G. Burroughs Mider Lecture
Established in 1968 in honor of the first NIH director of laboratories and clinics. The lecture, part of the Wednesday Afternoon Lecture Series, is presented by an NIH intramural scientist to recognize and appreciate outstanding contributions to biomedical research.
Research in the Subramaniam lab over the last decade has been guided by the vision that emerging tools in 3D electron microscopy hold great promise for imaging cells, viruses and protein complexes at high resolution in their native states, thus bridging a major gap in structural biology. In his talk, he will review examples of recent progress ranging from determination of protein structures at atomic resolution to imaging viruses, cells and tissue at nanometer resolution.
Dr. Staudt pioneered the use of gene expression profiling to discover molecularly and clinically distinct cancer subtypes and to predict response to therapy. He defined molecular subtypes of lymphoma that were previously unrecognized but are now viewed as distinct diseases that arise from different stages of B cell differentiation, utilize different oncogenic mechanisms and offer new therapeutic targets.
Over the years, Dr. Germain and his colleagues have made key contributions to our understanding of Major Histocompatibility Complex (MHC) class II molecule structure–function relationships, the cell biology of antigen processing, and the molecular basis of T cell recognition. More recently, his laboratory has been focused on the relationship between immune tissue organization and dynamic control of adaptive immunity at both the initiation and effector stages.
The promise of treating cancer with the host’s own immune system has long held allure for scientists and physicians, but successes have been modest and inconsistent until recently. For the past two decades, Dr. Mackall’s research has focused on developing immune-based therapies for childhood cancer. She began by describing the impact of standard cancer therapies on T-cell homeostasis and identifying factors that limit T-cell restoration in children and adults.
GATA binding factor 2 (GATA2) was initially cloned in 1991 as a critical regulator of murine endothelial development, the complete absence of which was incompatible with life. Subsequent work confirmed that it was also critical for hematopoiesis, erythropoiesis, and macrophage function. After almost 20 years of characterization of patients with disseminated mycobacterial infections who had monocytopenia, B cell and NK (natural killer) cell cytopenia, Steve Holland’s group found heterozygous mutations in the same transcription factor, GATA2, accounting for their disease.
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