Dr. Scott Abrams joined the Faculty of Roswell Park Cancer Institute (RPCI) in 2008 and, in 2013, was promoted to Professor of Oncology and Member in the Department of Immunology. He holds a joint appointment as Research Professor on the Graduate Faculty at the State University of New York at Buffalo. Moreover, in 2013, he was appointed as Director of Graduate Studies in the Department of Immunology at RPCI and, in 2014, was reappointed to the UB Graduate Faculty with Distinction.
Dr. Abrams came to RPCI from the Laboratory of Tumor Immunology and Biology, National Cancer Institute (NCI), National Institutes of Health (NIH), in Bethesda, MD, where he served as an Investigator. He has been honored by the NCI/NIH with five consecutive Performance Awards from 2003–2007, and was the recipient of six NIH Federal Technology Transfer Awards for the discovery of human T lymphocyte peptide epitopes reflecting ras codon 12 mutations. The identification of such mutated ras peptide sequences has also culminated in patent approval in both Europe and the U.S.
Currently, Dr. Abrams serves on several external grant review panels. He has authored or co-authored more than 100 journal articles, reviews and book chapters, and has received numerous national and international invitations to speak.
Dr. Abrams' research focus is in tumor immunology; specifically, how solid tumors impair the normal process of myeloid cell production leading to the generation of myeloid-derived suppressor cells (MDSCs) which potently suppress antitumor immunity. Although much attention in this field has been devoted to unraveling mechanisms by which MDSCs mediate such immune suppression, a larger gap has remained in the understanding of the molecular or transcriptional mechanisms that initiate their development. Thus, over the past several years, the Abrams laboratory has been testing the central hypothesis that tumor-induced downregulation of interferon regulatory factor-8 (IRF8) compromises normal myelopoiesis, resulting in myeloproliferative phenotypes heavily characteristic of MDSCs. Emphasis has been placed on IRF8, since IRF8 is well-recognized as a key transcriptional player in normal myeloid cell development and differentiation.
Now published in a series of research articles, including The Journal of Clinical Investigation, his work defines a new paradigm in MDSC biology reflecting early transcriptional cues that profoundly affect MDSC development in neoplastic disease, such as breast cancer. The Abrams Lab has also engaged in a number of collaborations with other RPCI investigators reflecting shared research interests. For example, through the newly awarded RPCI-UPCI Ovarian Cancer SPORE, Dr. Abrams works with Drs. Odunsi and Moysich to study the association between MDSCs and ovarian cancer prognosis. The long-term goals of his research program are to advance an understanding of how the neoplastic process impairs the host immune response, thereby providing new insights into the design of strategies that can more effectively battle this extraordinarily complex family of diseases.
Banik D, Khan ANH, Walseng E, Segal BH, and Abrams SI. Interferon regulatory factor-8 is important for histone deacetylase inhibitor-mediated antitumor activity. PLoS One 7(9): e45422, 2012. doi:10.1371/journal.pone.0045422. PMCID: PMC3446900
Waight JD, Netherby C, Hensen ML, Miller A, Hu Q, Liu S, Bogner PN, Farren MR, Lee KP, Liu K, and Abrams SI. Myeloid-derived suppressor cell development is regulated by a STAT/IRF-8 axis. J. Clin. Invest. 123:4464-4478, 2013. PMCID: PMC3784535
Farren MR, Carlson LM, Netherby CS, Li P-K, Gabrilovich DI, Abrams SI, and Lee KP. Tumor induced STAT3 signaling impairs dendritic cell differentiation by downregulating PKC (beta) II expression. Sci. Signal. 7(313):ra16, 2014. doi: 10.1126/scisignal.2004656. PMCID: PMC4033697
Waight JD, Banik D, Griffiths EA, Nemeth MJ and Abrams SI Regulation of the interferon regulatory factor-8 (IRF-8) tumor suppressor gene by the signal transducer and activator of transcription 5 (STAT5) transcription factor in chronic myeloid leukemia. J. Biol. Chem. 289:15642-15652, 2014. PMCID: PMC4140919
Messmer MN, Netherby CS, Banik D, and Abrams SI. Tumor-induced myeloid dysfunction and its implications for cancer immunotherapy. Cancer Immunol. Immunother. 64: 1 – 13, 2015. PMCID: PMC4282948