This program provides up to two years of funding to the most promising PhD students. 

Selected by Harvard Medical School leadership, the fellows are also enrolled in the Therapeutics Graduate Program (TGP), a new curriculum that focuses on pharmacology, toxicology, and drug discovery, emphasizing research in both HMS labs and real-world internships.

Meet the fellows

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I grew up in Hong Kong, but I spent part of my adolescence in the Netherlands. I graduated as a double major in Chemistry and English from Amherst College, where my research focused on small molecule probes to research protein tyrosine phosphatases in Anthony Bishop’s lab. I joined Harvard’s Chemical Biology PhD program to continue developing new small molecules for emerging target classes in a world-class setting with supportive, collaborative colleagues and mentors.

  • How does your research hold promise for therapeutic innovation?

    Inhibiting the deubiquitinating enzymes (DUBs) offers the exciting potential to degrade pathogenic proteins as a novel therapeutic strategy. I am working on a platform that combines chemoproteomics, a novel DUB-targeting small molecule library, and orthogonal validation assays for DUB inhibitor discovery. In terms of therapeutic innovation, my work holds promise towards first-in-class DUB drugs, medicinal chemistry insights for what makes a good DUB inhibitor, as well as a generalizable chemoproteomic platform applicable to other target classes.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was very excited and honoured to be named a Fujifilm Fellow. Fujifilm is a company I grew up with, so it was particularly encouraging to receive support from a familiar name.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    After growing up in Los Angeles, California, I moved to Pittsburgh, Pennsylvania to attend Carnegie Mellon University, where I studied biological chemistry, politics, and public policy. Inspired by the intellectual diversity of the Harvard scientific community, I chose to pursue my doctoral work in the Chemical Biology PhD Program, where I could explore my interests in therapeutic development across many techniques, disciplines, and institutional frameworks.

  • How does your research hold promise for therapeutic innovation?

    Due to their pharmacological availability at the cell surface and diverse signaling capabilities, G Protein-Coupled Receptors (GPCRs) serve as the targets for roughly one-third of all FDA-approved therapeutics. My thesis work focuses on a highly unusual class of GPCRs that are responsible for cell adhesion in many biological contexts and resulting in disease states, including cancer, ADHD, and developmental disorders of the nervous system. To date, however, no drugs have been generated that target these Adhesion GPCRs. My project aims to characterize the basic mechanisms by which these receptors turn on and off, to identify potential ways to modulate their activities with novel therapeutics.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was absolutely humbled and honored to hear that I was selected as a Fujifilm Fellow. It is immensely heartening to know that an organization of leading scientific minds and industrial leaders has chosen to put a direct stake in not only my thesis work but also my future in this amazing scientific community that I have only recently become a part of.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I am a first-generation college student from Mystic, Connecticut. I attended Boston University, where I received a B.A. in Biochemistry and Molecular Biology and an M.A. in Biotechnology in 2017. My undergraduate and master’s research was dedicated to a synthetic biology project which aimed to develop a macrophage-based delivery system of protein therapeutics to solid tumor microenvironments. After graduation, I was chosen to be a post-baccalaureate scholar at the Novartis Institutes for Biomedical Research (NIBR), which was an incredible and formative experience for me. There I worked on many projects but spent most of my time on a project that elucidated a new transcription factor’s role in the toxicity of diphtheria toxin. I have always been interested in the drug discovery and development process, but my experience at NIBR solidified my love of research and the desire for my research to be translational. With these insights, I joined the Systems, Synthetic, and Quantitative Biology PhD Program at Harvard Medical School because of the interdisciplinary, collaborative, and cutting-edge research and the community of kind and welcoming scientists!

  • How does your research hold promise for therapeutic innovation?

