Abstract
The Willingham et al., 2012, published in PNAS in 2012. The key experiments being replicated are those reported in Figure 6A-C and Table S4. In these experiments, Willingham et al., 2012 test the safety and efficacy of anti-CD47 antibody treatment in immune competent mice utilizing a syngeneic model of mammary tumor growth in FVB mice. The Reproducibility Project: Cancer Biology is a collaboration between the eLife.
Highlights
Phagocytosis is an essential process utilized by an organism for pathogen or apoptotic cell clearance (Poon et al, 2014)
CD47 expression is increased in several cancer types including acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), non-Hodgkin lymphoma (NHL), primary effusion lymphoma, multiple myeloma, leiomyosarcoma, and bladder cancer, and targeting of CD47 on cancer cells with an anti-CD47 blocking antibody can promote phagocytosis by macrophages in vitro (Chan et al, 2009; Jaiswal et al, 2009; Majeti et al, 2009; Chao et al, 2010a; Edris et al, 2012)
Treatment with an anti-CD47 blocking antibody synergized with rituximab treatment to promote phagocytosis in vitro and to eliminate cancer cells in an in vivo xenograft model of nonHodgkin lymphoma (Chao et al, 2010b)
Summary
Phagocytosis is an essential process utilized by an organism for pathogen or apoptotic cell clearance (Poon et al, 2014). Willingham et al, 2012 showed that anti-CD47 antibody treatment reduced tumor growth and increased lymphocytic infiltration to the tumor site without unacceptable toxicity, demonstrating that anti-CD47 therapy is effective in reducing solid tumor growth in immune competent hosts This key experiment demonstrates that CD47 is a therapeutic target for solid tumors and follows similar reports from the same laboratory that demonstrated that anti-CD47 antibody treatment reduced growth of primary human cancer xenografts of several hematopoietic cancers and of solid leiomyosarcoma tumors (Jaiswal et al, 2009; Majeti et al, 2009; Chao et al, 2010a; Edris et al, 2012).
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