Immunotherapy for Pediatric Cancer

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The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute Natural Killer Cells:

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Presentation transcript:

Immunotherapy for Pediatric Cancer Stephan A. Grupp, Michael Verneris, Paul M. Sondel, Laurence J.N. Cooper Biology of Blood and Marrow Transplantation Volume 14, Issue 1, Pages 33-43 (January 2008) DOI: 10.1016/j.bbmt.2007.10.014 Copyright © 2008 American Society for Blood and Marrow Transplantation Terms and Conditions

Figure 1 Kaplan-Meier curves showing the overall and event-free survival (OS, EFS) for patients undergoing tandem autologous HSCT for high-risk NBL. The patients received carboplatin/etoposide/cyclophosphamide for the first HSCT, and melphalan/TBI for the second. (A) Overall survival (OS) from diagnosis. (B) EFS from diagnosis. Biology of Blood and Marrow Transplantation 2008 14, 33-43DOI: (10.1016/j.bbmt.2007.10.014) Copyright © 2008 American Society for Blood and Marrow Transplantation Terms and Conditions

Figure 2 T cell recovery as assessed by peripheral blood CD4+ T cell count at indicated times after tandem autologous HSCT. The groups include: patients receiving PBSC (no T cells), patients receiving T cell augmentation at day +12 and day +2 after the second PBSC infusion, and 4 patients from the day +2 group who experienced engraftment syndrome (Eng Synd). Biology of Blood and Marrow Transplantation 2008 14, 33-43DOI: (10.1016/j.bbmt.2007.10.014) Copyright © 2008 American Society for Blood and Marrow Transplantation Terms and Conditions

Figure 3 Possible outcomes following NK-Cell inhibitory receptor interaction with target cells such as AML blasts. (A) Engagement of CD94/NKG2A with nonpolymorphic HLA-E (limited polymorphism) results in no killing; (B) lack of HAL-E expression on leukemia cells prevents CD94/NKG2A signaling, creating a situation where NK cells may not be inhibited; (C) KIR binding to self-HLA-A, or -B, or -C on leukemia cells results in NK inhibition; (D) a lack of HLA-A, -B, or -C on leukemia cells results in no KIR engagement and enhanced NK-cell killing, and (E) KIR that do not recognize HLA-A, -B, and -C on leukemia cells (as in the setting of KIR-ligand mismatched transplant) can result in increased killing. Biology of Blood and Marrow Transplantation 2008 14, 33-43DOI: (10.1016/j.bbmt.2007.10.014) Copyright © 2008 American Society for Blood and Marrow Transplantation Terms and Conditions

Figure 4 Individual NK-cells differ in inhibitory receptor expression. Shown is a FACS plot of peripheral blood NK cells (gated on CD56+CD3−) from a healthy donor. Four distinct populations of cells can be identified by staining for KIR cocktail (CD158a, CD158b, and CD158e) vs CD94. The majority of NK cells express CD94 (and NKG2A, not shown) and are inhibited by HLA-E (right upper and lower quadrant). A small fraction of cells express KIR, but not CD94 (left upper quadrant), and these cells have the potential to be "alloreactive." The KIRnegCD94neg fraction is hyporesponsive. Biology of Blood and Marrow Transplantation 2008 14, 33-43DOI: (10.1016/j.bbmt.2007.10.014) Copyright © 2008 American Society for Blood and Marrow Transplantation Terms and Conditions

Figure 5 Schematic of hu14.18-IL2 (EMD 273063) immunocytokine linking GD2+ tumor cells and IL-2R+ lymphocyte [75]. Biology of Blood and Marrow Transplantation 2008 14, 33-43DOI: (10.1016/j.bbmt.2007.10.014) Copyright © 2008 American Society for Blood and Marrow Transplantation Terms and Conditions