Julio A. Aguirre-Ghiso, PhD, is an Endowed Professor of Cell Biology and founding Director of the Cancer Dormancy and Tumor Microenvironment Institute at the Albert Einstein Cancer Center in New York City, where he co-directs the Gruss-Lipper Biophotonics Center and co-leads the Tumor Microenvironment and Metastasis Program also at the Cancer Center. He is also a member of the Stem Cell Institute and Aging Research Institute at Einstein. Previously, he was an Endowed Mount Sinai Chair of Cancer Biology in the Departments of Medicine (Hematology and Medical Oncology), Otolaryngology, and Oncological Sciences and Co-Leader of the Cancer Mechanisms Program at The Tisch Cancer Institute at Icahn School of Medicine School of Medicine in New York City, where he retains and Adjunct Professor position. He is also President of the Metastasis Research Society and has served at several leadership levels at AACR. He received his PhD from the University of Buenos Aires, Argentina in 1997 and completed his post-doctoral training as a Charles H. Revson Fellow at Mount Sinai School of Medicine in 2003. He became an Assistant Professor at SUNY-Albany the same year and since 2008 he was at ISMMS where he joined as Associate Professor and reached the rank of Professor in 2014 and of Endowed Chair in 2020. His work focuses on understanding the biology of residual cancer cells that persist in a dormant state after initial therapy. His research team led, along with others, a paradigm shift, revealing novel cancer biology that diverges from the notion that cancer is perpetually proliferating. His work has been published in top tier journals such as Nature, Nature Cell Biology, JEM, Nature Cancer, Science and Cancer Cell among others. His team discovered that reciprocal crosstalk between disseminated tumor cells and the microenvironment regulates the inter-conversion between dormancy and proliferation of metastasis. His lab has also provided mechanistic advances to the understanding of the process of early dissemination in breast cancer and how it contributes to dormancy and metastatic progression. His work also has mechanistically explored how adaptive pathways such as the unfolded protein response allow cancer cells to persist while quiescent. This knowledge enables targeting residual cancer before it becomes clinically detectable and thus preventing recurrences. His research, which has been applied in clinical studies, is revealing ways to maintain residual cancer dormancy, kill dormant cancer cells, and utilize markers to determine the dormant or active state of disseminated cancer cells.

Dr. Beatty is an Associate Professor, Medicine, in the Division of Hematology/Oncology at the University of Pennsylvania Perelman School of Medicine. Dr. Beatty directs the Clinical and Translational Research Program in the Abramson Cancer Center Pancreas Program. Dr. Beatty’s clinical expertise is in the area of early clinical trials for the treatment of gastrointestinal malignancies including pancreas, esophageal and colon carcinomas. He has led the first clinical study of CD40 immunotherapy for pancreas cancer, the first in-human study of a novel inhibitor of indoleamine 2,3 deoxygenase, and first-in-human studies of chimeric antigen receptor (CAR) T cells for the treatment of pancreas cancer.

In addition to the translation of immunotherapeutic strategies for the treatment of gastrointestinal malignancies, Dr. Beatty’s clinical research is focused on translating novel imaging strategies to the clinic to understand therapeutic responses to immunotherapy. A priority of his research program is to develop and translate novel treatment strategies for pancreatic cancer, esophageal cancer, colon cancer, and glioblastoma.

Based on early clinical findings supporting a role for immunotherapy in pancreatic carcinoma, Dr. Beatty’s laboratory is using preclinical models of cancer to advance our understanding of the role of the immune system in regulating tumor biology with the primary goal to inform the development of novel immunotherapeutics for translation to the clinical setting.

Dr. Coussens is chairwoman of the department of cell, developmental & cancer biology, associate director for basic research in the Knight Cancer Institute at Oregon Health & Sciences University and holds the Hildegard Lamfrom Endowed Chair in Basic Science.

Dr. Coussens’ research focuses on dissecting the roles of normal immune cells in regulating various facets of solid tumor development, identifying leukocyte activities that are co-opted by early tumors to support ongoing cancer development, and in understanding the role leukocytes play in regulating responses to cytotoxic, targeted and immune-based therapies. Utilizing mouse models of mesothelioma, cutaneous, head and neck, pancreas and mammary carcinoma, her research identified critical immune-regulated pathways for therapeutic targeting that are being clinically translated in combination with chemotherapy in women with metastatic triple negative breast cancer, pancreas cancer, and head & neck squamous cancer.

In recognition of her research contributions for revealing underlying mechanisms of cancer development, Dr. Coussens’ has been acknowledged with multiple awards in recognition of her scientific contributions including the American Association for Cancer Research (AACR) Gertrude B. Elion Award (2001), the AACR-Women in Cancer Research Charlotte Friend Memorial Lectureship (2012), the 13^th Rosalind E. Franklin Award from the National Cancer Institute (2015), a Doctor in Medicine (honoris causa) from the University of Buenos Aires in Argentina (2018), the 12^th AACR-Princess Takamatsu Memorial Lectureship (2018), a Career Award from the European Academy of Tumor Immunology (2018), the 2018 Susan G. Komen Brinker Award for Scientific Distinction in Basic Science, and recently elected as Fellow of the American Association for Advancement of Science (AAAS; 2018) and Fellow of the AACR Academy (2019).

Ronald Wek, Ph.D., is the Showalter Professor of Biochemistry and is internationally recognized for his research on eIF2 phosphorylation and translational control in cellular adaptation to stresses, including perturbations in the endoplasmic reticulum and nutritional deficiencies. Since 1992, Dr. Wek has led a research laboratory at Indiana University School of Medicine that focuses on cellular stress response pathways and gene expression and their roles in health and disease. Dr. Wek’s research group contributed to the discovery and characterization of the eIF2 kinases PERK (EIF2AK3) in the Unfolded Protein Response and GCN2 (EIF2AK4) during nutritional deficiency. Because multiple eIF2 kinases respond to different stress conditions, this pathway is referred to as the Integrated Stress Response. Dysregulation of the eIF2 kinases and their associated stress response pathways have far-reaching biomedical significance for understanding the etiology and treatment of cancers, diabetes and related metabolic disorders, neuropathologies and infectious diseases. Dr. Wek’s research defined many of these translational control mechanisms and contributed to the understanding of the regulation and function of key target genes downstream of PERK and GCN2, including the transcription factors, ATF4 and CHOP (DDIT3), and feedback regulator GADD34 (PP1R15A).

Dr. Wek’s research has involved extensive collaborations at Indiana University and many other laboratories nationally and internationally. Dr. Wek has published over 130 research articles, reviews and commentaries, with over 12,000 citations and a current h-index of 56. He is supported by numerous grants from National Institutes of Health (NIH) and other support agencies and has served on numerous and diverse review panels for the NIH and other granting agents. Dr. Wek is an Associate Editor of the Journal of Biological Chemistry and an active member of the American Society of Biochemistry and Molecular Biology (ASBMB).

Wek received his Ph.D. from University of California, Irvine where he trained in molecular genetics. He then did a postdoctoral fellowship at the NIH with Dr. Alan Hinnebusch. This early training provided the groundwork for Dr. Wek’s pioneering research in the roles that eIF2 phosphorylation plays in adaptation to external and internal stresses encountered by cells and tissues.