Samuel Blackman, MD, PhD

Samuel C. Blackman is a physician-scientist and experienced cancer drug developer and biopharmaceutical executive, who has been involved in the early-stage clinical development of numerous cancer therapeutics over the past 17 years. He is currently an Entrepreneur-in-Residence at Google Ventures.

Sam was the co-founder and Head of Research and Development of Day One Biopharmaceuticals where he led the acquisition and development of OJEMDA™ (tovorafenib) through FDA approval and commercialization. Prior to founding Day One in 2018, Dr. Blackman held positions of increasing responsibility in large pharmaceutical companies (Merck, GlaxoSmithKline) and biotechnology companies (Seattle Genetics, Juno Therapeutics, Silverback Therapeutics, Mavupharma). He is also a member of the board of directors of Presage Biosciences and Bonum Therapeutics, as well as a a board member of the Pediatric Brain Tumor Foundation and CureSearch. Sam is a graduate of the pediatric hematology/oncology fellowship program at the Dana Farber Cancer Institute and Children’s Hospital Boston, and the pediatric residency program at Cincinnati Children’s Hospital Medical Center. Dr. Blackman received his B.A. in Philosophy from the University of Chicago, and his M.D. and Ph.D. in Pharmacology from the University of Illinois at Chicago.

Jean-Francois Emile, MD, PhD

Dr. Jean-Francois Emile obtained his MD of medicine in 1994, and his PhD of immunology in 1997 at the University of Paris and started his academic career as assistant professor in Necker hospital. He has been Professor of pathology since 2003.

Since 1993, J.F. Emile actively contributed to the French histiocytosis network, and had several international collaborations. J.F. Emile contributed to 135 publications on histiocytoses (Pubmed). H-index 84 (Web of Science, Clavirate). He contributed to the description of new types of histiocytosis, to a better understanding of these diseases through description of the molecular somatic alterations, and to the development of targeted therapies.

His present positions include Professor of Pathology at the University of Versailles SQY, University Paris-Saclay, France. Head of research unit EA4340-BECCOH at the University of Versailles SQY, University Paris-Saclay. Head of the pathology laboratory of the Ambroise Paré hospital, Assistance Publique – Hôpitaux de Paris, in Boulogne, France. Head of Biobank of the Ambroise Paré hospital.

Juliane Gust, MD, PhD

Juliane Gust is an Assistant Professor of Pediatric Neurology at Seattle Children’s/University of Washington. As a pediatric neurologist and physician-scientist, she is interested in the effects of cancer therapy and systemic inflammation on the developing brain. Her current work focuses on determining the pathomechanisms of neurotoxicity associated with chimeric antigen receptor (CAR) T cell therapy, as well as the use of CAR T cells to target brain tumors. In her laboratory, she uses animal modeling and in vivo imaging approaches to dissect cellular mechanisms of immune-neurovascular interaction. She is also actively involved in several clinical research consortia in cancer immunotherapy.

Sidd Jaiswal, MD, PhD

Sid Jaiswal is an investigator at Stanford University in the Department of Pathology, where his lab focuses on understanding the biology of the aging hematopoietic system. As a post-doctoral fellow, he identified a common, pre-malignant state for blood cancers by reanalysis of large sequencing datasets. This condition, termed "clonal hematopoiesis", is characterized by the presence of stem cell clones harboring certain somatic mutations, primarily in genes involved in epigenetic regulation of hematopoiesis. Clonal hematopoiesis is prevalent in the aging population and increases the risk of not only blood cancer, but also cardiovascular disease and overall mortality, possibly by alteration of myeloid cell function. Recent work from the lab has identified the genetic mechanisms of positive selection for many mutant clones. Other work has identified that clonal hematopoiesis is surprisingly associated with protection from Alzheimer’s disease, which may be due to infiltration of mutant cells into the brain. Dr. Jaiswal’s longstanding goal is to identify clinical interventions to reduce the risk of adverse consequences in those with pre-malignant states like clonal hematopoiesis. Understanding the biology of these mutations and how they contribute to the development of cancer and other age-related diseases is the current focus of work in the lab. Dr. Jaiswal’s longstanding goal is to identify clinical interventions to reduce the risk of adverse consequences in those with pre-malignant states like clonal hematopoiesis.

Astrid van Halteren, MD, PhD

Ilia Voskoboinik, MD, PhD

Professor Ilia Voskoboinik is a group leader at the Peter MacCallum Cancer Centre, where he leads the Killer Cell Biology Laboratory within the Cancer Immunology Research Program. His research spans biochemistry, human genetics, cell biology, and immunology, with a focus on elucidating the molecular mechanisms underlying congenital diseases.

Professor Voskoboinik completed his Ph.D. in Toxicology in 1998 before undertaking postdoctoral research at the Karolinska Institute in Stockholm. He then returned to Australia to join the Department of Genetics at the University of Melbourne, where he investigated the biochemical and cellular mechanisms of Menkes disease, a congenital disorder of copper metabolism.

Since joining the Peter MacCallum Cancer Centre in 2003, his research has centred on cytotoxic T lymphocytes and natural killer cells, with particular emphasis on their cellular and biochemical mechanisms, paediatric primary immunodeficiencies, and predisposition to haematological cancers. His work has contributed to significant discoveries, including elucidating the process of perforin pore formation - a critical step in cytotoxic lymphocyte-mediated killing, the mechanisms protecting cytotoxic lymphocytes from their own effector proteins, the cellular basis of familial haemophagocytic lymphohistiocytosis (FHL) hyperinflammation, and the link between impaired cytotoxic lymphocyte function and atypical FHL as well as haematological malignancies.