Colleagues: Recently Tenured

LAUREN ATLAS, PH.D., NCCIH, NIMH, NIDA

Senior Investigator, Affective Neuroscience and Pain Laboratory, NCCIH, NIMH, NIDA

Education: University of Chicago (B.A. in psychology); Columbia University, New York (Ph.D. in psychology)

Training: Postdoctoral fellow, Department of Psychology, New York University, New York (2011–2014)

Came to NIH: In 2014 as a clinical investigator, NCCIH

Outside interests: Stained glass; scuba diving; bird watching; samba dancing

Website: https://irp.nih.gov/pi/lauren-atlas

Research interests: I am a psychologist and cognitive neuroscientist who is interested in how expectations shape pain, emotional experience, and clinical outcomes (e.g., placebo effects). My lab integrates experimental psychology, neuroimaging, computational approaches, and psychophysiology to understand how psychological and contextual factors influence subjective experience. We pursue three main lines of research.

First, we measure how subjective pain is linked to nociception and whether individual differences modulate these relationships. We have shown that autonomic responses are more related to subjective pain than noxious input (PMID: 31107415) and that pain sensitivity is more stable across visits in women than in men (PMID: 35189353).

Our second line of work addresses the brain mechanisms by which expectations shape pain, and we have identified dissociations between effects of verbal instructions and associative learning (PMID: 36317867; PMID: 27171199).

Finally, we ask how social factors influence pain and expectations, both in terms of patient-provider relationships (PMID: 34126294) and health disparities in pain (PMID: 37293681). Current work includes the role of nonverbal reactions to pain (i.e., facial expressions), whether we can reduce biases in pain assessment, and whether brain mechanisms of pain modulation are unique to pain or shared across areas of affect and emotion.

AARON CYPESS, M.D., PH.D., NIDDK

Senior Investigator and Chief, Translational Physiology Section, Diabetes, Endocrinology, and Obesity Branch, NIDDK

Education: Princeton University, Princeton, New Jersey (B.A. in chemistry); Rockefeller University, New York (Ph.D. in biochemistry); Cornell University Medical College, New York (M.D.)

Training: Internal medicine intern and resident, Beth Israel Deaconess Medical Center (BIDMC), Boston (2001–2003); endocrinology clinical and research fellow, BIDMC Joslin Diabetes Center (2003–2006); clinical investigation fellow, BIDMC Harvard-MIT Division of Health Sciences and Technology (2006–2008)

Before coming to NIH: Assistant professor of internal medicine, Harvard Medical School (Boston); staff physician, Joslin Diabetes Center and Beth Israel Deaconess Medical Center

Outside interests: Biking; hiking with my wife and kids; Shabbat meals with family and friends

Website: https://www.niddk.nih.gov/about-niddk/staff-directory/biography/cypess-aaron

Research interests: The goal of my research group is to understand the roles of brown and white adipose tissue (BAT and WAT) in human physiology and identify approaches to turn that knowledge into treatments for obesity-related metabolic diseases (PMID: 35196429). Until recently, BAT was thought to be nonexistent and metabolically irrelevant in adult humans in part because there were no methods to localize and quantify BAT mass and measure its activity. Using a combination of molecular techniques and whole-body imaging, we showed that BAT is present in women and men in defined anatomical depots and has an activity that correlates inversely with age and obesity, suggesting several physiological roles for BAT in adult human metabolism (PMID: 19357406).

In parallel with these advances, our group is developing a pharmacological approach to treat obesity-related metabolic disease through the activation of the beta-3 adrenergic receptor (AR). The beta-3 AR has a distinct tissue expression in humans, with particularly high amounts in the BAT, the WAT, and the hepatobiliary system. Over the past decade, we pioneered the use of the beta-3 AR agonist mirabegron (Myrbetriq) in the setting of metabolic research (PMID: 25565203). We recently showed in a clinical trial that chronic mirabegron treatment increased BAT metabolic activity and resting energy expenditure, and it led to higher plasma concentrations of several typically beneficial metabolites, including high-density lipoprotein, total bile acids, and the adipokine adiponectin. Moreover, mirabegron increased insulin sensitivity, glucose effectiveness, and insulin secretion (PMID: 31961826). These discoveries have opened up several new areas of research as we determine the mechanisms underlying mirabegron’s effects and the physiological roles of human BAT as both a thermogenic and an endocrine organ.

Going forward, the translational research projects in the group will focus on human BAT and WAT structure and function at the molecular, genetic, and anatomical levels; beta-3 AR physiology and therapeutics; and metabolic imaging.