    Chronic pain management is a significant unmet medical need due to the high prevalence and the dearth of safe and efficacious treatments. There has been limited success in developing new pain therapeutics of different drug classes or with different mechanisms of action to current standards of care. However, recently approved protein therapeutics for treating migraine, a chronic neurological condition causing painful and debilitating headaches, provide evidence for protein-based drugs as chronic pain treatments. My project in the Silver Lab aims to develop novel protein-based therapeutics to address the unmet need for chronic and inflammatory pain treatment.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was incredibly honored when I heard that I had been named a Fujifilm Fellow! I immediately shared the great news with my biggest cheerleaders: my family. I am very thankful to FUJIFILM for the support and cannot wait to share my experience and findings with the scientific community.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I grew up in Switzerland, where I completed my bachelor’s and master’s degree in Nanoscience at the University of Basel. Nanoscience is an interdisciplinary course of studies that combines biology, chemistry, and physics. During my master’s, I did several research projects in chemistry and microbiology, which further deepened my interdisciplinary background. One of these projects was in the lab of Thomas Bernhardt at Harvard Medical School. It was during this project that I got fascinated by the mechanisms behind bacterial growth and cell division. Given the thrilling experience at HMS, and the nourishing and highly collaborative environment, I decided to pursue a PhD in the Biological and Biomedical Sciences Program here at Harvard.

  • How does your research hold promise for therapeutic innovation?

    The rise of antibiotic resistance makes bacterial infections harder to treat as an increasing amount of antibiotics become less effective. This leads to increased mortality, morbidity, and increased health care costs due to bacterial infections. To stop this emerging global health crisis, it is important to develop new therapeutics that are effective against antibiotic-resistant bacteria. Since bacterial cell division is an essential step in the bacterial life cycle and the mechanisms are very different from that in human cells, cell division is an interesting target for new antibiotics. Understanding the molecular mechanisms underlying bacterial cell division is crucial to find new methods for the treatment of diseases and the development of antibiotics.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was very honored to be named a Fujifilm Fellow, and I’m looking forward to continuing my scientific endeavors as part of the Fujifilm Fellowship. I’m very grateful for FUJIFILM’s contribution towards life sciences and education.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I am a second-year graduate student in the Biological and Biomedical Sciences (BBS) program. I am from Tokyo, Japan, and first came to Boston in 2013 to pursue my BA/MA degree in biochemistry and molecular biology at Boston University. I worked as an undergraduate researcher for three years in the Whitty Research Group, where I deepened my interest in protein-protein interactions. With Dr. Adrian Whitty’s encouragement, I applied to the BBS program for my graduate studies. I chose to study at Harvard because of its highly collaborative environment with many talented individuals.

  • How does your research hold promise for therapeutic innovation?

    I will be studying how PTEN, a phosphatase inactivated in many tumor cells, is regulated by N-terminal ubiquitination. There is currently little known about the effects of ubiquitination on structure and activity of PTEN. A deeper understanding of PTEN regulation would help guide the development of a novel PTEN-based anti-tumor therapeutics.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was surprised for being named as a Fujifilm fellow. I am very grateful for this honor and the support from a famous Japanese company.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I grew up in Southern California and graduated from Northwestern University, where I studied Neuroscience and Biochemical Engineering. I have always been fascinated by the remarkable complexity of the brain and its control over every aspect of life. I’ve found that the neuroscience community at Harvard Medical School is rich with scientists who both share these curiosities and inspire the field at large.

  • How does your research hold promise for therapeutic innovation?

    Parkinson’s disease is characterized by a progressive loss of dopamine neurons in the midbrain, resulting in a depreciation of voluntary movement control. The current therapies aim to mitigate motor deficits through global dopamine replacement, yet the role of dopamine is not completely understood on circuits modulating action selection, reward-seeking, and motivation. My research background includes investigating the role dopamine plays in guiding behavioral decisions in healthy brains to further understand the neural circuitry affected by Parkinson’s disease. Describing how different neural ensembles respond to dopamine input to produce complex behavioral sequences can uncover novel strategies for symptom management and therapeutic treatment in patients with Parkinson’s disease.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    When I learned I was selected for the fellowship, I was honored to receive the support. I’m so excited to be included in FUJIFILM’s mission for advancing therapeutic science and building a collaborative scientific community.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    After growing up on Long Island, New York, I attended Cornell University, where I studied Biology and minored in English and Biomedical Engineering. Hoping to pursue a career in the field of therapeutics, I decided to pursue a PhD at Harvard Medical School.

