Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Sylvie Jacod"'
Autor:
Alessandra Nardin, Jean-Pierre Abastado, Aurélie Boyer, Sylvie Jacod, Claire Boccaccio, Andrew Kaiser
Publikováno v:
Journal of Immunotherapy. 25:88-96
Dendritic cells (DC) are essential for the generation of primary adaptive immune responses, but their full immunostimulatory capacities are only reached upon maturation. The authors compared several clinical-grade adjuvants of bacterial origin to det
Autor:
Arnaud Fontanet, Jean-Hervé Colle, Jacques Thèze, Jean-Louis Moreau, Sylvie Jacod, Marcel Joussemet, Olivier Lambotte, Jean-François Delfraissy
Publikováno v:
Journal of acquired immune deficiency syndromes (1999). 42(3)
Despite an increase in plasma IL-7 levels, the CD4 T-cell pool decrease progressively in HIV-infected patients. Here we report on our tests to check the hypothesis that defects in the IL-7 receptor system might be involved in this phenomenon. The cel
Autor:
Gottfried E. Konecny, Diane Provencher, Noa Ben-Baruch, Jalid Sehouli, Paul Cottu, Chen Wang, Gabriele Feisel, Sylvie Jacod, Fritz Jänicke, Hsiao-Wang Chen, Beth Y. Karlan, Lynda D. Roman, Martin Pölcher, Paul Haluska, Vincent Houe, Matthias W. Beckmann, Judy Dering, Dennis J. Slamon, Isabelle Ray-Coquard, Achim Rody
Publikováno v:
Journal of Clinical Oncology. 32:5529-5529
5529 Background: IGF signaling has been implicated in the pathogenesis and progression of ovarian cancer (OC). Ganitumab (GAN; AMG 479) is an investigational, fully human, monoclonal antibody inhib...
Autor:
Robert D. Loberg, Seamus O'Reilly, Matthias W. Beckmann, Vincent Houe, Gottfried E. Konecny, Dennis J. Slamon, Lorraine Elit, Sylvie Jacod, John A. Glaspy, Beth Y. Karlan, Paul Cottu, Linda D. Bosserman, Diane Provencher, Isabelle Ray-Coquard, Paul Haluska
Publikováno v:
Journal of Clinical Oncology. 31:5515-5515
5515 Background: IGF signaling has been implicated in the pathogenesis and progression of ovarian cancer (OC). Single agent activity and safety of ganitumab (AMG 479), a fully human monoclonal antibody against IGF-1R that blocks binding of IGF1 and I