Colleagues: Recently Tenured
VERONICA A. ALVAREZ, PH.D., NIAAA
Senior Investigator; Chief, Section on Neuronal Structure, Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism
Education: University of Buenos Aires, Buenos Aires, Argentina (B.S. in biology; Ph.D. in neuroscience)
Training: Postdoctoral training in neurobiology at Harvard Medical School (Boston) and the Vollum Institute, Oregon Health and Science University (Portland, Ore.)
Came to NIH: In 2008
Outside interests: Running; hiking; spending time with family
Research interests: I am interested in the neurobiology of addiction. The focus of my research is to understand the cellular mechanisms that control reward-motivated and compulsive behaviors. Specifically, the goal of my lab is to find out how cocaine and alcohol affect synapses and neuronal connectivity to drive the development of compulsive drug-seeking behaviors that characterize individuals suffering from cocaine abuse or alcohol-use disorder. In my laboratory at NIAAA we combine multiple techniques ranging from cellular and synaptic approaches all the way to behavioral analysis and in vivo manipulations in wild-type and genetically engineered mouse models. We expect that our studies will provide information about the short-term and long-term effects of stimulant drugs and alcohol on synapses and on the way that different brain regions talk to each other and integrate information. In addition, we hope our findings will lead to the identification of neuronal markers associated with higher vulnerability to addiction and aid in the development of new therapies to treat drug abuse and dependence.
YOGITA CHUDASAMA, PH.D., NIMH
Senior Investigator; Chief of the Section on Behavioral Neuroscience and Director of the Rodent Behavioral Core, National Institute of Mental Health
Education: Cardiff University, Cardiff, Wales, United Kingdom (B.Sc. in applied psychology; Ph.D. in behavioral neuroscience)
Training: Postdoctoral fellowship at the Department of Experimental Psychology, University of Cambridge (Cambridge, England); postdoctoral fellowship at NIMH’s Laboratory of Neuropsychology
Before returning to NIH: Associate professor, Department of Psychology at McGill University (Montreal)
Came to NIH: In 2003 for training in NIMH (2003–2006); visiting professor (2013–2014) in the National Institute on Drug Abuse; joined NIMH in 2015
Outside interests: Hiking; traveling; exploring
Research interests: I am interested in understanding the neural circuits underlying the control of executive functions (control of attention and inhibition, working memory, reasoning, problem solving, and planning). Impairments in executive function, which are characteristic of people with neuropsychiatric disorders such as schizophrenia, persist long after acute symptoms subside and severely compromise the patients’ psychosocial function and quality of life. My lab uses rodent models to dissect complex executive behavior into its cognitive components and to examine how large-scale neural circuits contribute to each component. In recent years, we have demonstrated that executive behaviors are not restricted to the prefrontal cortex but depend heavily on a broad network of interconnected structures that include the hippocampus, basal ganglia, and midline thalamic nuclei. We are particularly interested in the complex interplay among these structures in cognition and their related pharmacology.
My lab is also trying to understand the functional anatomy of social and emotional development. There is significant overlap in the brain structures that govern executive and social behavior. For these studies, we use the common marmoset (Callithrix jacchus), a New World monkey. Marmosets provide many opportunities for studying the same circuitry and have well-developed social behaviors that cannot be well modeled in rodents. One major interest is in how marmosets solve problems through social cooperation.
Applying a combined approach in rodents and primates provides us with a unique perspective on the detailed circuits that support executive behaviors that often go awry in people who suffer from poor control over their decisions, memories, and actions.
MICHAEL T. COLLINS, M.D., NIDCR
Senior Investigator and Chief, Skeletal Clinical Studies Section, Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research
Education: Catholic University of America, Washington, D.C. (music); University of Maryland at College Park (B.G.S. in premedical general studies); University of Maryland at Baltimore (M.D.)
