Colleagues: Recently Tenured
KAREN ADELMAN, PH.D., NIEHS
Senior Investigator; Head, Transcriptional Responses to the Environment Group, Laboratory of Molecular Carcinogenesis
Education: State University of New York, Buffalo, N.Y. (B.S. in biology); Génétique Cellulaire et Moléculaire, Université de Paris VI, Paris (Ph.D. in molecular and cellular genetics)
Training: Postdoctoral training in the Department of Microbiology and Immunology and the Department of Molecular Biology and Genetics at Cornell University (Ithaca, N.Y.)
Came to NIH: In August 2005
Selected professional activities: Member, American Society of Biological Chemists and co-organizer 2012 Thematic Session on Gene Regulation at Experimental Biology Meeting; co-organizer 2013 Federation of American Societies for Experimental Biology meeting.
Outside Interests: Spending time with her children (ages 4 and 1); photography; traveling; cooking
Research interests: We investigate the interplay between signals from the environment and transcription by RNA polymerase II (Pol II). The wrapping of DNA-containing genes around nucleosomes prevents access to the DNA. Although this wrapping may help keep stress-responsive genes silent under normal conditions, it poses a problem to the transcription machinery during times of stress. We seek to understand how cells modulate chromatin around stress-responsive promoters to respond to environmental insult or injury.
We use genomic approaches in Drosophila and murine models to quantify alterations in Pol II distribution and gene expression that occur when a cell receives specific stimuli from the environment. We recently found that many genes in signal-responsive pathways are preloaded with Pol II before full-scale gene activation. Pol II is engaged in early transcription elongation, but pauses after synthesizing a short (25 to 60 nucleotides) mRNA transcript. Surprisingly, we observed that this paused Pol II plays a critical role in establishing an accessible chromatin architecture around gene promoters that facilitate further gene activation. We are further investigating paused Pol II’s role in other inducible gene systems.
AMY BERRINGTON DE GONZÁLEZ, PH.D., NCI-DCEG
Senior Investigator, Radiation Epidemiology Branch
Education: University of Manchester, Manchester, England (B.S. in mathematics); University of Kent, Canterbury, England (M.Sc. in applied statistics); University of Oxford, Oxford, England (Ph.D. in cancer epidemiology)
Training: Postdoctoral training in the Cancer Epidemiology Unit, University of Oxford
Before coming to NIH: Assistant professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health (Baltimore); research lecturer in the Nuffield Department of Clinical Medicine, University of Oxford
Came to NIH: In February 2008
Selected professional activities: Member of two radiation research committees at the National Academy of Sciences and a U.K. Health Protection Agency committee
Outside interests: Literature and music
Research interests: Over the past three decades in the U.S., radiation exposure from medical sources has increased sixfold. My goal is to provide information for public health and clinical purposes by quantifying the potential cancer risks from both conventional and emerging medical technologies that involve ionizing radiation. I use theoretical risk-projection modeling and conduct epidemiological studies of medically exposed populations.
I have conducted a series of risk-projection studies to estimate the potential cancer risks from emerging technologies, including computed topography (CT) colonography and use of low-dose-radiation CT scanning to obtain an interior view of the colon; and lung CT screening. My collaborators and I developed the NCI Radiation Risk Assessment Tool (RadRAT), computer software that estimates lifetime cancer risks from low-dose radiation exposures.
Examination of second-cancer (different cancer from original diagnosis) risks after radiotherapy provides insights into the long-term effects of high-dose fractionated radiation exposure. I conducted several studies using NCI’s Surveillance Epidemiology and End Results cancer registries to evaluate second-cancer patterns and risks related to radiotherapy treatment. I am using medical records from Kaiser Permanente Health Plans to develop a cohort of breast cancer survivors and studying the late effects of various breast cancer treatments. I am also doing a pilot study to assess the feasibility of conducting the first multicenter study of second-cancer risks from proton therapy and intensity-modulated radiation therapy.
