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
Dr. Andrew Singleton has published more than 600 articles on a wide variety of topics. He leads a laboratory of about 50 staff, including five principal investigators and three group leaders. Singleton’s lab works on the genetic basis of neurological disorders including Parkinson's disease, Alzheimer’s disease, dystonia, ataxia, dementia with Lewy bodies, and amyotrophic lateral sclerosis (ALS). His team seeks to identify genetic variability that causes or contributes to disease and to use this knowledge to understand the underlying molecular processes.
Dr. Kaplan's research has focused on identifying mechanisms of immune dysregulation, organ damage and premature vascular disease in systemic autoimmunity. More specifically, she investigates how innate immunity (in particular, type I interferons and myeloid cells) promote end-organ damage in systemic lupus erythematosus, rheumatoid arthritis and other systemic autoimmune diseases.
Advancing Therapies for Children and Adults with Rare Tumors or Genetic Tumor Predisposition Syndromes
Dr. Widemann is the Chief of the National Cancer Institute’s (NCI’s) Pediatric Oncology Branch. Trained as a pediatric oncologist with expertise in drug development and early clinical trials for children with refractory cancers she applied her expertise to study genetic tumor predisposition syndromes (GTPS), in particular neurofibromatosis type 1 (NF1) and very rare pediatric and adult solid tumors.
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