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.
Leveraging the Intramural Research Program to Effect Foundational Progress in Neurodegenerative Disease
In this lecture, Dr. Singleton will cover his laboratory’s work aimed at unraveling the genetics of Parkinson’s disease. This work has resulted in the identification of a large number of causal risk variants and risk loci forming the basis for much of the current mechanistic research and providing targets for therapeutic intervention. He will discuss how genetics has evolved into highly collaborative team science, and how using the capabilities and position of the Intramural Research Program has been critically important in shaping this work.
Recent discoveries have led to a resurgence of interest in neutrophils as shapers of immune dysregulation and as triggers of organ damage in chronic inflammatory diseases. These important advances have emphasized that neutrophils are significantly more versatile and heterogenous than was previously thought and that they may play fundamental roles in the pathogenesis of systemic autoimmune diseases, such as systemic lupus erythematosus, as well as in the development of vascular damage.
Advancing Therapies for Children and Adults with Rare Tumors or Genetic Tumor Predisposition Syndromes
Dr. Widemann will define rare tumors and genetic tumor predisposition syndromes and their unmet medical need. This will be followed by approaches taken in the NIH intramural research program, which provides unique resources to study rare tumors. She will highlight this in examples of NF1, RASopathies, and other rare tumors in children and adults. In addition to providing examples of advances, Dr. Widemann will highlight remaining challenges and future directions.
Dr. Segre’s research at NHGRI explores human skin bacterial, fungal and viral communities, enabling studies of alterations associated with pediatric atopic dermatitis, primary immunodeficiency and emerging pathogens. Dr. Segre’s research also focuses on integrating whole genome sequencing of hospital pathogens to track possible nosocomial transmissions. These studies integrate DNA sequence technology, algorithm development and clinical studies to explore the diversity of microbes in and on humans in health and disease.
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.
The page was last updated on Thursday, January 29, 2015 - 2:30pm