a subsequent Tumor inoculation. The in vivo Resistance can be correlated with the induction of a humoral response specific for the idiotype expressed by the Tumor. No such protection can be achieved when B cells are used as APC. These data show that effector cells in Tumor-bearing animals can be recruited and activated using dendritic cells, providing long-lasting immune surveillance.
Christiane Dosne Pasqualini - One of the best experts on this subject based on the ideXlab platform.
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Concomitant Tumor Resistance: The Role of Tyrosine Isomers in the Mechanisms of Metastases Control
Cancer Research, 2012Co-Authors: Raúl A. Ruggiero, Paula Chiarella, Juan Bruzzo, Roberto Meiss, Oscar D. Bustuoabad, Christiane Dosne PasqualiniAbstract:Concomitant Tumor Resistance (CR) is a phenomenon in which a Tumor-bearing host is resistant to the growth of secondary Tumor implants and metastasis. Although previous studies indicated that T-cell–dependent processes mediate CR in hosts bearing immunogenic small Tumors, manifestations of CR induced by immunogenic and nonimmunogenic large Tumors have been associated with an elusive serum factor. In a recently published study, we identified this factor as meta -tyrosine and ortho -tyrosine, 2 isomers of tyrosine that would not be present in normal proteins. In 3 different murine models of cancer that generate CR, both meta - and ortho -tyrosine inhibited Tumor growth. Additionally, we showed that both isoforms of tyrosine blocked metastasis in a fourth model that does not generate CR but is sensitive to CR induced by other Tumors. Mechanistic studies showed that the antiTumor effects of the tyrosine isomers were mediated in part by early inhibition of the MAP/ERK pathway and inactivation of STAT3, potentially driving Tumor cells into a state of dormancy in G 0 -phase. Other mechanisms, putatively involving the activation of an intra–S-phase checkpoint, would also inhibit Tumor proliferation by accumulating cells in S-phase. By revealing a molecular basis for the classical phenomenon of CR, our findings may stimulate new generalized approaches to limit the development of metastases that arise after resection of primary Tumors or after other stressors that may promote the escape of metastases from dormancy, an issue that is of pivotal importance to oncologists and their patients. Cancer Res; 72(5); 1043–50. ©2012 AACR .
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Tyrosine Isomers Mediate the Classical Phenomenon of Concomitant Tumor Resistance
Cancer Research, 2011Co-Authors: Raúl A. Ruggiero, Paula Chiarella, Juan Bruzzo, Roberto Meiss, Pedro Di Gianni, Martín A. Isturiz, Susana Linskens, Norma Speziale, Oscar D. Bustuoabad, Christiane Dosne PasqualiniAbstract:Concomitant Tumor Resistance (CR) is a phenomenon originally described in 1906 in which a Tumor-bearing host is resistant to the growth of secondary Tumor implants and metastasis. Although recent studies have indicated that T-cell–dependent processes mediate CR in hosts bearing immunogenic small Tumors, manifestations of CR induced by immunogenic and nonimmunogenic large Tumors have been associated with an elusive serum factor. In this study, we identify this serum factor as tyrosine in its meta and ortho isoforms. In three different murine models of cancer that generate CR, both meta-tyrosine and ortho-tyrosine inhibited Tumor growth. In addition, we showed that both isoforms of tyrosine blocked metastasis in a fourth model that does not generate CR but is sensitive to CR induced by other Tumors. Mechanistic studies showed that the antiTumor effects of the tyrosine isoforms were mediated, in part, by early inhibition of mitogen-activated protein/extracellular signal-regulated kinase pathway and inactivation of STAT3, potentially driving Tumor cells into a state of dormancy. By revealing a molecular basis for the classical phenomenon of CR, our findings may stimulate new generalized approaches to limit the development of metastases that arise after resection of primary Tumors, an issue of pivotal importance to oncologists and their patients. Cancer Res; 71(22); 7113–24. ©2011 AACR.
Cynthia Kenyon - One of the best experts on this subject based on the ideXlab platform.
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DAF-16/FOXO targets genes that regulate Tumor growth in Caenorhabditis elegans
Nature Genetics, 2007Co-Authors: Julie Pinkston-gosse, Cynthia KenyonAbstract:Cancer is an age-related disease, and inhibiting insulin/insulin-like growth factor 1 (IGF-1) signaling extends lifespan and increases Tumor Resistance in C. elegans and mammals. To investigate how the insulin/IGF-1 pathway couples these two processes, we analyzed putative transcriptional targets of the C. elegans FOXO transcription factor DAF-16, which promotes both longevity and Tumor Resistance. Twenty-nine of 734 genes tested influenced germline-Tumor cell proliferation or p53-dependent apoptosis. About half of these genes also affected normal aging, thereby linking these two processes mechanistically. Many of these 29 genes are orthologs of known human Tumor suppressors or oncogenes, suggesting that others may be as well. Our findings implicate nuclear-pore modification in p53-dependent cell death, because inhibiting nuclear-pore genes that are upregulated by DAF-16 blocks p53-dependent cell death in the Tumor, but not normal, p53-independent, germline cell death.
Veronique Flamand - One of the best experts on this subject based on the ideXlab platform.
