Immune Checkpoints in the Tumor Environment:
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1 Immune Checkpoints in the Tumor Environment: Novel Targets and the Clinical Promise of Combined Immunotherapies Monday, 28 October (AM) Parkside Ballroom B, Convention Centre Level 1 Phosphatidylserine (PS)-Mediated Immune Suppression in Tumors Support for this educational activity is provided by Peregrine Pharmaceuticals, Inc.
2 Chairman Welcome Dear Colleagues, On behalf of my distinguished faculty and Peregrine Pharmaceuticals, Inc., it is my pleasure to welcome you to what promises to be an interesting breakfast discussion at the 15 th Annual World Conference on Lung Cancer. The program titled Immune Checkpoints in the Tumor Environment: Novel Targets and the Clinical Promise of Combined Immunotherapies will highlight the discoveries that have been made about novel immune checkpoints, including PD-1, CTLA-4 and related molecules including exposed phosphatidylserine (PS) in the tumor environment. We will explore strategies to utilize this knowledge for optimizing patient outcomes. I believe that given the growing interest in the potential applications of immunotherapy in cancer treatments as well as the management of lung cancer, you will find this program quite interesting. Sincerely, Scott J. Antonia, MD, PhD H. Lee Moffitt Cancer Center Tampa, Florida
3 Program Scott J. Antonia, MD, PhD, H. Lee Moffitt Cancer Center (Symposium Chair and Moderator) - Introduction Dmitry L. Gabrilovich, MD, PhD, The Wistar Institute Myeloid-Derived Suppressor Cells as Negative Regulator of Immune Responses in Cancer Rolf A. Brekken, PhD, University of Texas Southwestern Engagement of Phosphatidylserine (PS) by PS-Targeting Antibodies Blocks a Global Immunosuppressive Checkpoint in the Tumor Microenvironment Inducing Multiple Downstream Anti-Tumor Response Mechanisms David E. Gerber, MD, University of Texas Southwestern Clinical Experience and Prospects with Checkpoint Immunotherapy in Lung Cancer
4 Biographies Scott J. Antonia, MD, PhD Department Chair and Program Leader, Thoracic Oncology and Program Leader of Immunology Program, H. Lee Moffitt Cancer Center, Tampa Florida Professor of Oncology, University of South Florida College of Medicine, Tampa, Florida Dr. Antonia is currently the Department Chair and Program Leader of the Thoracic Oncology Department, Associate Professor in the Department of Interdisciplinary Oncology and Program Leader of the Immunology Program at the H. Lee Moffitt Cancer Center and Research Institute in Tampa, Florida. He is also a Professor of Oncology at the University of South Florida College of Medicine in Tampa. Prior to being named chair of Thoracic Oncology in 2010, he was associate chairman of the Sarcoma Department. He joined the Moffitt Cancer Center in Dr. Antonia received his M.D. and his Ph.D. in Immunology from the University of Connecticut Health Center in Farmington, Connecticut. In addition, he completed an internal medicine residency at Yale University School of Medicine and pursued additional training at Yale through a medical oncology fellowship and post-doctoral fellowship in Immunobiology. Dr. Antonia s work focuses on translational research. Using his molecular biology and cellular background in the development of immunotherapeutic strategies for the treatment of cancer patients, he has developed strategies designed to thwart the immunosuppressive mechanisms used by tumors to evade T-cell mediated rejection. His clinical interests focus on immunotherapy and immunobiology, in particular, gene-modified tumor cell vaccine trials at both pre-clinical and clinical stages. He has designed and conducted numerous cutting-edge studies with novel immunotherapeutics and has two patents for technology he has developed. He has been awarded a K24 grant from the National Cancer Institute to support his clinical research and is the principal investigator for a Thoracic SPORE project. Dr. Antonia is also conducting several ongoing investigator-initiated clinical trials testing novel tumor vaccines, and tumor vaccine augmentation strategies for the treatment of various cancers. Dr. Antonia also serves as chairman of Moffitt s Scientific Review Committee and medical director of the Tumor Vaccine Production Facility at Moffitt. He was named the Moffitt Physician of the Year in 2005 and Mentor of the Year in Dr. Antonia has published papers in several peer-reviewed journals, including Science, Clinical Cancer Research, Current Opinions in Oncology, and Cancer Research.
