Colleagues: Recently Tenured
RAMAPRASAD SRINIVASAN, M.D., PH.D., NCI
Senior Investigator, Head, Molecular Cancer Section, Urologic Oncology Branch, National Cancer Institute (NCI)
Education: Bangalore Medical College, Bangalore, India (MBBS); University of Texas MD Anderson Cancer Center and Graduate School of Biomedical Sciences, Houston (Ph.D.)
Training: Oncology and Hematology Fellow, National Institutes of Health, NCI and National Heart, Lung, and Blood Institute (1999–2003); Resident, University of Texas Health Science Center, Houston, Department of Internal Medicine (1997–1999); Resident, State University of New York at Stony Brook, New York, Department of Internal Medicine (1996–1997)
Came to NIH: In 1999 as a Research Fellow, NCI
Outside interests: Travel; reading; running; tennis; cooking
Research interests: My lab leads efforts to develop novel treatment strategies for patients with kidney cancer within the Urologic Oncology Branch and the Center for Cancer Research. My work is focused on developing and evaluating individualized, mechanism-based proof-of-concept studies based on the recognition that there are inherent genetic and molecular differences between various subtypes of kidney cancer. I pioneered the evaluation of systemic treatment strategies in patients with von Hippel-Lindau disease (VHL) and co-led an international study that ushered in the FDA approval of the HIF2-alpha inhibitor belzutifan, heralding a paradigm shift in the management of VHL (N Engl J Med 385:2036-2046, 2021).
Our work has also led to the development of a new standard of care in patients with metastatic kidney cancer associated with hereditary leiomyomatosis and renal-cell cancer. I am currently investigating a variety of newer targeted agents as well as novel immunotherapy approaches in clear cell and papillary kidney cancer, as well as in hereditary kidney cancer syndromes.
SHUO GU, PH.D., NCI
Senior Investigator, RNA Mediated Gene Regulation Section, RNA Biology Laboratory, Center for Cancer Research (CCR), National Cancer Institute (NCI)
Education: Tsinghua University, Beijing (B.S. in biology); City of Hope Medical Center, Duarte, California (Ph.D. in molecular biology)
Training: Postdoctoral training in molecular biology, Departments of Pediatrics and Genetics, Stanford University at Palo Alto, California (2011–2013)
Before coming to NIH: Research Fellow, Stanford School of Medicine
Came to NIH: In 2014 as a Stadtman Investigator, NCI-CCR
Outside interests: Reading; running; swimming
Research interests: My laboratory studies how microRNAs(miRNAs), a class of small noncoding RNAs, are regulated. We aim to understand how sequence alterations at miRNA 5' and 3' ends diversify miRNA function. We became interested in this problem through the study of miRNA isoforms (isomiRs), which are abundantly detected in cells.
My laboratory has made significant contributions to elucidating the mechanisms of isomiR biogenesis and function. We developed a novel algorithm that allows us to detect and annotate isomiRs from next-generation sequencing data with high confidence (Bioinformatics 35:1576-1578, 2019). Using this method, we demonstrated that isomiR profiles are cell-, tissue-, and disease-specific.
By combining genetic studies with biochemical and structural approaches, our work established the tertiary structure of pre-miRNAs as well as their specific interactions with DROSHA as major determinants for 5’ isomiR production (Cell Rep 26:447-459, 2019). Our studies also yielded insights into how 5’ isomiR biogenesis is regulated in cancer. For 3’ isomiRs, our discovery that uridylation can alter the way miRNAs recognize their targets revealed that 3’ isomiRs possess unique functions (Mol Cell 75:511-522, 2019).
We also uncovered a mechanism by which a subset of miRNAs is degraded via 3’ uridylation (Nat Commun 11:2765, 2020). By investigating the selective actions of the major uridylation enzymes, our recent studies support a model in which TUT4 mediates mono-uridylation while TUT7 carries out oligo-uridylation on mature miRNAs, resulting in altered target-site selection and changes in miRNA stability, respectively (Nat Commun 13:5260, 2022).