  • How does your research hold promise for therapeutic innovation?

    For patients that have genetic blood diseases like sickle cell anemia or hemophilia, bone marrow transplants replace unhealthy blood stem cells with healthy blood stem cells. Great progress has been achieved in the field of gene therapy, which can correct the genetic mutations that cause diseases. However, transplants require that stem cells be removed from patients’ bone marrow so that gene therapy can be performed in a laboratory. When hematopoietic stem cells are taken out of our bodies and placed in a dish, the cells become stressed and can lose their capacity to make blood.

    My thesis aims to improve transplantation by better understanding how hematopoietic stem cells respond to and survive stress. With this knowledge, strategies to cure hematopoietic diseases by gene therapy and bone marrow transplant will be more effective at normalizing patients’ blood.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    When I learned that I was named a Fujifilm Fellow, I was excited to share the news with my unconditionally supportive parents and laboratory. I am so happy to be supported by Fujifilm, which shares my enthusiasm for the future of cell-based therapies.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I am from Lusaka, Zambia, and I came to the United States to pursue a higher education. I attended Paine College in Augusta, Georgia, where I studied biology. During my undergraduate training, I had the opportunity to conduct research in laboratories at my home campus, Children’s Hospital Los Angeles, and Novartis Institutes for BioMedical Research (NIBR). After graduating from college, I was selected for the Post-Baccalaureate Scholars Program at NIBR, where I studied pulmonary epithelial cell biology for two years. After two years of research experience in pulmonary biology, I decided to pursue a doctoral degree in the PhD Program in Biological Sciences in Public Health (BPH). In particular, I chose the BPH program because it offered a holistic training in biomedical research to tackle global health challenges.

  • How does your research hold promise for therapeutic innovation?

    Worldwide, asthma affects more than 350 million people. While advances in diagnosis and therapeutic management have been made, asthma remains a progressive disease with no cure. Because poorly controlled asthma is significantly associated with high mortality and morbidity, developing new drugs and therapeutic strategies is readily needed.

    To advance our knowledge about the cause and development of asthma and to find potential drug targets, my research focuses on the pulmonary epithelium. Under normal conditions, the pulmonary epithelium serves as a protective physical barrier. It is the first line of defense against inhaled external insults such as environmental pollutants, allergens, and viruses, all of which are major risk factors for asthma. Repeated insults could eventually damage the pulmonary epithelium, which contributes to the development of asthma. In my work, I am investigating how external stimuli, such as allergens, compromise the normal defense function of the pulmonary epithelium, contributing to the progression of asthma. Understanding the role of the airway epithelium presents potential therapeutic targets for the development of new drugs and/or new therapeutic strategies for the treatment of asthma.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was very excited and honored to be named a Fujifilm Fellow. I am grateful for the financial support from FUJIFILM Corporation.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I was born in Ecuador, but my family and I moved to the United States when I was 8 years old in search for better economic and educational opportunities. I completed my undergraduate studies at Hunter College, where I was a member of the Research Initiative for Scientific Enhancement (RISE) program. Being a RISE fellow gave me the opportunity to pursue research opportunities in biomedical sciences at Hunter College and encouraged me to pursue summer research at other institutions. As a result, I applied and was accepted to two summer internships at Harvard University. Upon the completion of my undergraduate degree, I sought out additional research opportunities in the biomedical sciences and did a two-year post-baccalaureate at Harvard University.

    I decided to pursue my PhD in the Biological and Biomedical Sciences (BBS) program at Harvard Medical School because it is a welcoming setting that is devoted to cultivating an atmosphere that encourages students to think creatively and critically as they develop into independent investigators.