ARYA BIRAGYN (BIRA ARYA), PH.D., NIA
Senior Investigator; Chief, Immunotherapeutics Section, Laboratory of Molecular Biology and Immunology
Education: Lomonosov Moscow State University, Moscow, Russia (M.S. in genetics); Engelgardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow (Ph.D. in molecular biology)
Training: Postdoctoral training in the Department of Animal Sciences, University of Illinois at Urbana-Champaign and in NCI’s Laboratory of Immuno-regulation and the Lymphoma Development Program
Before coming to NIH: After training at NIH, was a scientist at the Science Applications International Corporation (Frederick, Md.)
Came to NIH: In 1992 for training at NCI; returned in 2000 as NCI staff scientist; became NIA tenure track investigator in 2003
Selected professional activities: Adjunct associate professor, Johns Hopkins University, Baltimore; Editorial board member for the Journal of Biological Chemistry
Outside interests: Participating in charity activities to improve health care in Mongolia; member of Project C.U.R.E.; bicycling; skiing
Research interests: Our laboratory is studying the role and function of regulatory cells in cancer metastasis. We discovered a new subset of regulatory B cells, tBregs, which are induced by cancer to generate regulatory T cells (Tregs) and suppress immune responses. To control Tregs and tBregs, we developed a novel technology by fusing a chemokine and a toxin into what we call a “chemotoxin.” Chemotoxins kill cells that express certain chemokine receptors. We demonstrated that C-C chemokine receptor type 4 (CCR4) is a key chemokine receptor that regulates trafficking of Tregs. Chemotoxin can also be used to control breast cancer metastasis to the lung and combat leukemia in mice, suggesting that it can be an effective treatment for human cancers and T-cell lymphoma and leukemia.
My laboratory also has expertise in vaccines. We successfully generated several potent cancer vaccines, such as chemokine-based simple vaccines for human use by targeting an embryonic antigen that is expressed in several human malignancies. We recently created a novel Alzheimer disease (AD) vaccine that combats AD and significantly extends the life span of a mouse model used in AD research.
KAI GE, PH.D., NIDDK
Senior Investigator; Chief, Adipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology
Education: Fudan University, Shanghai (B.S. in biochemistry); Shanghai Institute of Biochemistry, Chinese Academy of Sciences, Shanghai (Ph.D. in molecular biology)
Training: Postdoctoral training with Lasker Awardee Robert Roeder at Rockefeller University (New York); postdoctoral training in the Molecular Genetics Program at the Wistar Institute (Philadelphia)
Came to NIH: In September 2003
Outside interests: Visiting museums and zoos with his daughter; playing badminton and ping-pong; reading National Geographic and other educational publications
Research interests: Obesity is the single most important risk factor for type 2 diabetes, which accounts for 90 to 95 percent of all cases. A better understanding of the mechanisms that regulate adipogenesis—the generation of fat—may lead to novel approaches to the treatment of obesity and type 2 diabetes.
My laboratory studies regulatory mechanisms of gene expression. We use adipogenesis as a model to study epigenetic regulation of gene expression and cell differentiation. Epigenetic mechanisms change these in a heritable way through pathways other than DNA sequence alteration.
We have identified novel epigenetic regulators including histone methyltransferases and demethylases with unique properties. We have also shown that histone methylation regulates the expression of both positive and negative master regulators of adipogenesis. Our current efforts include the investigation of adipogenesis regulation by these novel epigenetic factors and using adipogenesis as a model system to study the biological functions of many newly identified epigenetic regulators.
