Suzanne Ostrand-rosenberg PhD

Dr. Suzanne Ostrand-Rosenberg, Ph.D. is more than 37 years of experience as the PI of a laboratory studying the immune system’s response to malignancies. Throughout this period Suzanne lab’s long-term goal has been to manipulate an individual's immune response to reject cancer cells. In the 1990’s we were instrumental in demonstrating that CD4+ T helper lymphocytes are essential for immune-mediated tumor rejection. Recently, we were among the first labs to appreciate that myeloid-derived suppressor cells (MDSC) are highly immune-suppressive cells present in virtually all cancer patients, and are a significant obstacle to active cancer immunotherapies. Our work demonstrating that MDSC is induced by a variety of pro-inflammatory mediators was described in a Science Magazine “News Focus” article and is the basis for the concept that chronic inflammation increases cancer risk and cancer progression by inducing MDSC which inhibits anti-tumor immunity.

Our lab was also the first to demonstrate that macrophages, the other major pro-tumor myeloid cell population that infiltrates solid tumors, undergo cross-talk with MDSC which enhances the pro-tumor activity of both cell populations. Studies to date have identified a variety of physiological conditions and molecules that drive the accumulation and suppressive potency of MDSC and macrophages. However, the neutralization of these cells has been unsuccessful because of the multiple pro-inflammatory mediators that drive their accumulation and function. Our preliminary studies, which are the basis for this application, demonstrate that the ubiquitously expressed alarmin, HMGB1, and the pro-inflammatory mediator S100A8/A9, are master regulators that activate MDSC by binding to the Receptor for Advanced Glycation Endproducts (RAGE). These observations led us to hypothesize that pro-tumor MDSC and TAMs may be neutralized by targeting RAGE, HMGB1, and S100A8/A9. If our hypothesis is correct, then our studies will provide a global and universal strategy for eliminating the suppressive activity of these myeloid cell populations and provide a more favorable environment for immunotherapy in cancer patients.