Training: Internal medicine residency and chief resident in medicine, University of Maryland at Baltimore; Endocrine Fellowship Training, NIH Inter-institute Endocrine Training Program, National Institute of Child Health and Human Development
Came to NIH: In 1986 as a biologist in the National Institute of Mental Health (as an undergraduate); returned in 1995 for endocrine fellowship training in NICHD; in 1998, joined the NIDCR as a clinical associate; became a NIDCR staff clinician in 1999 and a tenure-track investigator in 2006
Selected professional activities: Associate program director, NIH Inter-Institute Endocrine Training Program: chair, Medical Advisory Committee, Fibrous Dysplasia Foundation; advisory boards MAGIC Foundation and Yale Center for X-Linked Hypophosphatemia; FDA Advisory Committee for Reproductive Health Drugs; consultant to U.S. Department of Justice
Outside interests: Spending time with family and friends; enjoying food, music, and nature
Research interests: The mission of my group is to understand the spectrum, natural history, and underlying pathophysiology of diseases of mineral homeostasis and the skeleton, to improve the care of patients with these diseases, and to mentor the next generation of clinician-scientists to do the same. This mission is accomplished through the study of pathophysiologically and mechanistically related human diseases, natural-history studies, translational investigation, and clinical trials. The primary diseases and pathophysiological conditions under investigation include fibrous dysplasia of bone and McCune-Albright syndrome (FD/MAS). FD/MAS is a multisystem disease caused by somatic activating mutations of the cAMP-regulating protein Gs alpha subunit. It is defined by a mosaic combination of a skeletal dysplasia, café-au-lait skin macules, and endocrine dysfunction, which can include an excess of the recently discovered phosphate- and vitamin D-regulating hormone fibroblast growth factor 23 (FGF23).
One of the major thrusts of my research is to identify molecules with inhibitory and stimulatory activity at the mutations in Gs alpha subunit that cause FD/MAS. Not only will my work provide an in-depth study of the underlying molecular and cellular pathophysiology involved in the Gs alpha subunit/cAMP pathway, but it will also identify compounds from which to develop drugs to treat FD/MAS. I lead an active clinical research program in FD/MAS in the NIDCR that includes ongoing natural-history studies as well as several completed and ongoing clinical trials. The output of this clinical work has largely defined the current care of patients with FD/MAS.
Arising out of the FD/MAS work is an active research program on mineral metabolism. The work focuses on FGF23 physiology and biology. In particular, we are looking at diseases of FGF23 excess; osteomalacic disorders such as tumor-induced osteomalacia and X-linked hypophosphatemic rickets; and FGF23 deficiency, such as familial tumoral calcinosis (a condition characterized by abnormal deposition of calcium phosphate crystals in tissue). These diseases, and FGF23 biology in general, are further explored through our basic and translational studies that seek to identify new disorders of FGF23, the cellular and molecular pathophysiology of disorders of FGF23, and novel mechanistically related treatments for these disorders.
NEAL FREEDMAN, PH.D., M.P.H., NCI-DCEG
Senior Investigator, Metabolic Epidemiology Branch, National Cancer Institute–Division of Cancer Epidemiology and Genetics
Education: Brown University, Providence, R.I. (Sc.B. in biochemistry and colonial American history); University of California, San Francisco (Ph.D. in biomedical sciences); Harvard School of Public Health, Boston (M.P.H. in quantitative methods)
Training: Cancer Prevention Fellow, Nutritional Epidemiology Branch, NCI-DCEG
Came to NIH: In 2005 for training; became a tenure-track investigator in DCEG in 2009
Selected professional activities: Associate editor for American Journal of Epidemiology and Tobacco Regulatory Science; NCI-DCEG principal investigator for the Prostate, Lung, Colon, and Ovary (PLCO) Cohort Study
Outside interests: Spending time with family; hiking and being outside; reading; doing photography; baking; and enjoying delicious food
Research interests: I am interested in the role of diet and lifestyle in cancer with a particular focus on tobacco products and on liver cancer.
In my tobacco research, my research group and I seek to understand how long-term trends in tobacco use affect disease risks. For example, we have chronicled the impact of historically different cigarette smoking patterns in men and women. In the past, men in the United States smoked more than women, started smoking at a younger age, and tended to have higher smoking-associated disease risks. But today, U.S. women smoke at a similar rate—and start at a similar age—as men. Our work has shown that these changes have resulted in now-similar disease risks among U.S. men and women who smoke cigarettes.