JOHNNY TAM, PH.D., NEI
Senior Investigator, Clinical and Translational Imaging Section, Ophthalmic Genetics and Visual Function Branch, National Eye Institute (NEI)
Education: University of California at San Diego (B.S. in bioengineering and B.A. in mathematics); University of California at San Francisco and University of California at Berkeley, California (joint Ph.D. program in bioengineering)
Training: Postdoctoral training in superresolution microscopy and biophysics, Institute of Photonic Sciences (ICFO), Castelldefels, Spain (2012-2014)
Before coming to NIH: Whitaker International Postdoctoral Fellow, ICFO
Came to NIH: In 2014 as a Research Fellow, NEI
Outside interests: Spending time with family, especially with my young children
Research interests: I am an engineer with a passion for developing new imaging technologies for clinical applications in ophthalmology and vision science. My lab brings together experts from diverse fields spanning biology, microscopy, optics, computer science, engineering, genetics, and ophthalmology to invent, design, build, and implement fully custom optical instruments capable of resolving individual neurons, capillaries, and epithelial cells in the living human eye. Our imaging approach is based on adaptive optics, a technology that is widely used in modern ground-based large astronomical telescopes for correcting distortions to light traveling through earth’s atmosphere.
Highlights of our lab’s multidisciplinary accomplishments to date, successfully translated to the living human eye, include: 1) establishing that retinal epithelial cell mosaicism can be used to longitudinally track cells in health and disease (JCI Insight 4:e124904, 2019); 2) surpassing the optical diffraction limit of light in the living human eye to reveal the smallest cellular structures in the eye (Optica 8:333-343, 2021); 3) developing novel methods for visualizing transient red blood cell stasis patterns in the choriocapillaris (iScience 26:105755, 2023); 4) leveraging generative artificial intelligence approaches to improve image annotation and analysis (IEEE Trans Med 40:2820-2831, 2021); and 5) revealing that photoreceptors and retinal pigment epithelial cells are differentially affected in genetic eye diseases such as choroideremia (Commun Biol 5:898, 2022) and vitelliform macular dystrophy (Invest Ophthalmol Vis Sci 63:27, 2022).
ANDREA MARZI, PH.D., NIAID
Senior Investigator, Immunobiology and Molecular Virology Unit, National Institute of Allergy and Infectious Diseases (NIAID)
Education: Friedrich Alexander University Erlangen, Nürnberg, Germany
(B.Sc. and M.Sc. in biology, Ph.D. in virology)
Training: National Microbiology Laboratory, Public Health Canada, Winnipeg, Canada (2007–2008); Laboratory of Virology, Rocky Mountain Labs (RML), NIAID (2008–2012)
Came to NIH: In 2008 as a Postdoctoral Fellow, RML, NIAID
Outside interests: Baking; reading; going on walks and hikes with my dog and husband; jigsaw puzzles; golfing
Research interests: My research focuses on filoviruses (Ebola and Marburg viruses), particularly on host–pathogen interactions and medical countermeasure development.
Although Ebola virus (EBOV) has been extensively studied over the past few decades, there still are gaps in our understanding of the mechanism of pathogenesis. Using our established capacity for in vitro and in vivo experiments in the BSL-4 laboratory at the RML, we are leveraging molecular approaches including virus reverse-genetics systems combined with animal models to gain insight into potential mechanisms of pathogenesis.
In 2019, the first EBOV vaccine was approved for human use: a live-attenuated vesicular stomatitis virus (VSV)-based vector expressing the EBOV glycoprotein (VSV-EBOV; Ervebo by Merck) as viral antigen. This vaccine was extensively characterized in preclinical studies at RML (Science 349:739-42, 2015; PNAS 110:1893-8, 2013) and deployed in phase 3 clinical trials during the West African EBOV epidemic in Guinea in 2015.
