NIH Research Festival
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Masur Auditorium, Building 10
Super enhancers, as the name may connote, offer seemingly heroic regulation of gene expression. While snippets of DNA known as enhancers have long been appreciated to bind with transcription factors to ramp up gene activity, regions of DNA called super enhancers are exceptionally busy parts of the genome that control lineage-defining genes — to paraphrase the movie Spinal Tap, they turn their volume up to 11 just when that extra push is needed. Mutations in super enhancers have been noted in various diseases, and they may play important roles in the dysregulation of gene expression in cancer.
NIH researchers have been at the forefront of this three-year-old field. The Collins lab in 2013 identified “stretch enhancers” as gene groups analogous to super enhancers; and with the O’Shea lab they explained how T cell super enhancers relate to the function of this specialized cell. In the summer of 2016, the Hennighausen lab discovered super enhancers in the mammary genome and used CRISPR/Cas9 to dissect one in mice. In this plenary session, NIH researchers present their latest work on these master control switches. Francis Collins, M.D., Ph.D. (NHGRI), will discuss the epigenomics of type 2 diabetes as revealed by one set of super enhancers. Rafael Casellas, Ph.D. (NIAMS), will illuminate the role of nuclear architecture in gene expression in B cells. And Keiko Ozato, Ph.D. (NICHD), will present how super enhancer are rapidly organized to control inflammatory gene expression.
Masur Auditorium, Building 10
The NIH intramural program has helped to pioneer the field of clinical imaging, from the earliest development of MRI technology and Louis Sokoloff’s now classic PET scan techniques to map and measure brain function, to recent breakthroughs such as MRI-guided closed-chest heart repair.
This plenary session highlights the latest research of three NIH PIs who are extending this fine tradition of intramural-based clinical imaging advances. Shawn Chen, Ph.D. (NIBIB), will discuss nanotheranostics, the integration of diagnostic and therapeutic function in one system using the benefits of nanotechnology, which may be essential for personalized medicine. Jessica Gill, Ph.D., R.N. (NINR), will present her discoveries of mechanisms underlying differential responses to traumatic brain injury as a way to inform interventions to support recovery. And PET expert Robert Innis, M.D., Ph.D. (NIMH), will present his most recent method for imaging proteins as a biomarker for neuro-inflammation.
Masur Auditorium, Building 10
Cell-based immune therapies, such as immunotherapy for cancer, are among the hottest topics in clinical research. A centuries-old concept of stimulating the immune system to fight a non-infectious disease, immunotherapy became a viable treatment that doctors could exert some degree of control over as a result of pioneering research at the NCI in the 1960s and 1970s on monoclonal antibodies (Michael Potter) and Interleukin-2 (Robert Gallo). Building on such advances, NCI’s Steven Rosenberg, M.D., Ph.D. was the first to recognize the potential of Il-2 and apply it as a novel anti-cancer agent, in 1984. Rosenberg has spent most of his 40-year-career at the NIH improving various techniques, most recently developing chimeric antigen receptor therapy and T cell receptor gene-engineered cell therapy to fine-tune and turbo-charge the killing of cancer cells.
Rosenberg’s body of research has given rise to numerous methods to harness the immune system to fight cancer and other chronic, non-infectious diseases. And many of Rosenberg’s NIH colleagues are now at the forefront of these pursuits. This plenary session features Steve Rosenberg, providing an historical context that only he can best deliver, as well as an update on his latest clinical work. Nicholas Restifo, M.D. (NCI), will discuss new immunotherapies for patients with advanced cancer. And John Tisdale, M.D. (NHLBI), will present his research combining hematopoietic stem cell methods with immunotherapy for the treatment of the genetic-based sickle cell disease.
This page was last updated on Friday, March 12, 2021