Although the prevalence of cigarette smoking has declined substantially in the United States over the past 50 years, cigarettes continue to be responsible for nearly a third of cancer mortality. Yet other tobacco products are also commonplace including smokeless tobacco, cigars, and emerging products such as electronic cigarettes and water pipes. In our studies, we aim to understand the health risks of using each of these types of tobacco products and of using multiple products.
We are also investigating how diet and lifestyle are associated with liver cancer. Liver cancer is the second leading cause of cancer death in the world. Strong risk factors have been identified including aflatoxin (toxins produces by certain fungi found on agricultural crops), alcohol, chronic hepatitis B and C infections, and diabetes. My work has suggested an important role for diet in liver cancer, and we are currently following up one of the most promising leads—coffee. There is an inverse relationship between coffee intake and the incidence of liver cancer and other liver diseases, suggesting that drinking coffee may have benefits for the liver. We are using a broad range of classical and molecular epidemiologic approaches to better understand the potential impact of coffee drinking on liver disease and on health.
JANET E. HALL, M.D., M.Sc., NIEHS
Senior Investigator; Head of the Reproductive Physiology and Pathophysiology Group, Neuroendocrinology of Reproduction and Aging, National Institute of Environmental Health Sciences
Education: McMaster University, Hamilton, Ontario, Canada (B.A./B.P.E in English and physical education; M.Sc.in medical sciences; M.D.)
Training: Residency in internal medicine and chief resident at McMaster University; clinical and research fellowships in endocrinology and metabolism at Massachusetts General Hospital (Boston)
Before coming to NIH: Professor of medicine, Harvard Medical School (Boston); associate chief of the Reproductive Endocrine Unit and associate physician at Massachusetts General Hospital
Came to NIH: In 2015
Selected professional activities: Extramural funding from NICHD and NIA; former president of the Endocrine Society; associate editor, Endocrine Reviews
Outside interests: Boston HealthCare for the Homeless and the Carroll School of Lincoln, which serves children with language-based learning disabilities
Research interests: I study human reproductive physiology and pathophysiology with a view to translating this information so it can benefit women who have reproductive disorders. The focus of my research is on the neuroendocrine interactions that govern normal reproduction and the changes that occur with aging. We have used this information as a backdrop to provide insights into the pathophysiology of clinical reproductive endocrine disorders. At Harvard, I studied the mechanisms underlying the critical events of the menstrual cycle, how sleep and circadian factors influence these processes, and how signals from the ovary contribute to repeated cycles of follicle development and ovulation. In addition, we investigated the neuroendocrine underpinnings of reproductive disorders including congenital gonadotropin-releasing hormone (GnRH) deficiency, hypothalamic amenorrhea, polycystic ovarian syndrome, and premature ovarian insufficiency. My group investigated the integrated changes that occur with reproductive aging and is finalizing the analysis of neuroimaging studies that investigate how aging influences the way estrogen affects cognitive processes.
Since moving to NIEHS, I am continuing several longstanding collaborations as well as developing new studies. I am maintaining my Massachusetts General Hospital (MGH) program—and working to move it to NIH—in which I use pulsatile GnRH for ovulation induction in patients with GnRH deficiency. I continue to be involved in genotype and phenotype studies in collaboration with colleagues from MGH and the National Institute of Child Health and Human Development. Within this collaborative group I lead the genotype-phenotype studies in women with hypothalamic amenorrhea (a condition in which hypothalamic signaling to other parts of the reproductive system is interrupted because of physiologic stresses such as nutritional imbalance). At NIEHS, my group has established a protocol to investigate factors leading to the variability in neuroendocrine responsiveness to physiologic environmental stresses in normal women that will provide critical insights into the pathophysiology of hypothalamic amenorrhea. I am also collaborating with investigators in NIEHS’s Epidemiology Branch to determine the impact of environmental toxins on reproductive function. In the next year, my group will re-establish our neuroimaging program, which seeks to understand the effects of endocrine disruptors on cortical and hypothalamic function.