  • How does your research hold promise for therapeutic innovation?

    There is a major need to develop drugs that target obesity and obesity-linked disorders, such as diabetes and NASH, which are leading causes of death worldwide. A well-established approach to reverse obesity is activation of calorie-burning in brown adipose tissues (BAT). BAT has the unique capacity to catabolize fat and glucose in futile thermogenic cycles that are protective against obesity. The major protein effector of thermogenesis in BAT is uncoupling protein 1 (UCP1). To date, UCP1 has been considered “undruggable,” lacking obvious modes of small molecule pharmacological engagement for therapeutic activation. My host lab recently discovered that UCP1 contains a functional cysteine residue that when post-translationally modified can increase protein activity. This newfound site represents the first known activation site of UCP1.

    My research will apply new mass spectrometric and chemical technologies to identify small molecules that can modify this newfound active site on UCP1. We predict that chemical modification of this site will activate the calorie burning activity of UCP1, effectively acting as a molecular switch to drive calorie burning. These molecules could hold major promise as treatments for obesity and diabetes, where excess calories are a major driver of disease and death.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I am extremely excited for the opportunity given to me to continue working towards novel scientific discovery. I am looking forward to future scientific experiences as part of being a Fujifilm fellow and the opportunity to share my findings with the science community.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I was born and brought up in southwestern India and moved to the United States to pursue a master’s degree in Biotechnology from Northwestern University, located in the beautiful city of Chicago. After graduation, I worked in a viral oncology laboratory at Northwestern as a Research Technician for a few years before starting my PhD at Harvard as part of the HMS PhD Program in Virology. I chose Harvard because of its emphasis on translational research and deep expertise in the development of therapeutics, in addition to being in Boston, which has become a hub of innovation in the life sciences industry.

  • How does your research hold promise for therapeutic innovation?

    Recent DNA sequencing efforts have revealed frequent perturbations in genes encoding members of the BAF complex family. We now know that dysregulation of chromatin architecture is implicated as a cause in many diseases, most prominently cancer. The overarching goal of my research is to leverage this information to gain insight into disease biology and reveal targets for therapeutic intervention. It is my hope that my work will contribute to the development of potent therapeutics to treat genetic diseases.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I am excited and honored to be named a Fujifilm Fellow. I’m thankful to FUJIFILM for their support and hope they continue doing the same to others in the future.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I am a Japanese American born in New York City, but I moved to Massachusetts at a young age. I attended the University of Massachusetts Amherst (UMass Amherst) for my bachelor’s degree, where I received a dual degree in chemistry and biochemistry and molecular biology. I first discovered research in my freshman year and became fascinated with gene editing and its tremendous potential to revolutionize medicine and science. After graduating from UMass Amherst, I worked as a research technician at Massachusetts General Hospital, working on an off-target detection platform for CRISPR/Cas9, a versatile gene-editing technology that is starting to be used in the clinic. I became convinced that I wanted to pursue a PhD and develop new technologies for therapeutic use. I joined the Harvard Biological and Biomedical Sciences program because of the breadth and diversity of exciting research and the welcoming and collaborative environment.

  • How does your research hold promise for therapeutic innovation?