RASIKA MATHIAS, SC.D., NIAID

Senior Investigator, Chief of Genomics and Precision Health Section, NIAID

Education: Stella Maris College, Chennai, India (B.Sc. in zoology); Johns Hopkins Bloomberg School of Public Health, Baltimore (Sc.D. in genetic epidemiology)

Training: Postdoctoral fellow, Inherited Disease Research Branch, NHGRI

Before coming to NIH: Professor of medicine, Johns Hopkins School of Medicine, Baltimore

Came to NIH: In 2024 as a senior investigator, NIAID

Outside interests: All things food; travel; photography

Research interests: I recently joined the Laboratory of Allergic Diseases where I have established the Genomics and Precision Health Section (GPHS). The section will work on bringing together genomics, transcriptomics, and epigenetics to understand disease risk, severity, and trajectory, with an emphasis on health disparities and clinical translation in precision health.

My primary interest is to look across the allergic diathesis of atopic dermatitis, asthma, and food allergy, because we have shown that there is a high degree of overlap in the genetic underpinnings of these related allergic diseases (PMID: 32777389). We will integrate genetics seamlessly with additional -omics, and do so by leveraging expansive preexisting resources in conjunction with new initiatives to deliver on the promise of genetic risk prediction and the ultimate translation of genetics into clinical practice for allergy. My lab has demonstrated the importance of allergen exposure and context-dependent genetic determinants of allergy (PMID: 34981778), and we will continue to focus on these factors for allergy risk and response to interventions like immunotherapy.

My research also places special emphasis on the inclusion of individuals representing the African Diaspora in research programs because often they bear a major burden from health disparities in these disease areas that is further compounded by the existing inequalities stemming from their lack of inclusion in biomedical research. One of the major programs that I have led for over a decade is the Consortium on Asthma among African-ancestry Populations in the Americas (CAAPA). In CAAPA, we have forged close collaborations with scientific teams in Nigeria, Brazil, Barbados, and Honduras, which I will continue to build upon at GPHS. CAAPA is the single largest multi-omics study on asthma in African ancestry populations and has made numerous inroads into dissecting the molecular underpinnings of the allergic diathesis in this group that bears significant prevalence and morbidity (PMID: 27725671).

FASIL TEKOLA-AYELE, PH.D., NICHD

Senior Investigator, Epidemiology Branch, Division of Population Health Research, NICHD

Education: Debub University, Ethiopia (B.S. in public health); Addis Ababa University, Addis Ababa, Ethiopia (M.P.H.); Brighton and Sussex Medical School, Universities of Brighton and Sussex, Brighton, England (Ph.D. in genetic epidemiology)

Training: Postdoctoral fellow, NHGRI (2010–2014); research fellow, NHGRI (2014–2016)

Before coming to NIH: Doctoral student at Brighton and Sussex Medical School

Came to NIH: In 2008 as predoctoral fellow; returned in 2010 as postdoctoral fellow, NHGRI

Outside interests: Jogging; gardening; spending time with family and friends

Website: https://irp.nih.gov/pi/fasil-tekola-ayele

Research interests: The early life period is critical for long-term health. Fetal growth abnormalities and cardiometabolic diseases are interconnected and cause a high burden of morbidity. Understanding the complex genetic and environmental factors that underlie these relationships is crucial to developing preventive and therapeutic interventions for maximizing health across the life span. The placenta is critical for fetal development and potentially underlies later-onset diseases, but it is understudied. Moreover, to date, perinatal genomic studies have failed to capture human ancestral diversity, which impedes biological understanding of diseases and could fuel disparities in genomic-informed health care in the future. In the genetic epidemiology research group, we study genetic mechanisms of fetal growth variations at the maternal-placental-fetal interface and their links with cardiometabolic outcomes in diverse human populations. Our studies so far demonstrated that genetic and epigenetic processes that regulate fetal development and placental response to maternal metabolic and psychosocial factors may offer mechanistic insights to early origins of cardiometabolic diseases in later life.

Highlights of our contributions include the following. 

1. Identifying multiancestral as well as African- and Amerindigenous- ancestry-related genetic loci associated with fetal growth (PMID: 32407400; PMID: 33590300).
2. Identifying high-priority genes in placenta that affect fetal growth via epigenetically and transcriptionally altered mechanisms, filling a major gap in functional understanding of birthweight genome-wide association study loci (PMID: 35501330).
3. Developing a genome-wide atlas of placenta-specific variably methylated regions, elucidating their regulatory functions, and demonstrating the importance of gene-environment integration in advancing phenotypic relevance of placenta research (PMID: 34155504).
4. Offering evidence on placental aging “clock” epigenome, and transcriptome as a potential link between maternal cardiometabolic status, fetal growth, and offspring risk of cardiometabolic diseases (PMID: 32078381; PMID: 33926514).