MITCHELL HO, PH.D., NCI-CCR
Senior Investigator; Chief, Antibody Therapy Section, Laboratory of Molecular Biology, National Cancer Institute–Center for Cancer Research
Education: East China Normal University, Shanghai, China (B.S. in biology); San Francisco State University, San Francisco, Calif. (M.A. in cellular and molecular biology); University of Illinois at Urbana-Champaign, Champaign, Ill. (Ph.D. in immunology)
Training: Postdoctoral training at NCI’s Laboratory of Molecular Biology
Came to NIH: In 2002 for training; in 2008 became tenure-track investigator in NCI’s Center for Cancer Research
Selected professional activities: Founding chair of the NIH Antibody Interest Group; member of the Board of Distinguished Advisors for the Antibody Society; chair of the Department of Biochemistry for the FAES Graduate School at the NIH
Outside interests: Swimming; hiking; aquariums
Research interests: I am a protein biochemist at the National Cancer Institute, and my research focuses on the use of antibody-engineering technology to advance the development of cancer therapeutics. By combining cutting-edge antibody technology with cellular functional assays, my laboratory has pioneered the production of inhibitory antibodies that attack tumor-specific glypicans. These glypicans are cell-surface heparan sulfate proteoglycans that modulate multiple signaling pathways known to be fundamental in cancer development. We have generated human monoclonal antibodies that have the unique ability to inactivate the wingless-related integration site (Wnt)–yes-associated protein (Yap) signaling pathways by binding to cryptic Wnt binding sites on glypican-3 (GPC3). Our Wnt-inhibitory antibodies not only serve as research tools to investigate the biological interaction of Wnt and GPC3 but also exhibit significant inhibition of GPC3-positive liver-tumor growth in mice. To further enhance the antitumor efficacy, we have constructed chimeric proteins composed of an antibody fragment fused to an immunotoxin. Our immunotoxin causes the regression of liver cancer in mice via dual inhibition of both Wnt-Yap signaling and protein synthesis. Our work established GPC3 as a therapeutic target for immunotoxins and other antibody-toxin/drug conjugates in liver cancer. Furthermore, we are also evaluating additional glypicans as new targets in antibody-based cancer therapies.
Our lab also focuses on the protein mesothelin because of its high expression in mesothelioma and other solid tumors. The molecular interaction between mesothelin and the protein mucin 16 (MUC16, also known as cancer antigen 125) may facilitate the implantation and spread of tumors. We experimentally identified the functional binding domain (named IAB) in mesothelin for MUC16. Moreover, we have generated the anti-mesothelin antibodies that target poorly immunogenic epitopes close to the cell membrane. Our anti-mesothelin antibodies show promising potential for the treatment and diagnostics of mesothelioma and other cancers.
LINDSAY M. MORTON, PH.D., NCI-DCEG
Senior Investigator, Radiation Epidemiology Branch, National Cancer Institute–Division of Cancer Epidemiology and Genetics
Education: Dartmouth College, Hanover, N.H. (B.A., Senior Fellow with Honors, concentration in biology); Yale School of Public Health, New Haven, Conn. (Ph.D. in epidemiology with a focus on cancer epidemiology)
Training: Postdoctoral fellow in NCI-DCEG; research fellow in NCI-DCEG
Came to NIH: In 2004 for training; became tenure-track investigator in Radiation Epidemiology Branch in 2008
Selected professional activities: Childhood Cancer Survivor Study Steering Committee; Lymphoma Research Foundation Scientific Advisory Board; Cancer Research editorial board member
Outside interests: Swimming; playing outside (hiking, kayaking, and more); cooking; spending time with friends and family
Research interests: I am studying multiple primary cancers to evaluate the carcinogenic effects of radiotherapy and chemotherapy as well as to identify other environmental and genetic risk factors for second cancers. Second cancers are a leading cause of morbidity and mortality among cancer survivors. Treatments for first primary cancers are an important cause of subsequent malignancy. There is still much to learn about treatment-related second cancers, particularly whether inherited susceptibility could modify risks and the magnitude of risks associated with current treatment approaches. Beyond the consideration of treatments, many second cancers are likely caused by shared environmental and inherited risk factors, but few studies in the past have collected data on additional risk factors.
