| Robert David Schreiber | |
| Birth Date: | April 1946 |
| Birth Place: | Rochester, New York |
| Citizenship: | U.S. |
| Nationality: | American |
| Field: | Scientist
|
| Work Institutions: | Scripps Research Institute |
| Alma Mater: | State University of New York at Buffalo |
| Known For: | Research in cancer immunology |
Robert D. Schreiber (born 1946) is an immunologist and currently is the Alumni Endowed Professor of Pathology and Immunology at Washington University School of Medicine. Schreiber has led a major revision in our understanding of how the immune system interacts with cancer. His work on the cancer immunoediting[1] hypothesis has helped reveal that the immune system is not only capable of destroying cancers, but can also drive them into a dormant state that, in some cases, results in an improved state of malignancy.
Schreiber obtained his B.A. and PhD in biochemistry from the State University of New York at Buffalo. His postdoctoral training was with Han Mueller-Eberhart at the Scripps Clinic studying the complement system. He joined the Scripps faculty in 1976 and rose to associate member with tenure at Scripps before joining Washington University in St. Louis as Professor of Pathology. He was given the Alumni Endowed Professorship in 1990 and became an affiliate of the Ludwig Institute for Cancer Research in 2001.
Schreiber's work focuses on the concept of immune surveillance in cancer pathogenesis. For over 50 years, scientists have argued about the role of the immune system in preventing the initiation of cancer. The original immune surveillance hypothesis proposed that tumor cells arise naturally and are normally eradicated by the immune system. Tumors would, therefore, only arise if the tumor could develop a mechanism to evade the immune system, or if the immune system were compromised. This hypothesis was directly tested in a landmark paper published by Osias Stutman (1974).[2] In this paper, Stutman tested whether athymic, nude mice which lack an adaptive immune system have an increased incidence of tumors. His finding that the incidence of tumor formation was the same in nude mice, as compared to wild type mice, led to the strong belief, for over 20 years, that the immune system played no role in preventing the initiation or the prevention of tumors. This finding was consistent with the idea that most tumors arise in individuals with normal immune systems.
With the explosion of new information about the role of the innate immune system over the last two decades, and with the knowledge that the innate immune system was intact in the nude mice that Stutman had used, Schreiber repeated these experiments using a strain of mice he bred to lack both innate and adaptive immunity. These mice lacked the recombination activating gene (RAG) required for adaptive immune responses and the STAT1 gene that is required for innate responses. Schreiber's lab was the first to generate STAT1 deficient mice and has worked to characterize the important role of this gene in innate immunity.[3]
In 2001, in a landmark paper, Schreiber reported that RAG2 knockout mice, which lack an adaptive immune system (T and B cells), had a dramatically increased rate of tumor formation compared to wild type mice.[4] This study invalidated the conclusions of the Stutman study, and revived the idea that the immune system could play a critical role. Subsequent work showed that tumors escape immune recognition by losing their antigenicity in a process he named cancer immunoediting.[1]
These studies have been critical in forming the scientific basis of many of the immune mediated strategies currently being tested in patients as anti-tumor regimens. Not only do these studies confirm that the immune system can, in fact, play an important role in destroying tumors, but they support the idea that better understanding of immunological recognition and regulation will lead to breakthroughs in our ability to eradicate tumors using the immune system.