Following the successful strategy of the VSV-EBOV, we are developing and characterizing VSV-based vaccines for other human pathogenic filoviruses including Marburg virus and Sudan virus (eBioMed 89:104463, 2023; Lancet Microbe 4:e171-e178, 2023). Accompanying these efforts is the development of animal models for novel filoviruses such as Lloviu virus (J Infect Dis 2023; DOI:10.1093/infdis/jiad226) in order to conduct countermeasure efficacy studies and also to evaluate the pathogenic potential of these new viruses. My long-term goal is to develop approaches that can be applied to any highly pathogenic and emerging virus threatening global public health.
EMMIE DE WIT, PH.D., NIAID
Senior Investigator, Laboratory of Virology, Rocky Mountain Laboratories (RML), National Institute of Allergy and Infectious Diseases (NIAID)
Education: Utrecht University, Utrecht, the Netherlands (M.S. in biology); Erasmus University Rotterdam, Rotterdam, the Netherlands (Ph.D. in virology)
Training: Postdoctoral training in virology, Erasmus Medical Center, Rotterdam (2007-2009); and Laboratory of Virology, RML, NIAID (2009-2016)
Before coming to NIH: Postdoctoral Researcher, Erasmus Medical Center, Rotterdam
Came to NIH: In 2009 as a Postdoctoral Fellow, RML, NIAID
Outside interests: Cycling; hiking; camping; baking
Research interests: In my lab, we study the pathogenesis of emerging respiratory viruses that cause severe lower respiratory tract disease. The COVID-19 pandemic highlighted the devastating effect of emerging respiratory viruses on global public health and economies. It also showed the difficulty of treating viral lower respiratory tract infections, underscoring that our current understanding of their pathogenesis is insufficient to drive the development of effective treatments. Our main goal is therefore to increase our understanding of the pathogenesis of emerging respiratory viruses to such an extent that we can devise new treatment strategies.
This became very urgent when SARS-CoV-2 emerged only months after I started my lab. We quickly pivoted to studying SARS-CoV-2 in January 2020 and were able to help inform public health decisions through our own work and collaborations with other labs. In February 2020, we developed a nonhuman primate model of SARS-CoV-2 infection (Nature 585:268-272, 2020). This model was used by labs worldwide for preclinical testing of all COVID-19 vaccines that were approved for human use. In March 2020, we showed that remdesivir treatment was effective in preventing lower respiratory tract disease in rhesus macaques (Macaca mulatta), data that contributed to the licensing of remdesivir for use in COVID-19 patients (Nature 585:273-276, 2020). We also used this model to investigate why older people are more likely to develop severe COVID-19 (Life Sci Alliance 5:e202101314, 2022) and to assess the threat posed by emerging variants of concern (Sci Adv 7:eabj3627, 2021).
Now that our pandemic response work is slowing down, we are developing human distal lung organoid models to help us bridge the gap between animal models and human clinical data, enabling us to study the pathogenesis of our viruses of interest on a molecular level in the human host.
Many emerging respiratory viruses also cause neurological complications, and we have also started to study these viruses. Especially during Nipah virus infection, neurological complications are a major cause of death in humans. The pathogenesis of Nipah virus neurological disease is rarely studied and poorly understood. We are trying to fill that gap by developing in vitro (for example, cerebral organoids) and in vivo models.
KELLY FERGUSON, PH.D., NIEHS
Senior Investigator, Epidemiology Branch, Perinatal and Early Life Epidemiology Group, with a secondary appointment in the Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences (NIEHS)
Education: University of Michigan, Ann Arbor (B.S. in biopsychology and cognitive science); University of Michigan School of Public Health (M.P.H. in occupational and environmental epidemiology and Ph.D. in environmental health sciences).
Training: Postdoctoral Research Fellow and NIEHS P30 Center Scientist, Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor (2014-2015)
Before coming to NIH: Research Assistant Professor, Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor
Came to NIH: In 2016 as a Tenure Track Investigator, Epidemiology Branch, NIEHS Division of Intramural Research
Outside interests: Outdoor activities like biking, hiking, and swimming at home in North Carolina or back in Michigan; cooking up new recipes (current focus area: pies); University of Michigan football.