I lead a multicenter study of gastrointestinal (GI) cancers (stomach, pancreas, esophagus) among survivors of Hodgkin lymphoma and cancers of the testis, breast, and cervix. The study represents the first comprehensive effort beyond the atomic bomb survivor studies in Japan to quantify the radiation dose–response relationship for upper-GI cancers. Additionally, it is one of just a few studies to quantify chemotherapy-related risks for solid tumors. We have found that the radiation-related risks for all three GI organs increase linearly with increasing dose. We also identified that radiation-related stomach cancer risk after Hodgkin lymphoma was particularly high for patients who also received the chemotherapy drug procarbazine. The increased risks of GI cancer often persist 25 years or more after the first-cancer diagnosis.
In the arena of second-cancer risk among childhood-cancer survivors, I have partnered with the Childhood Cancer Survivor Study to conduct the first large-scale studies of genetic susceptibility to treatment-related second cancers, a major cause of morbidity and mortality in childhood-cancer survivors. We have completed genotyping of over 5,000 childhood-cancer survivors and are combining these data with long-term follow-up and detailed treatment information. Individuals with certain hereditary disorders, such as ataxia telangiectasia (a rare inherited disorder that affects the nervous system, immune system, and other body systems and is characterized by progressive difficulty with coordinating movement), have increased sensitivity to the effects of radiation. But less is known about genetic susceptibility to radiation-related carcinogenesis beyond these rare disorders, and very little is known about genetic susceptibility to chemotherapy-related carcinogenesis. Data from this study will be shared through the Childhood Cancer Survivor Study and the database of Genotypes and Phenotypes (dbGaP) to create a resource to investigate genetic susceptibility to a range of adverse effects in childhood-cancer survivors. These studies hold promise for informing decisions regarding front-line therapy and/or post-treatment surveillance, as well as providing insight into mechanisms of treatment-related carcinogenesis.
JUNG-HYUN PARK, PH.D., NCI-CCR
Senior Investigator, Experimental Immunology Branch, National Cancer Institute–Center for Cancer Research
Education: University of Cologne, Cologne, Germany (B.S. in biology); Julius Maximilian University of Würzburg, Würzburg, Germany (M.S. in biology; Ph.D. in immunology)
Training: Postdoctoral training at the Korea Research Institute of Bioscience and Biotechnology (Daejeon, South Korea); research fellow at NCI-CCR’s Experimental Immunology Branch
Before coming to NIH: Research associate at the Korea Research Institute of Bioscience and Biotechnology
Came to NIH: In 2001 as a research fellow; became a tenure-track investigator in 2008
Selected professional activities: Deputy editor, ImmuneNetwork; co-chair, NIH–Cytokine Interest Group; faculty, NIH–University of Pennsylvania Immunology Graduate Partnership Program
Outside interests: Playing the violin; reading and trying to understand books on philosophy
Research interests: My research focuses on understanding the mechanisms of cytokine-receptor regulation and signaling in immune cells. Specifically, I am interested in interrogating the molecular pathways that control cytokine-receptor signaling in T cells, which are key players in immune surveillance and immune activation. Multiple developmental and environmental cues control cytokine signaling in parallel to cytokine-receptor expression. T cells can show variations in their cytokine responsiveness, resulting in distinct cell-fate choice and effector T-cell generation. Why some T cells choose to respond to a cytokine but other T cells in the same environment remain unresponsive is a fundamental question in immunology that fascinates the members of my lab.
Recently, we discovered a transcriptional basis for such distinct cytokine responsiveness during T-cell development in the thymus. We reported that the zinc finger protein ThPOK induces the expression of suppressor of cytokine signaling molecules to desensitize cytokine-receptor signaling. We also identified another mechanism to desensitize cytokine receptors: a soluble form of the common gamma-chain cytokine receptor (c), which was generated by alternative splicing and was expressed by activated T cells. We found that soluble c (sc) proteins bind to interleukin (IL)–7 and IL-2 receptors even in the absence of cytokines, and they inhibit c cytokine signaling but promote pro-inflammatory IL-17 expression. Thus, sc is a novel immunomodulatory molecule that controls cytokine responsiveness in activated T cells. As we continue to investigate the mechanisms that control cytokine responsiveness, we hope to gain a better understanding of the molecular basis for distinct cytokine signaling in T-cell development, differentiation, and homeostasis.
This page was last updated on Wednesday, April 13, 2022