Harvard Catalyst Program for Faculty Development and Diversity Inclusion (PFDD) Faculty Fellowship

Harvard Catalyst Program for Faculty Development and Diversity Inclusion (PFDD) Faculty Fellowship (formerly PFDD Faculty Fellowship) is a two-year, non-degree Faculty Fellowship Program for Harvard junior faculty designed to address faculty need for additional support to conduct clinical and/or translational research and to free junior faculty from clinical and teaching demands at a key point in their career development. Each Faculty Fellow will receive $100,000 over a two-year period to support their scholarly efforts. Faculty Fellows are required to devote appropriate time toward the development of their academic career, to meet regularly with their mentors, and to present at the annual Minority Health Policy Meeting. For more information about Catalyst see: http://catalyst.harvard.edu


Doctoral degree (e.g. MD, PhD, DO, DMD, DDS). Harvard appointment at the level of instructor or assistant professor. Applications will also be considered from clinical or research fellows who are in the process of appointment/promotion to instructor and/or assistant professor at Harvard. U.S. Citizenship or Permanent Residency.

Harvard Catalyst PFDD Faculty Fellowship application deadline for 2018 has passed.

In the News

Growing Talent: Fellowships help diverse junior faculty thrive

Recipients of the 2016-2018 HMS Office for Diversity Inclusion and Community Partnership Faculty Fellowship and the Harvard Catalyst Program for Faculty Development and Diversity Inclusion Faculty Fellowship were celebrated at a breakfast in March at Harvard Medical School.

The fellows are accomplished HMS junior faculty who will spend a portion of their time over the next two years conducting individual mentored research projects at their respective HMS-affiliated institutions. They will receive $100,000 over the two-year fellowship to support their scholarly research and fellowship-related activities.

HMS News | May 18, 2016 | More...

2009-2017 PFDD Faculty Fellows



Mélissa Léger-Abraham, PhD, Instructor, Harvard Medical School, Department of Biological Chemistry and Molecular Pharmacology

Mentor:  Gerhard Wagner, PhD, Elkan Rogers Blout Professor, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School

Department Chair: Stephen Blacklow, PhD, MD, Gustavus Adolphus Pfeiffer Professor; Chair, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School

Project Title:“Structure-Function Analysis of Translation Initiation Using CRISPR/Cas9 in the Human Parasite Leishmania”


Project Description: Leishmaniasis is a parasitic disease that affects more than 350 million people worldwide and is endemic in vast areas of the tropics, subtropics, and the Mediterranean basin. Native populations, travelers, and military personnel who spend time in affected areas are most at risk. Parasites cause four clinical syndromes; these include a visceral form of the disease, which is lethal, and a cutaneous form, which is the most widespread. The goal of our research project is to validate translation initiation factors in parasites, as targets for specific anti-parasitic drugs against Leishmaniasis. We are establishing a CRISPR/Cas9 genome-editing platform to knockout specific translation initiation factors in Leishmania and will use a quantitative proteomic technique (SILAC labeling coupled to mass spectrometry analysis) to monitor changes in Leishmania protein expression induced by knockout or overexpression of translation initiation factors. We will also use biophysical techniques, such as X-ray crystallography and nuclear magnetic resonance, to determine the molecular structures of candidate translation initiation factors (and their associated protein complexes), to identify differences and similarities between the factors found in human cells and their orthologs in parasites. We expect our findings to translate into novel anti-parasitic drugs. They will also offer a proof of concept for this approach in treating other parasitic infections that significantly burden human health but currently have limited treatment options.

Biography: Mélissa Léger-Abraham, PhD, is an Instructor at Harvard Medical School in the Department of Biological Chemistry and Molecular Pharmacology. Her research focuses on understanding the structural basis for protein translation in parasites that cause two important human diseases, Leishmaniasis and Malaria. Dr. Léger-Abraham was originally born in Montreal, Canada. She is the daughter of a French-Canadian father and a Haitian mother. She obtained her PhD in Biochemistry at the Université de Montréal. She conducted her postdoctoral studies in the laboratory of Professor Gerhard Wagner at Harvard Medical School. Her research combines techniques in molecular biology (including CRISPR/Cas9 genome editing), protein biochemistry, and structural biology (X-ray crystallography and nuclear magnetic resonance). Her goal is to identify and structurally characterize key components in the parasite protein translation machinery to develop a new class of ­­specific anti-parasitic agents.