5 Dmitry L. Gabrilovich, MD, PhD Christopher M. Davis Professor in Cancer Research, Program Leader, Translational Tumor Immunology, The Wistar Institute, Philadelphia, Pennsylvania Dr. Gabrilovich is currently the Christopher M. Davis Professor in Cancer Research and Program Leader, Translational Tumor Immunology at The Wistar Institute, Philadelphia, Pennsylvania. The Wistar Institute is the nation s first independent institution devoted to medical research and training and has been designated a National Cancer Institute Cancer Center in basic research. Prior to joining Wistar, Dr. Gabrilovich was the Robert Rothman Endowed Chair in Cancer Research and Head, Section of Dendritic Cell Biology at the Moffitt Cancer Center in the Department of Immunology and a Professor of Oncologic Sciences and Molecular Medicine at the University of South Florida. Prior to this, Dr. Gabrilovich was a Research Fellow at the Imperial College in London, United Kingdom and at the University of Texas Southwestern Medical Center in Dallas, Texas. Dr. Gabrilovich earned his MD from Kabardino-Balkarian State University Medical School in Nalchik, Russia and his Ph.D. in Immunology from the Central Institute of Epidemiology in Moscow, Russia. Dr. Gabrilovich s research has been focused on abnormalities in the function of various myeloid cells, which play a major role in regulation of immune responses. One group of cells is professional antigen-presenting cells, dendritic cells (DC). These cells are responsible for induction of the anti-tumor immune response. He was one of the first investigators who demonstrated the defects in the function of dendritic cells in cancer. Dr. Gabrilovich and his team have found that defects in differentiation of DC are associated with accumulation of immature myeloid cells in tumorbearing animals and patients with cancer. Under normal conditions, these cells represent an intermediate stage of myeloid cell differentiation. In cancer, however, they lose the ability to differentiate into mature myeloid cells, including granulocytes, DC, and macrophages. They become functionally defective and acquire the ability to suppress immune responses. Dr. Gabrilovich together with investigators from other institutions coined the term myeloid-derived suppressor cells (MDSC) which is now widely used to characterize these cells. He is one of the pioneers in discovering that murine and human MDSC have a significant role in the suppression of anti-tumor immune response. Since 2007, when the term was introduced by Dr. Gabrilovich and colleagues, more than 600 papers studying these cells were published. Dr. Gabrilovich s lab is focused on understanding the mechanisms of tumor-associated immunosuppression as well as on the development of new effective cancer immunotherapeutics. His work explores different aspects of immature myeloid cell biology in cancer. Specifically, how cellular and molecular mechanisms of T-cell suppression and tolerance are induced as a result of abnormal differentiation of myeloid cells and abnormal DC function. Their main focus is on the role of reactive oxygen species and peroxynitrite in regulation of T-cell function. His work demonstrates that reactive oxygen species produced by immature myeloid cells in vitro and in tumor-bearing animals in the presence of tumor-derived soluble factors are substantial contributors to the immunosuppression mediated by these cells in cancer.
6 Rolf A. Brekken, PhD Effie Marie Cain Research Scholar in Angiogenesis Research and Associate Professor, Hamon Center for Therapeutic Oncology, University of Texas Southwest Medical Center, Dallas, Texas Dr. Brekken is the Effie Marie Cain Research Scholar in Angiogenesis Research and an Associate Professor, in the Departments of Surgery and Pharmacology and a Principal Investigator in the Hamon Center for Therapeutic Oncology Research, University of Texas Southwest Medical Center in Dallas, Texas. He is a member of the faculty of the school s Integrative Biology and Cancer Biology Graduate programs in the UT Southwestern Graduate School of Biomedical Sciences. Dr. Brekken received his Bachelor of Arts degree from Luther College in Decorah, Iowa and his PhD (Cell and Molecular Biology) from UT Southwestern Graduate School of Biomedical Sciences. His postdoctoral fellowship was conducted in the Department of Vascular Biology at the Hope Heart Institute in Seattle, Washington where he studied how the extracellular matrix contributes to vascular function in and growth of tumors. Dr. Brekken s research interests include angiogenesis and extracellular matrix remodeling in tumors and the development and evaluation of novel therapies for cancer. His laboratory is particularly interested in the biology of novel therapies and how the intricacies of the tumor microenvironment affect therapeutic efficacy. He is an author on over 100 peer reviewed scientific papers and is a senior editor of Cancer Research. David E. Gerber, MD Associate Professor, Internal Medicine, Division Hematology-Oncology University of Texas Southwest Medical Center, Dallas, Texas Dr. Gerber is currently an Associate Professor of Internal Medicine in the Hematology-Oncology Division at the University of Texas Southwestern Medical Center in Dallas, Texas where he joined the faculty in Dr. Gerber earned his M.D. from Cornell University Medical College in New York, New York, and completed his internship and residency in Internal Medicine at the University of Texas Southwestern Medical Center in Dallas, Texas. He completed his fellowship in medical oncology at Johns Hopkins University School of Medicine in Baltimore, Maryland. Dr. Gerber is board certified in Internal Medicine and Medical Oncology. Dr. Gerber research interests are focused particularly in lung cancer, which have generated over 40 peer-reviewed publications. He has also authored two books and 12 book chapters on this topic with his studies contributing to invitations to lecture both nationally and internationally. Within the Harold C. Simmons Cancer Center at University of Texas Southwestern, Dr. Gerber serves as Co-Leader of the Experimental Therapeutics Scientific Program which aims to identify novel targets for tumor targeting, perform laboratory testing of new treatment strategies, and develop new biomarkers and clinical trials. He is also Co-Director of the Lung Cancer clinical research team. On an international level, he serves on American Society of Clinical Oncology (ASCO) and International Association for the Study of Lung Cancer (IASLC) committees related to lung cancer research and treatment; he also serves on the editorial board of the Journal of Clinical Oncology, and as a grant reviewer for the United States Department of Defense and the American Cancer Society.
