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The Second Annual AACR–Cancer Research Institute Lloyd J. Old Award in Cancer Immunology

ThesecondannualAmericanAssociation forCancerResearch andCancerResearch Institute (AACR–CRI) Lloyd J.OldAward in Cancer Immunologywas presented toDr.RobertD. Schreiber on WednesdayApril 9, 2014, at the 105thannual AACRmeetingheld in San Diego, CA. Dr. Lloyd J. Old (1933–2011) was the founding scientific and medical director of CRI and an honorary member of the AACR. Dr. Old's singular focus on developing immune-based solutions for cancer, and his collaborative style of leadership for decades, shepherded basic discoveries in tumor immunity from the bench and animal models into clinical research. His efforts in large measure provided the foundation for the current success and excitement in cancer immunology and immunotherapy. It is thus fitting to consider Dr. Old as the father ofmodern tumor immunology and the original standard-bearer of cancer immunotherapy. The AACR–CRI Lloyd J. Old Award recognizes an active investigator who has conducted outstanding and innovative research in cancer immunology that has had a farreaching impact on the field. Jill O'Donnell-Tormey, PhD, Chief Executive Officer and Director of Scientific Affairs at CRI, and James P. Allison, PhD, recipient of the inaugural Lloyd J. Old award and a deputy editor of this journal, presented the award to Dr. Schreiber. Dr. Schreiber is the Alumni Endowed Professor of Pathology and Immunology, Professor of Molecular Microbiology, Director of the Center for Human Immunology and Immunotherapy Programs, and co-leader of the Tumor Immunology Program at the Siteman Cancer Center at the Washington University School of Medicine in Saint Louis (WUSTL), Missouri. Dr. Schreiber is being recognized for his pioneering work that led to our understanding of the roles of the immune system in protecting against tumor outgrowth and in shaping tumor immunogenicity leading to tumor progression. Dr. Schreiber began his award lecture with a historic summary of the cancer immunosurveillance and cancer immunoediting concepts, which date back to 1909 with the prediction by Nobel laureate Paul Ehrlich that host immunity should protect against cancer by preventing the outgrowth of continuously arising transformed cells (1). In 1951, Sir Peter Medawar, a Nobel laureate and the father of transplantation, performed a series of studies on skin grafting in mammals and defined the components of immunity required for rejecting foreign cells (2). With the development of inbred strains of mice,many investigatorswere able to study tumor immunity in the following decade (3–6)—including Lloyd Old, namesake of this award. Collectively, this work led to the recognition that tumors express specific antigens that can be recognized by the immune system, which in turn was capable of destroying the transformed cells without affecting the normal tissues from which they were derived. Moreover, tumor immunity could be transferred to isogenic hosts. These observations formed the basis for the cancer immunosurveillance hypothesis proposed by Burnett and Thomas in the late 1950s to early 1960s, positing that host immunity, and specifically T cells, would be able to detect and destroy developing tumor cells almost immediately following their transformation (7, 8). The logical predictions that followed from this hypothesis were that immunodeficient individuals should develop more cancers than those with an intact immune system. However, when these predictions were tested experimentally using nude mice (the only immunodeficient mouse strain that was available at the time), no evidence could be found for an effective cancer immunosurveillance mechanism that affected either spontaneous or carcinogen-induced cancers (9, 10). On the basis of these findings, the cancer immunosurveillance hypothesis was abandoned in the mid-1970s, and the field went on to develop arguments to explain why cancer immunosurveillance could not occur. However, by the early 1990s, things began to change. By then, it became apparent that nude mice maintained some basal Tcell functions and thus were not ideal models of immunodeficiency. In addition, newer well-defined geneticmousemodels of complete immunodeficiency were generated and monoclonal antibodies (mAb) capable of depleting or neutralizing key immune components of innate and adaptive immunity were developed that could induce immunodeficiency in wild-type mice on any genetic background. Moreover, an explosive growth had taken place in the understanding of the composition and function of the immune system such that the roles of immunity in promoting both host defense as well as immunopathologic processes were better understood (11). These events thus set the backdrop for Schreiber's entrance into the field of tumor immunology in the early 1990s. At that time, Dr. Schreiber was a well-known cytokine biologist particularly recognized for his work on the cytokine interferon gamma (IFNg). In the course of this work, Schreiber doi: 10.1158/2326-6066.CIR-14-0094