DAVID LEOPOLD, PH.D., NIMH
Senior Investigator; Chief, Section on Cognitive Neurophysiology and Imaging; Director, Neurophysiology Imaging Facility
Education: Duke University, Durham, N.C. (B.S.E. in biomedical engineering); Baylor College of Medicine, Houston (Ph.D. in neuroscience)
Training: Postdoctoral training in the Physiology of Cognitive Processes Department at the Max Planck Institute for Biological Cybernetics (Tübingen, Germany)
Came to NIH: In January 2004 to establish the Unit on Cognitive Neurophysiology and Imaging and to head the Neurophysiology Imaging Facility Core
Outside interests: Hiking; bird watching; reading about history
Research interests: My overarching research goal is to understand the large-scale organization of brain activity related to visual perception. In perception, stimuli of varying complexity—simple (color, brightness), intermediate (shape, geometric arrangement), and complex (identity, meaning)—are processed simultaneously. In the lab, we combine behavioral, neurophysiological, imaging, and neuropharmacological techniques to gain insights into how the brain interprets the visual world. We are particularly interested in the functional interactions between diverse brain areas.
In one series of studies, we trained monkeys to report how they perceived a visual stimulus by pressing response keys. We then presented them with a bi-stable visual illusion (in which a stimulus property, such as direction of movement or three-dimensional shape, appears to change spontaneously every few seconds) and measured whether, at each moment, neural responses were linked to the monkey’s reported subjective perception. We found that neural responses in certain regions of the visual cortex and thalamus consistently reflected the perceived stimulus, even though the physical stimulus was always the same. These results illustrate that the visual brain actively interprets the images on the retina.
We also study how the brain processes faces and other high-level visual stimuli. In one study, we are determining how the brain responds during the observation of dynamic social behaviors. We measure brain activity in monkeys as they repeatedly view videos of other monkeys. Luckily for us, they are quite content to watch movies of their kin, even if the movies are “re-runs.” We plan to use a similar method, using movies depicting complex human social situations, to study activity in the brains of patients with schizophrenia.
KEVIN F. O’CONNELL, PH.D., NIDDK
Senior Investigator, Genetics of Simple Eukaryotes Section, Laboratory of Biochemistry and Genetics
Education: University of New Hampshire, Durham, N.H. (B.A. in microbiology); University of Massachusetts, Worcester, Mass. (Ph.D. in molecular genetics and microbiology)
Training: Postdoctoral training in the Laboratory of Molecular Biology, University of Wisconsin (Madison)
Came to NIH: In February 2002
Selected professional activities: Member, American Society for Cell Biology; Editorial Board Member, Prion
Outside interests: Devoting most of his time to his wife and daughters
Research interests: My laboratory uses the worm Caenorhabditis elegans as a model system to address questions concerning the assembly and function of the centrosome. The centrosome is an organelle that serves as the cell’s primary microtubule-organizing center (MTOC) and duplicates once per cell cycle. Through its ability to form polarized arrays of microtubules, the centrosome participates in critical cellular processes such as intracellular transport, the generation and maintenance of cellular polarity, cell motility, and cell division.
Because the mechanisms that govern centrosome duplication and behavior in C. elegans are likely to be highly conserved, our findings should prove valuable in understanding analogous processes in humans and diseases such as autosomal recessive primary microcephaly, cancer, infertility, and various ciliopathies that are linked to centrosome defects. Ciliopathies are caused by defects in the function or structure of cilia; examples include obesity, polycystic kidney, situs inversus (major internal organs in reversed positions), and Joubert syndrome (a rare brain malformation that affects the cerebellar vermis, an area of the cerebellum that controls balance and coordination).
By combining molecular genetics with biochemistry, my lab has identified several factors required for the centrosome duplication pathway. These factors include the master cell-cycle regulator ZYG-1, the protein spindle defective–2 (SPD-2), and the protein phosphatase 2A–suppressor of Ras-6 (PP2A-SUR-6). These factors and three other proteins form the core conserved machinery that drives centrosome duplication.