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murine dendritic cells pulsed in vitro with Tumor antigen induce Tumor Resistance in vivo
European Journal of Immunology, 1994Co-Authors: Veronique Flamand, Thierry Sornasse, Kris Thielemans, Christian Demanet, Marleen Bakkus, Herve Bazin, Francoise Tielemans, Jacques Urbain, Muriel MoserAbstract:The aim of this work is to induce Tumor Resistance to a B cell lymphoma in BALB/c mice using elements of the immune system. It has indeed been shown by us and by others that antigen-presenting cells (APC) like dendritic cells can induce efficient immune responses and can even substitute for Freund's adjuvant. Here we show that mice immunized with syngeneic dendritic cells pulsed in vitro with Tumor antigen (BCL1 idiotype expressed by lymphoma cells) are protected against a subsequent Tumor inoculation. The in vivo Resistance can be correlated with the induction of a humoral response specific for the idiotype expressed by the Tumor. No such protection can be achieved when B cells are used as APC. These data show that effector cells in Tumor-bearing animals can be recruited and activated using dendritic cells, providing long-lasting immune surveillance.
Raúl A. Ruggiero - One of the best experts on this subject based on the ideXlab platform.
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Concomitant Tumor Resistance
Cancer Letters, 2012Co-Authors: Paula Chiarella, Juan Bruzzo, Roberto Meiss, Raúl A. RuggieroAbstract:Abstract Concomitant Tumor Resistance (CR) is a phenomenon in which a Tumor-bearing host is resistant to the growth of secondary Tumor implants. This phenomenon has been described in human and animal systems and it can be generated by both immunogenic and non-immunogenic Tumors. The relevance of CR to the mechanisms of metastases control has been highlighted by numerous observations showing that the removal of human and murine Tumors may be followed by an abrupt increase in metastatic growth, suggesting that a primary Tumor may exert a controlling action on its metastases which could be considered as secondary Tumor implants developed spontaneously during the primary Tumor growth. A more profound understanding of the different mechanisms claimed to be associated with the phenomenon of CR could contribute to develop new and more harmless means to manage malignant diseases, especially by limiting the development of metastases that arise after resection of primary Tumors or after other stressors that may promote the escape of metastases from dormancy.
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Concomitant Tumor Resistance: The Role of Tyrosine Isomers in the Mechanisms of Metastases Control
Cancer Research, 2012Co-Authors: Raúl A. Ruggiero, Paula Chiarella, Juan Bruzzo, Roberto Meiss, Oscar D. Bustuoabad, Christiane Dosne PasqualiniAbstract:Concomitant Tumor Resistance (CR) is a phenomenon in which a Tumor-bearing host is resistant to the growth of secondary Tumor implants and metastasis. Although previous studies indicated that T-cell–dependent processes mediate CR in hosts bearing immunogenic small Tumors, manifestations of CR induced by immunogenic and nonimmunogenic large Tumors have been associated with an elusive serum factor. In a recently published study, we identified this factor as meta -tyrosine and ortho -tyrosine, 2 isomers of tyrosine that would not be present in normal proteins. In 3 different murine models of cancer that generate CR, both meta - and ortho -tyrosine inhibited Tumor growth. Additionally, we showed that both isoforms of tyrosine blocked metastasis in a fourth model that does not generate CR but is sensitive to CR induced by other Tumors. Mechanistic studies showed that the antiTumor effects of the tyrosine isomers were mediated in part by early inhibition of the MAP/ERK pathway and inactivation of STAT3, potentially driving Tumor cells into a state of dormancy in G 0 -phase. Other mechanisms, putatively involving the activation of an intra–S-phase checkpoint, would also inhibit Tumor proliferation by accumulating cells in S-phase. By revealing a molecular basis for the classical phenomenon of CR, our findings may stimulate new generalized approaches to limit the development of metastases that arise after resection of primary Tumors or after other stressors that may promote the escape of metastases from dormancy, an issue that is of pivotal importance to oncologists and their patients. Cancer Res; 72(5); 1043–50. ©2012 AACR .
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Tyrosine Isomers Mediate the Classical Phenomenon of Concomitant Tumor Resistance
Cancer Research, 2011Co-Authors: Raúl A. Ruggiero, Paula Chiarella, Juan Bruzzo, Roberto Meiss, Pedro Di Gianni, Martín A. Isturiz, Susana Linskens, Norma Speziale, Oscar D. Bustuoabad, Christiane Dosne PasqualiniAbstract:Concomitant Tumor Resistance (CR) is a phenomenon originally described in 1906 in which a Tumor-bearing host is resistant to the growth of secondary Tumor implants and metastasis. Although recent studies have indicated that T-cell–dependent processes mediate CR in hosts bearing immunogenic small Tumors, manifestations of CR induced by immunogenic and nonimmunogenic large Tumors have been associated with an elusive serum factor. In this study, we identify this serum factor as tyrosine in its meta and ortho isoforms. In three different murine models of cancer that generate CR, both meta-tyrosine and ortho-tyrosine inhibited Tumor growth. In addition, we showed that both isoforms of tyrosine blocked metastasis in a fourth model that does not generate CR but is sensitive to CR induced by other Tumors. Mechanistic studies showed that the antiTumor effects of the tyrosine isoforms were mediated, in part, by early inhibition of mitogen-activated protein/extracellular signal-regulated kinase pathway and inactivation of STAT3, potentially driving Tumor cells into a state of dormancy. By revealing a molecular basis for the classical phenomenon of CR, our findings may stimulate new generalized approaches to limit the development of metastases that arise after resection of primary Tumors, an issue of pivotal importance to oncologists and their patients. Cancer Res; 71(22); 7113–24. ©2011 AACR.