Natasha M. Archer, MD, MPH,
Instructor, Harvard Medical School;
Department of Pediatrics,
Boston Children's Hospital

Mentor: David Nathan, MD, Robert A. Stranahan Distinguished Professor of Pediatrics and Professor of Medicine, Harvard Medical School; President Emeritus, Dana-Farber Cancer Institute

Division Chief: David A. Williams, MD, Leland Fikes Professor of Pediatrics, Harvard Medical School; Chief, Division of Hematology/Oncology, Department of Pediatrics, Boston Children's Hospital

Project Title: “The Effect of Fetal Hemoglobin on Plasmodium Falciparum Invasion and Growth”

Project Description: P. falciparum, the deadliest of malaria parasites, massively but sequentially degrades hemoglobin subunits beginning with plasmepsin I and II cleavage at α 33-34. Fetal hemoglobin (HbF) is composed of 2 α and 2 γ chains. Due to enhanced α/γ relative to α/β dimer stability, the α chains of HbF may be relatively more resistant to parasitic plasmepsin I and II cleavage as compared to HbA conferring protection from intraerythrocyte growth of P. falciparum to neonates and those with hemoglobinopathies such as hemoglobin (Hb) S, C and E and β-thalassemia, all characterized by high HbF. While others have demonstrated increased invasion but decreased P. falciparum growth in high HbF-containing human and human γ-transgenic murine red cells, the fraction of HbF in erythrocytes required for malaria inhibition, and the mechanism by which HbF exerts this effect, are unknown. Characterizing HbF’s role in P. falciparum infection will help lead to further understanding of how HbF and medications that increase it, such as hydroxyurea, will affect patients with hemoglobinopathies who live in malaria endemic regions.

Biography:  Natasha M. Archer, MD, MPH, is a pediatric hematologist/oncologist at Dana-Farber/Boston Children’s Cancer and Blood Disorders Center, an instructor in pediatrics at Harvard Medical School, and associate physician in the Division of Global Health Equity at Brigham and Women’s Hospital.  She is also the senior health and policy advisor for Hematology at Partners In Health (PIH), a Boston-based non-profit health care organization. Dr. Archer’s research focuses on the delivery of effective hematology care in resource-limited settings. Dr. Archer has helped the PIH team in Mirebalais, Haiti set up a program for newborn screening and disease management for sickle cell disease. Her ongoing clinical research focuses on ways to effectively diagnosis and manage anemia in Haiti. In addition, Dr. Archer’s translational research explores the relationship between hemoglobin and malaria infectivity. Dr. Archer completed her fellowship in pediatric hematology/oncology at Dana-Farber/Boston Children’s in 2014 and her medicine and pediatrics residency in the Harvard Combined Internal Medicine/Pediatrics Residency training program. She completed the Doris and Howard Hiatt Global Health Equity Residency in 2011. Dr. Archer earned her BS from Yale University in 1999, her MD from Yale University School of Medicine in 2006, and her MPH from Harvard School of Public Health in 2011.


Kathryn T. Hall, PhD, MPH, MA,
Assistant Professor in Medicine, Division of Preventive Medicine,
Brigham and Women's Hospital and Harvard Medical School”

Mentor: Kenneth J. Mukamal, MD, MPH, MA, Associate Professor of Medicine, Harvard Medical School; Associate Physician, Department of Medicine, Beth Israel Deaconess Medical Center

Division Chief: JoAnn Manson, MD, DrPH, Professor of Medicine and Elizabeth Fay Brigham Professor of Women's Health at Harvard Medical School, and Chief of the Division of Preventive Medicine and Co-Director of the Connors Center for Women's Health and Gender Biology at Brigham and Women's Hospital in Boston

Project Title: Epidemiological, Pharmacogenomic and Clinical Impact of Catechol-O-Methyltransferase on Cardiovascular Disease”