7 Immunosuppressive signals from PS help tumors evade immune surveillance. Antibody-mediated Phosphatidylserine (PS) blockade overrides immunosuppressive signaling. Phospholipids are distributed asymmetrically in the plasma membrane of most normal eukaryotic cells. Unlike neutral phospholipids that are distributed randomly across the bilayer membrane, phosphatidylserine (PS) is localized predominantly in the inner membrane leaflet. The asymmetric distribution of PS is maintained actively by an ATP-dependent aminophospholipid translocase. During apoptosis, PS is externalized to the outer plasma membrane leaflet where it functions as an eat me signal that facilitates the recognition and clearance of dying cells. PS-dependent engulfment of apoptotic cells triggers a series of events that leads to the generation of potent immunosuppressive signals associated with Myeloid Derived Suppressor Cells (MDSCs) and M2 macrophages that quell any potential autoimmune responses. Thus, PS exposure represents an evolutionarily conserved mechanism of immune suppression. Tumors have hijacked this biology such that exposure of PS in the tumor microenvironment is critical in maintaining the immunosuppressive state of tumors. Externalized PS is abundant in the tumor microenvironment : it is found on tumor vascular endothelial cells, on tumor-derived microvesicles, and constitutively on some tumor cells. Moreover, the exposure of PS is increased significantly on tumor cells in response to chemotherapy and radiotherapy. Externalized PS interacts with PS receptors on immune cells where it actively promotes expansion of immunosuppressive cells that enhance tumor progression and prevent induction of adaptive tumor immunity. Based on these observations, we propose that PS exposure is a global immune checkpoint that is exploited by successful tumor for growth and progression. To explore the possibility of reversing the immunosuppressive effects of exposed PS, we raised a family of PS-targeting antibodies that bind or target PS with high affinity. For example, bavituximab, a chimeric PS targeting antibody is currently in multiple clinical trials, with the initiation of a Phase III trial in non-small cell lung cancer underway. Data obtained in pre-clinical tumor models indicate that antibody mediated PS blockade reactivates tumor immunity on multiple levels. It repolarizes tumor associated macrophages from an immunosuppressive to a tumoricidal phenotype, it decreases the presence of immunosuppressive MDSCs and promotes their differentiation, it promotes dendritic cell maturation into functional antigen presenting cells, and induces tumor specific cytotoxic T-cell immunity. Thus, antibody mediated PS blockade promotes innate and adaptive tumor immunity. Impressive anti-tumor effects have been obtained in cancer patients by blockade of immune checkpoints (e.g., antibodies specific for PD-1, PD-L1, and CTLA-4). However, only a limited number of patients benefit from these therapies. Mechanistic studies indicate that blockade of these immune checkpoints are most effective when there is a de novo or pre-existing antitumor immune response. Unfortunately, pre-existing tumor specific immune activity is limited in cancer patients because of the exposure of PS in the tumor microenvironment. Our results in animal models indicate that antibody-mediated PS blockade with bavituximab reverses PS-mediated immunosuppression and initiates therapeutically effective adaptive antitumor immunity. Thus, treatment with bavituximab in combination with blockade of downstream immune checkpoints could potentially result in robust and long-lasting antitumor immunity that significantly improves clinical outcomes. For more information please see Yin et al 2013 Cancer Immunology Research 1: doi: /
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