The Experts below are selected from a list of 2568 Experts worldwide ranked by ideXlab platform
Jeffrey H Lipton - One of the best experts on this subject based on the ideXlab platform.
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cd56bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.
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cd56 bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.
Amina Kariminia - One of the best experts on this subject based on the ideXlab platform.
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cd56bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.
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cd56 bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.
Carlos Bachier - One of the best experts on this subject based on the ideXlab platform.
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tbo Filgrastim versus Filgrastim during mobilization and neutrophil engraftment for autologous stem cell transplantation
Biology of Blood and Marrow Transplantation, 2015Co-Authors: Mohammed M Elayan, Justin Horowitz, Jose M Magraner, Paul J Shaughnessy, Carlos BachierAbstract:Abstract There are limited data available supporting the use of the recombinant granulocyte colony–stimulating factor (G-CSF), tbo-Filgrastim, rather than traditionally used Filgrastim to mobilize peripheral blood stem cells (PBSC) or to accelerate engraftment after autologous stem cell transplantation (ASCT). We sought to compare the efficacy and cost of tbo-Filgrastim to Filgrastim in these settings. Patients diagnosed with lymphoma or plasma cell disorders undergoing G-CSF mobilization, with or without plerixafor, were included in this retrospective analysis. The primary outcome was total collected CD34 + cells/kg. Secondary mobilization endpoints included peripheral CD34 + cells/μL on days 4 and 5 of mobilization, adjunctive use of plerixafor, CD34 + cells/kg collected on day 5, number of collection days and volumes processed, number of collections reaching 5 million CD34 + cells/kg, and percent reaching target collection goal in 1 day. Secondary engraftment endpoints included time to neutrophil and platelet engraftment, number of blood product transfusions required before engraftment, events of febrile neutropenia, and length of stay. A total of 185 patients were included in the final analysis. Patients receiving Filgrastim (n = 86) collected a median of 5.56 × 10 6 CD34 + cells/kg, compared with a median of 5.85 × 10 6 CD34 + cells/kg in the tbo-Filgrastim group (n = 99; P = .58). There were no statistically significant differences in all secondary endpoints with the exception of apheresis volumes processed (tbo-Filgrastim, 17.0 liters versus Filgrastim, 19.7 liters; P P = .04). In conclusion, tbo-Filgrastim demonstrated similar CD34 + yield compared with Filgrastim in mobilization and post-transplantation settings, with no clinically meaningful differences in secondary efficacy and safety endpoints. Furthermore, tbo-Filgrastim utilization was associated with cost savings of approximately $1406 per patient utilizing average wholesale price.
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tbo Filgrastim versus Filgrastim during mobilization and neutrophil engraftment for autologous stem cell transplantation
Biology of Blood and Marrow Transplantation, 2015Co-Authors: Mohammed M Elayan, Justin Horowitz, Jose M Magraner, Paul J Shaughnessy, Carlos BachierAbstract:Abstract There are limited data available supporting the use of the recombinant granulocyte colony–stimulating factor (G-CSF), tbo-Filgrastim, rather than traditionally used Filgrastim to mobilize peripheral blood stem cells (PBSC) or to accelerate engraftment after autologous stem cell transplantation (ASCT). We sought to compare the efficacy and cost of tbo-Filgrastim to Filgrastim in these settings. Patients diagnosed with lymphoma or plasma cell disorders undergoing G-CSF mobilization, with or without plerixafor, were included in this retrospective analysis. The primary outcome was total collected CD34+ cells/kg. Secondary mobilization endpoints included peripheral CD34+ cells/μL on days 4 and 5 of mobilization, adjunctive use of plerixafor, CD34+ cells/kg collected on day 5, number of collection days and volumes processed, number of collections reaching 5 million CD34+ cells/kg, and percent reaching target collection goal in 1 day. Secondary engraftment endpoints included time to neutrophil and platelet engraftment, number of blood product transfusions required before engraftment, events of febrile neutropenia, and length of stay. A total of 185 patients were included in the final analysis. Patients receiving Filgrastim (n = 86) collected a median of 5.56 × 106 CD34+ cells/kg, compared with a median of 5.85 × 106 CD34+ cells/kg in the tbo-Filgrastim group (n = 99; P = .58). There were no statistically significant differences in all secondary endpoints with the exception of apheresis volumes processed (tbo-Filgrastim, 17.0 liters versus Filgrastim, 19.7 liters; P
Mahmoud Aljurf - One of the best experts on this subject based on the ideXlab platform.
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cd56bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.
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cd56 bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.
Cindy Toze - One of the best experts on this subject based on the ideXlab platform.
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cd56bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.
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cd56 bright natural killer regulatory cells in Filgrastim primed donor blood or marrow products regulate chronic graft versus host disease the canadian blood and marrow transplant group randomized 0601 study results
Haematologica, 2017Co-Authors: Amina Kariminia, Sabine M Ivison, Jacob Rozmus, Susanna Sung, Avani Varshney, Mahmoud Aljurf, S Lachance, Irwin Walker, Cindy Toze, Jeffrey H LiptonAbstract:Randomized trials have conclusively shown higher rates of chronic graft-versus-host disease with Filgrastim-stimulated apheresis peripheral blood as a donor source than unstimulated bone marrow. The Canadian Blood and Marrow Transplant Group conducted a phase 3 study of adults who received either Filgrastim-stimulated apheresis peripheral blood or Filgrastim-stimulated bone marrow from human leukocyte antigen-identical sibling donors. Because all donors received the identical Filgrastim dosing schedule, this study allowed for a controlled evaluation of the impact of stem cell source on development of chronic graft-versus-host disease. One hundred and twenty-one evaluable Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow patient donor products were immunologically characterized by flow cytometry and tested for their association with acute and chronic graft-versus-host disease within 2 years of transplantation. The immune populations evaluated included, regulatory T cells, central memory and effector T cells, interferon γ positive producing T cells, invariate natural killer T cells, regulatory natural killer cells, dendritic cell populations, macrophages, and activated B cells and memory B cells. When both Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow were grouped together, a higher chronic graft-versus-host disease frequency was associated with lower proportions of CD56bright natural killer regulatory cells and interferon γ-producing T helper cells in the donor product. Lower CD56bright natural killer regulatory cells displayed differential impacts on the development of extensive chronic graft-versus-host disease between Filgrastim-stimulated apheresis peripheral blood and Filgrastim-stimulated bone marrow. In summary, while controlling for the potential impact of Filgrastim on marrow, our studies demonstrated that CD56bright natural killer regulatory cells had a much stronger impact on Filgrastim-stimulated apheresis peripheral blood than on Filgrastim-stimulated bone marrow. This supports the conclusion that a lower proportion of CD56bright natural killer regulatory cells results in the high rate of chronic graft-versus-host disease seen in Filgrastim-stimulated apheresis peripheral blood. clinicaltrials.gov Identifier: 00438958.