Biography
Samantha Bucktrout is a cellular immunologist who led a cancer immunology research group for Pfizer. During her five years at Pfizer, she contributed to clinical research targeting T-cells in type 1 diabetes and led the development of state-of-the-art antibody and protein therapeutics for cancer immunotherapy. Samantha Bucktrout’s basic research training includes two postdoctoral positions in groups of leading immunologists: the Bluestone Laboratory at the University of California, San Francisco and the Miller Laboratory at Northwestern University. Her research uncovered mechanisms of autoimmunity, describing the dendritic cell subsets that drive epitope spreading, and regulatory T-cell dysfunction in type 1 diabetes and multiple sclerosis. Her research has been published in Nature Immunology, Nature Medicine, and Immunity. A native of England, she graduated from the University of Aberdeen with a bachelor’s degree in biology and holds a doctorate in immunology from the University of Edinburgh.
Talk
Tumor-Immune Multiplexed Imaging To Guide Immunotherapeutic Selection
Clinical benefit to immunotherapy is thought to be hindered by the immune-suppressive tumor microenvironment. I will discuss the use of multiplexed imaging of intact tumor-stromal tissue interrogating tumor-immune relationships. Integration of molecular data and other clinical characteristics can be used to guide rational selection and enhance efficacy of emerging immunotherapeutics.
The development of effective anti-cancer therapies has been challenged by the overall complexity of tumors. The tumor heterogeneity is exacerbated during the progression of the cancer along with the tumor microenvironment (TME), comprised of many different cell populations, such as cancer-associated fibroblasts and various infiltrating immune cells, and non-cell components of extracellular matrix. These crucial parts of the surrounding stroma can function as both positive and negative regulators of all hallmarks of cancer development. Understanding the major events occurring in the TME that support primary tumor growth and how these events impact the modulation of the environment is of utmost relevance to assist the definition of efficient therapy strategies.