GEOFFREY SCHOENBAUM, M.D., PH.D., NIDA
Senior Investigator; Chief of the Behavioral Neurophysiology Neuroscience Section and of the Cellular Neurobiology Research Branch
Education: University of Georgia, Athens, Ga. (B.S. in biology); University of North Carolina, Chapel Hill, N.C. (M.D.; Ph.D. in neurobiology)
Training: Postdoctoral fellowship in the Department of Psychology at the University of North Carolina, Chapel Hill
Before coming to NIH: Professor of anatomy and neurobiology at the University of Maryland School of Medicine (Baltimore)
Came to NIH: In October 2011
Outside interests: Technical mountain biking; spending time with his family
Research interests: We are trying to better understand how neural circuits—particularly in the orbitofrontal cortex (OFC) of the brain—mediate simple associative learning and decision-making. By studying how neural circuits mediate simple behaviors in rats, we hope to understand how these circuits function in humans, how they are disrupted in clinical brain disorders, and possible treatments.
Using reinforcer devaluation (making a reinforcer undesirable through association with illness or satiation) and unit recordings that measure activity from OFC neurons, our laboratory was among the first to demonstrate a critical role for the OFC in goal-directed behavior. Recently, we have shown that the information supplied by the OFC both drives behavior and facilitates new learning.
We have also demonstrated that exposure to cocaine and other drugs of abuse induces long-lasting changes in the representation of information about expected outcomes in the OFC. These results suggest that features of addiction, such as loss of behavioral control and failed learning, may be partly due to drug-induced changes in OFC-dependent functions.
RACHAEL STOLZENBERG-SOLOMON, PH.D., M.P.H., R.D., NCI-DCEG
Senior Investigator, Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics
Education: University of California, Davis, Calif. (B.S. in dietetics); Vanderbilt University, Nashville, Tenn. (M.Ed. in health-science nutrition); The Johns Hopkins University School of Hygiene and Public Health, Baltimore (M.P.H. in nutrition and epidemiology; Ph.D. in epidemiology)
Training: Dietetic internship at Vanderbilt University Medical Center (Nashville, Tenn.); predoctoral and postdoctoral training in NCI’s Division of Cancer Prevention and Control; postdoctoral training in NCI’s Division of Cancer Epidemiology and Genetics
Before coming to NIH: Research dietitian at VA Medical Center (Nashville, Tenn.); clinical dietitian and senior clinical dietitian at The Johns Hopkins Hospital (Baltimore)
Came to NIH: In 1996 for training; in December 2002 as a tenure track investigator
Selected professional activities: Associate editor, American Journal of Epidemiology; editorial board member, Cancer Biomarkers Epidemiology and Genetics; adjunct associate professor, Yale University School of Hygiene and Public Health (New Haven, Conn.)
Outside interests: Spending time with family and two children; cooking international foods; jogging
Research interests: The principal focus of my research has been the etiology of pancreatic cancer. Using epidemiologic approaches, I have made several original observations into the nutritional, metabolic, and genetic determinants of this highly fatal disease.
I use prospective data from cohort studies in which a group of people who do not have pancreatic cancer are tracked over time. I was the first to demonstrate that higher serum insulin concentration and other markers related to insulin resistance increase pancreatic cancer risk. These findings support the hypothesis that diabetes may affect risk directly through insulin resistance.
Other modifiable factors that I have observed as contributors to pancreatic cancer are adiposity, high fat intake (particularly fat from animal foods), heavy alcohol use, poor teeth, and many other unhealthy lifestyle factors (including smoking, poor dietary quality, and physical inactivity). We estimated that at least 27 percent of pancreatic cancer is accounted for by an unhealthy lifestyle. I continue to research the mechanisms by which these factors contribute to pancreatic cancer.
Since 2006, I have been collaborating with a multidisciplinary team of investigators, at NCI-DCEG and extramurally, in a large-scale effort known as PanScan. We are conducting the first genome-wide association study (GWAS) for pancreatic cancer. The GWAS has already shown a link between certain alleles of the gene for ABO blood type and pancreatic cancer.
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