In our future research, we hope to identify potential molecular intervention targets for promoting long-term health and reducing health disparities.

ANISH THOMAS, M.D., NCI

Senior Investigator, Developmental Therapeutics Branch, NCI-CCR

Education: St. John’s Medical College, Bangalore, India (MBBS and M.D.)

Training: Research assistant, State University of New York (SUNY) Upstate Medical University, Syracuse, New York (2006–2010); internal medicine resident, SUNY Upstate Medical University (2007–2010); medical oncology and hematology fellowship, NCI and NHLBI (2010-2013) 

Came to NIH: In June 2010 as a postdoctoral fellow, NCI and NHLBI

Outside interests: Spending time with family

Website: https://ccr.cancer.gov/staff-directory/anish-thomas

Research interests: I am a medical oncologist and physician-scientist specializing in the care of patients with lung cancer, specifically small-cell lung cancer (SCLC), the most fatal form of lung cancer. Over the past decade, I have dedicated my efforts to establishing a cutting-edge translational research program at the NIH aimed at advancing our understanding and treatment of SCLC. The overarching goal of my group is to develop innovative strategies that improve the quality of life and outcomes of patients with this aggressive form of lung cancer.

Our approach integrates personalized patient care, clinical trials, in-depth tumor molecular profiling, and laboratory-based research to discover and evaluate new treatment approaches for SCLC. Using a bed-to-benchside approach (PMID: 35561672), we learn from individual patients. For example, we investigate the reasons behind the considerable variability in tumor responses among patients, aiming to predict outcomes at the individual level, and investigate the determinants leading to the preference of specific metastatic sites in certain patients.

Overall, our findings have contributed to the understanding that SCLC is not just one disease but comprises many subtypes, each with its own characteristics and risk factors. We have also identified vulnerabilities that are unique to these subtypes. Key insights from our work include:

1. Replication stress is a transformative vulnerability of SCLCs characterized by high neuroendocrine differentiation (PMID: 33848478).
2. Notch signaling is a driver of intrinsic immunity, which renders low neuroendocrine SCLC more sensitive to immunotherapy (PMID: 34162872).
3. Ataxia telangiectasia and Rad3 related (ATR), a key mediator of replication stress, is a tractable SCLC target. Targeting ATR improves overall survival of relapsed SCLC patients over standard therapies (PMID: 29252124; PMID: 37824137; PMID: 37227187).
4. Germline genotype defines a novel SCLC subset characterized by improved responses to DNA repair targeted drugs (PMID: 33504652).
5. Extrachromosomal DNA amplification contributes to MYC-driven SCLC heterogeneity and is associated with worse outcomes (PMID: 36715552).
6. SCLC subtypes can be profiled noninvasively using histone modifications in plasma circulating free DNA, providing a comprehensive view of the tumor gene expression patterns, as well as cell and tissue of origin (https://doi.org/10.1101/2022.06.24.497386).

We plan to continue to advance novel therapies for the benefit of SCLC patients and nurture the next generation of scientists and clinicians.

ACHIM WERNER, PH.D., NIDCR

Senior Investigator, Stem Cell Biochemistry Section, NIDCR

Education: University of Lübeck, Germany (B.S. in molecular biotechnology); University of Göttingen, International Max Planck Research School for Molecular Biology, Germany (Ph.D. in molecular biology)

Training: California Institute of Regenerative Medicine postdoctoral fellow, Department of Molecular and Cell Biology, University of California at Berkeley (2012–2017)

Before coming to NIH: K99 postdoctoral fellow, University of California at Berkeley

Came to NIH: In 2017 as a Stadtman tenure track investigator, NIDCR

Outside interest: Volleyball; tennis; running; watching TV shows. The Big Bang Theory is my all-time favorite.

Website: https://irp.nih.gov/pi/achim-werner

Research interests: My lab studies the molecular principles of how cell-fate decisions are determined during development. We focus our studies on ubiquitylation, an essential posttranslational modification that is required for cell division, differentiation, and migration in all metazoans.

We leverage the unique environment of the NIH intramural program and combine our core expertise in human pluripotent stem cell (hPSC) culture, proteomics, and ubiquitin biochemistry with animal models, clinical genetics, and human disease cohorts. This integration has allowed us to establish a collaborative research program that has identified previously unrecognized diseases manifesting with brain and craniofacial defects (PMID: 33523931) or autoinflammation (PMID: 33108101) and has uncovered molecular principles of how ubiquitylation regulates diverse aspects of neuroectodermal development (PMID: 37495603) and hematopoietic differentiation (PMID: 35793467; PMID: 38360993).

We believe that our studies will continue to determine pathogenic variants in undiagnosed disease patients and will facilitate the development of novel therapies for diseases of dysregulated ubiquitylation.