Research interests: Adverse pregnancy outcomes have extensive individual and societal repercussions, and the contribution of environmental factors is of increasing interest to researchers, policy makers, physicians, and parents. My research examines environmental chemical exposures in pregnancy and their associations with adverse pregnancy outcomes as well as long-term health effects in the mother and child. A major focus of my research is on exposure to phthalates, which are commonly used as plasticizers and in personal care products. Exposure to phthalates is widespread in the US and worldwide. Since coming to NIEHS, I have been investigating the relationship between exposure to phthalates in pregnancy and preterm birth. This work culminated in my work establishing a consortium of 16 U.S. cohorts and over 6,000 pregnant participants. In this study we found robust evidence of associations between prenatal urinary concentrations of several phthalate metabolites and preterm delivery (JAMA Pediatr 176:895-905, 2022).
Another major emphasis of my research has been on understanding how multiple chemical exposures may work together to impact health. In a multi-ethnic cohort from the Netherlands, we found that exposure to a mixture of chemicals, including phthalates, bisphenols (like BPA), and pesticides, was associated with reduced growth of the fetus in utero (Environ Health Perspect 129:117008, 2021). These findings are important since most studies examine chemicals one-at-a-time, ignoring their potentially cumulative impact.
Finally, my research highlights the importance of oxidative stress and inflammatory pathways as key mechanisms in the relationship between prenatal chemical exposures and adverse pregnancy outcomes. Using molecular markers of these processes, we have shown that exposure to chemicals in pregnancy is associated with inflammation, and that, at the same time, inflammation is central in the etiology of pregnancy outcomes like preterm birth and preeclampsia, as well as growth of the fetus during pregnancy (Pharmacol Ther 239:108181, 2022).
CHANDRA JACKSON, PH.D., NIEHS
Senior Investigator in the NIEHS Social and Environmental Determinants of Health Equity Group.
Education: Bethune-Cookman University (B.S. biology); Harvard T.H. Chan School of Public Health (M.S. in cardiovascular epidemiology); Johns Hopkins University (Ph.D. in cardiovascular epidemiology)
Training: Alonzo Smythe Yerby Postdoctoral Fellowship, Nutrition/Epidemiology, Harvard T.H. Chan School of Public Health (2012-2014)
Before coming to NIH: Research Associate, Population Health Research Program, Harvard Catalyst Clinical and Translational Science Center at Harvard Medical School, Boston (2014-2016)
Came to NIH: In 2017 as an Earl Stadtman Investigator (tenure-track), NIEHS Epidemiology Branch, and as an Adjunct Investigator, Intramural Research Program, National Institute on Minority Health and Health Disparities.
Outside interests: I enjoy daily nature walks and bike riding; domestic and international travel; many art forms such as wood working, painting, and sculpting; and attending concerts as well as comedy shows with friends and family.
Research interests: Sleep, an essential human need for maintaining biological homeostasis, is a seemingly simple behavior and yet complex physiological state (Lancet Public Health 8:e820-e826, 2023). It is not entirely endogenous and is, therefore, positively or negatively affected by modifiable physical (e.g. light; temperature; noise), as well as social (e.g. psychosocial stress) environmental factors. These factors vary by race, ethnicity, and socioeconomic status (Sleep 43:zsaa037, 2020). Preventing or minimizing the impact of environmental disturbances on sleep duration, quality, and timing could help populations avoid or delay a host of chronic diseases, such as cardiovascular disease, while addressing health disparities (J Hypertens 39:2210-2219, 2021).
My research group seeks to determine the social and biological pathways linking these upstream, modifiable physical and social environmental factors to sleep and cardiovascular health in the overall population and by race, ethnicity, and socioeconomic status.
This page was last updated on Wednesday, November 1, 2023