Colleagues: Recently Tenured


Senior Investigator and Chief, Immunity to Pulmonary Pathogens Section,
 Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases

Katy Bosio

Education: Washington State University, Pullman, Wash. (B.Sc. in microbiology); Colorado State University, Fort Collins, Colo. (Ph.D. in microbiology)

Training: Postdoctoral fellowships at the Food and Drug Administration Center for Biologics Evaluation and Research (Bethesda, Md.) and at the U.S. Army Medical Research Institute for Infectious Diseases (Frederick, Md.), studying innate immunity to Mycobacterium tuberculosis, Francisella tularensis, and Ebola and Marburg viruses

Before coming to NIH: Assistant professor, Department of Microbiology, Immunology, and Pathology, Colorado State University

Came to NIH: In 2007

Selected professional activities: Editorial board, Infection and Immunity; committee and co-chair, American Society for Microbiology Biodefense and Emerging Diseases meeting

Outside interests: Running; reading; hiking; cooking


Research interests: The focus of our research is to gain a better understanding of how aerosolized pathogens successfully infect and modulate the pulmonary environment to cause overt disease and death. Currently, our principal interest is the pathogenesis of aerosolized F. tularensis, the causative agent of pneumonic tularemia.

We are focused on uncovering the mechanisms by which F. tularensis modulates for innate and adaptive immunity. As an intracellular pathogen, F. tularensis is intimately associated with host cells. We have identified several major pathways by which the bacterium interferes with host-cell function, including accelerating decay of host mRNA, inhibiting transcription factors, and modulating host metabolism. F. tularensis can also affect generation of effective adaptive responses. We have developed several models to identify the specific cellular requirements for survival of tularemia and how the bacterium interferes with development of long-lived, antigen-specific, memory T cells. Identification of the microbial mechanisms and products embodied by F. tularensis that dampen mammalian immunity will aid in the development of novel vaccines and therapeutics for tularemia, as well as new therapies for unrelated diseases in which control of inflammation is required for survival.


Senior Investigator and Head, Unit on Behavioral Neurogenetics, National Institute of Child Health and Human Development

Harold Burgess

Education: University of Melbourne, Parkville, Victoria, Australia (B.S. in biochemistry); the Weizmann Institute of Science, Rehovot, Israel (Ph.D. in developmental neuroscience)

Training: Postdoctoral training, University of Pennsylvania (Philadelphia)

Came to NIH: In 2008

Selected professional activities: Academic Editor, PLOS One

Outside interests: Geocaching with his three kids; running; cultivating garlic; reading detective fiction


Research interests: My laboratory combines genetic and imaging techniques to study neural circuits required for sensory-guided behavior and motivational states. We use larval zebrafish to understand the functional development of neuronal circuits that allow the larvae to choose the best responses to environmental stimuli. The zebrafish model is a great system because the larval brain has the same basic organization as the human brain, but it is, of course, much smaller, containing only around 100,000 neurons, instead of the 100 billion or so in humans. The transparency of the fish at larval stages means that we can observe the firing of individual neurons in real time.

Larval behavior is innate and varies little among individual fish so it’s relatively easy to apply computational tools to quickly assess the contribution of identified neurons to behavior. For instance, one major behavioral test that my laboratory uses is the startle response. Defects in the startle response are observed in many psychiatric disorders, and the brainstem regions that control startle responses are highly conserved in fish. By performing genetic screens in larval zebrafish, we identify genes and neurons that tightly control the threshold for startle responses that are also relevant to mammals. We also study light-seeking behavior in larvae. Remarkably, part of this behavior is actually controlled by light-sensitive neurons within the brain itself rather than through the retina. We think these neurons are part of a primitive control system for motivational state, allowing us to understand how the fish perform goal-directed actions.


Senior Investigator and Deputy Chief, Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences

Francesco DeMayo

Education: Cornell University, Ithaca, N.Y. (B.S. in general studies); Michigan State University, East Lansing, Mich. (M.S. and Ph.D. in physiology)

Training: Postdoctoral training at Baylor College of Medicine (Houston)

Before coming to NIH: Cullen-Duncan-McAshan Endowed Chair in Cancer Research and Professor of Molecular and Cellular Biology and of Pediatrics, Baylor College of Medicine

Came to NIH: In 2015

Selected professional activities: Co-editor-in-chief of Biology of Reproduction

Outside interests: Bowling; bicycling; enjoying opera


Research interests: I lead the Pregnancy and Female Reproduction Group, which studies the mechanisms involved from the implantation of an embryo in the uterus to the birth of a baby. To identify the proteins that regulate the female reproductive tract during these processes, we use genetically engineered mice, human cells, and transcription-factor analysis. These tools allow us to examine factors that allow proper embryo implantation, adequate uterine support for embryo development, and on-time delivery. The timing of lung development is also critical for embryonic maturation. Our group investigates what regulates lung physiology and homeostasis and how lung cancer develops.

Our major areas of research include understanding uterine biology, specifically, how several transcription factors regulate the window of uterine receptivity; determining what regulates differentiation of the stroma, one of the three layers of the uterus; examining the role of transcription factors in another layer of the uterus called the myometrium; and using mouse models to explore the development of lung cancer.