Project Description:  This study is designed to determine if genetic variation in catechol-O-methyltransferase (COMT), a key enzyme in catecholamine metabolism, modifies incidence of cardiovascular disease (CVD) and aspirin treatment effects in men and racial/ethnic minority populations. Despite significant strides in prevention, CVD remains a leading cause of death. Pharmacogenomics, the study of genetic effects on drug response, has expanded understanding of CVD pathophysiology and, at least for specific genes and drugs, raised the possibility of personalized medicine. However, the potential of pharmacogenomics to guide improvements in personalized treatment remains largely unrealized. In particular, the impact of gene interactions with commonly used drugs is difficult to assess in epidemiologic studies and clinical trials. This is partly due to extraordinarily large sample sizes required for genome-wide studies of gene-drug interactions and lack of strong candidate genes. We recently identified COMT as a gene with plausible physiological links to both CVD and drug metabolism. In the Women’s Health Study (WHS), a placebo-controlled trial of aspirin for CVD prevention in predominantly Caucasian women, we showed that highly prevalent COMT variants were associated with incidence of major CVD. Importantly, we showed that COMT-associated CVD 3

protection was eliminated in women randomized to aspirin. Given widespread use of aspirin and evidence that COMT-drug sensitive alleles are more prevalent in minority populations, investigating this pharmacogenetic locus in male and minority racial/ethnic populations is imperative. Here I propose to use genetic data from a multiethnic longitudinal cohort and a clinical study to elucidate the generalizability and underlying mechanisms of COMT-CVD associations.

Biography:  Dr. Kathryn T. Hall received her PhD in Microbiology and Molecular Genetics from Harvard University in 1996. During her post-doctoral fellowship with Dr. Lee Nadler at Dana Farber Cancer Institute, she cloned and characterized CD100, the first semaphorin identified in the immune system. For the next 10 years, Dr. Hall tackled problems in biotech research and developed expertise in pharmaceutical drug development, first at Wyeth and then at Millennium Pharmaceuticals, where she became an Associate Director of Drug Development. While working in the pharmaceutical industry, Dr. Hall was struck by the health disparities in access to drugs and the tremendous variability in the responses of those who did receive treatment. To address these issues she developed public health media messages acquiring a Masters in Visual Media Arts from Emerson College. With the goal of continuing to examine and address these issues through academic biomedical research, Dr. Hall returned to Harvard Medical School in 2010, joining the Fellowship in Integrative Medicine at Beth Israel Deaconess Medical Center (BIDMC) in 2012 and receiving a Master’s in Public Health from Harvard School of Public Health in 2014.

Working with Ted Kaptchuk at BIDMC in the Program in Placebo Studies, Dr. Hall focused on catechol-O-methyltransferase (COMT) an enzyme that metabolizes catecholamines such as dopamine and epinephrine and has pleiotropic effects in a broad set of diseases and treatments. Her groundbreaking paper identifying COMT as the first genetic marker of placebo response was published in PLOS ONE and has been cited over 50 times since 2012. Dr. Hall coined the term “placebome” to describe the potential genomic perturbations that influence the placebo response and her review of the evidence and implications of its impact on the placebo response is in press at Trends in Molecular Medicine. Dr. Hall’s research captured media attention and her research has been the focus of numerous articles including features in Science and Discover magazine.

Dr. Hall’s current research builds on the emerging role of COMT in network medicine as a hub influencing disease and treatment outcomes from cardiovascular disease to cancer. Using data from the Women’s Health Study (WHS), a large placebo-controlled randomized clinical trial of aspirin for the prevention of cardiovascular disease, Dr. Hall working with Dr. Daniel Chasman at Brigham and Women’s Hospital made the novel observation that women homozygous for the low-activity form of the COMT enzyme had lower rates of major cardiovascular disease when randomized to aspirin compared to placebo; in contrast high-activity COMT homozygotes had increased rates of cardiovascular disease when randomized to aspirin compared to placebo. These original findings have important implications for personalized medicine and were recently published in Arteriosclerosis, Thrombosis and Vascular Biology, 2014. Currently with Dr. Kenneth Mukamal at BIDMC, Dr. Hall is examining COMT in diabetes and cancer. Dr. Hall will complete the Integrative Fellowship later this year and will join the Harvard Medical School faculty in August 2015.

PFDD Faculty Fellows Alumni