Specifically, our current projects include investigating how forkhead box protein O1 (FOXO1) and the progesterone receptor interact to regulate uterine receptivity for embryo implantation; establishing how WNK1 is involved in postimplantation support of the embryo; and how the progesterone receptor controls myometrial function during pregnancy and birth. We are also exploring the involvement of environmental factors in the development of squamous non-small-cell lung cancer.


Senior Investigator and Deputy Director, Division of Cancer Epidemiology and Genetics, National Cancer Institute

Montserrat Garcia-Closas

Education: University of Barcelona, Barcelona, Spain (M.D.); Harvard School of Public Health (M.P.H. in quantitative methods; Dr.P.H. in epidemiology)

Training: Postdoctoral training at NCI-DCEG

Came to NIH: In 1996 for training; became a tenure-track investigator in 1999 and a tenured senior investigator in 2007; left in 2008; returned in 2015

Before returning to NIH: Visiting scientist at the Department of Oncology and Strangeways Laboratory, University of Cambridge University (Cambridge, U.K.) in 2008–2010; professor of epidemiology at Division of Genetic and Epidemiology of the Institute of Cancer Research, University of London (London) in 2010–2015

Selected professional activities: Editorial board for Cancer Epidemiology, Biomarkers & Prevention; senior editor for Molecular and Genetic Epidemiology

Outside interests: Anything fun and relaxing–yoga, hiking, visiting new places, watching movies, photography, gardening, you name it


Research interests: I conduct large epidemiological studies to investigate biomarkers of breast- and bladder-cancer risk in combination with other exposure information. In particular, I am interested in the molecular characterization of tumors to identify exposure signatures and subtype-specific causes of cancer; identification of biomarkers of risk, including genetic and epigenetic changes; integration of biomarkers and other risk factors into cancer-risk prediction models; and evaluation of the utility of biomarkers in risk stratification to inform personal and public-health decisions in precision prevention.

The goal of my breast-cancer research is to facilitate the development and implementation of targeted prevention and screening strategies for different types of breast cancer. I am a co-leader of large-scale molecular-pathology studies within the international Breast Cancer Association Consortium. I have contributed to the development of one of the largest centralized collections of breast-tumor tissue with detailed data on risk factors and clinical outcomes. This resource has revealed important tumor markers that delineate the etiologic heterogeneity of breast cancer. At the University of London’s Institute of Cancer Research, I co-led the Breakthrough Generations Study, a large prospective cohort study of over 110,000 women in the United Kingdom aimed at evaluating risk factors for breast cancer. I am also an investigator in the ongoing international genotyping project OncoArray and am trying to identify inherited-susceptibility loci associated with specific subtypes of breast cancer.

In my bladder-cancer research, I am investigating the combined effects of genetic and environmental risk factors for this cancer. I have published the definitive study of the interaction between smoking history and the NAT2 genotype, which is one of the few consistent gene-environment interactions described to date. I contributed to the discovery of novel susceptibility loci for bladder cancer using genome-wide association studies, an area in which I continue to collaborate. In addition, I am engaged in epigenome-wide association studies of bladder cancer through NCI’s Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO) and identifying additional risk biomarkers.


Senior Investigator and Chief, Neuronal Ensembles in Drug Addiction, National Institute on Drug Abuse

Bruce Hope

Education: University of British Columbia, Vancouver, B.C. (B.Sc. in biochemistry; Ph.D. in neurological research)

Training: Postdoctoral training at the Laboratory of Molecular Psychiatry, Department of Psychiatry, Yale University, New Haven, Conn.

Before coming to NIH: Staff scientist at New England Medical Center (Boston) and assistant professor, Department of Pharmacology, at Tufts University School of Medicine (Boston); staff scientist at Massachusetts General Hospital (Boston); and instructor, Department of Psychiatry, Harvard Medical School (Boston)

Came to NIH: In 1996 as a visiting scientist in NINDS; then various positions in NIDA (1998–2009); became tenure-track investigator in NIDA in 2010

Selected professional activities: Associate editor for the Journal of Neuroscience and Synapse (2011–present); ad hoc reviewer for almost 40 journals

Outside interests: Swimming; ballroom dancing


Research interests: Use of drugs of abuse can cause learned associations to form between the drugs and the stimuli present in the drug-taking environment. With continued use, these stimuli can become cues that promote drug relapse. My group’s research is focused on figuring out how these memories are stored in the brain.

We have identified sparsely distributed patterns of neurons in the brain called neuronal ensembles that are selectively activated by drug-related cues and are thought to encode the learned associations that mediate drug-seeking behavior. Drug-related cues activate specific genes such as c-fos within these neuronal ensembles and allow us to identify them in the brain. We exploit the c-fos promoter to turn on different transgenes in transgenic rats, allowing us to manipulate specific neuronal ensembles and assess their role in drug-related memories.

We also developed a fluorescence-activated cell-sorting procedure for purifying these activated ensembles and found unique molecular alterations within their cell bodies and synapses. We have developed novel c-fos-GFP transgenic rats that produce green fluorescent protein in activated neurons and found unique synaptic alterations using slice electrophysiology. Using a combination of novel viruses and transgenic rats developed in collaboration with a colleague, we continue to search and characterize drug-related memory engrams that promote drug relapse.

If you have been tenured in the past few months, the NIH Catalyst will be in touch with you soon to invite you to be included on these pages. We will ask for your CV and a recent photo, review your website, and then draft an article for your review and edits.