    Retinitis pigmentosa (RP) is the most common form of inherited retinal dystrophy and affects approximately 1 in every 4,000 people. RP initially causes rod photoreceptor cell degeneration in the retina resulting in night blindness and can eventually lead to complete blindness upon cone photoreceptor cell dysfunction and degeneration. Gene replacement therapy is one promising therapeutic strategy but can be infeasible in many cases due to the genetic heterogeneity (with thousands of pathogenic mutations identified across more than 80 different genes) and because the causal mutations are not always known. One area of focus in our lab is developing generalized gene therapies that prolong cone photoreceptor cell survival regardless of genetic mutations. Our research holds great promise because a mutation-agnostic therapy will be able to treat more patients with RP and improve their quality of life.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was extremely surprised by the news and honored to be chosen as a Fujifilm fellow. I’m very grateful to see that such a famous company is willing to invest not only in science but also in the development of researchers.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I am originally from Nanjing, China. To fulfill my passion for biology, I left my homeland and my family to study life sciences in the Netherlands (HAN University of Applied Science). As an undergraduate student, I was fascinated with induced pluripotent stem cells (iPSCs) technology due to its therapeutic potential, such as in the study of neuron degeneration diseases. To gain a better comprehension of this, I studied iPSCs technology in Dr. Niels Geijsen’s lab at the Hubrecht Institute and upper motor neuron conversion from iPSCs in Dr. Paola Arlotta’s lab (in collaboration with Dr. Fengzhang’s lab) as my undergraduate internship.

    Throughout my time on both of my undergraduate internship projects, I found it fascinating how we could recapitulate what happens in a human body faithfully in a petri-dish and use it as a platform for disease mechanism discovery. I was eager to explore the research possibilities in this realm. With such a question, I was recruited by Dr. Justin Ichida, a fellow researcher from Harvard, who was starting a new lab at the University of Southern California.

    In Dr. Ichida’s lab, I embarked on a five-year journey applying stem cell technologies to studying and potentially treating Amyotrophic Lateral Sclerosis (ALS). I focused on the most common genetic cause of the disease, an extended hexanucleotide GGGGCC expansion in the 72nd open reading frame on chromosome 9 (C9ORF72). After days and nights of trying to get the best motor neuron conversion, gene editing efficiency, disease-relevant stress conditions, and downstream molecular readouts, I was eventually able to show that the motor neuron degeneration in C9ORF72 type ALS patients was caused by a cooperativity between the gain-of-function from toxic aggregates and the loss-of-function from C9ORF72 gene products on protein trafficking.

    The experience where I used my knowledge in stem cell biology to derive patient-specific motor neuron phenotypes for therapeutic compound high-throughput screening strengthened my belief that translational research could indeed one day provide effective therapeutic treatments. With this goal, I pursued other potential drugs for ALS. In collaboration with Dr. Berislav V. Zlokovic’s lab, I found that Active Protein C (APC), which was previously shown to block neuron apoptosis and to alleviate disease-mimicking phenotypes in rodent ALS models, rescued patient-specific motor neuron phenotypes via improving autophagosome functions.

    This was an exciting time for me as I had potentially discovered a new therapeutic pathway for ALS, but the final stage of submitting my APC manuscript, I abruptly needed to travel home to China to be by my mother’s side as she went through the final stage of cancer, and sadly her life. I was so incredibly frustrated that better therapies for breast cancers are not as readily available in China as they are in the US, and that as a whole how poor the prognosis is for late-stage cancers in general. Through my angst and grief came the vivid realization and understanding of the importance of scientific research. The helplessness and frustration for my mother have transformed me in many ways. It has given me drive and purpose to apply myself in cancer research. I want to replicate the story of Herceptin. I want to make immunotherapy more individualized. I no longer want to see desperate patients. I will devote my career to the disease that took my mother away in the hope of making the prognosis better for the next patient.

    Being one of the world’s leading cancer research organizations, Dana-Farber Cancer Institute has a long history of fighting cancer since 1947. Moreover, close collaboration with multiple hospitals such as Massachusetts General Hospital provides opportunities for close interactions between patients and researchers, so that the patients can benefit from the latest discoveries and innovative treatments. Overall, it is one of the best places for cancer research and it will be my great honor to further my research and study here.

  • How does your research hold promise for therapeutic innovation?

    Intratumor heterogeneity is a critical obstacle to conquer when designing the most effective therapeutic strategies for patients with cancer. The poor understanding of the genotypic and phenotypic variation of different clones within one tumor can cause ineffective treatment and drug resistance. Therefore, only by well-characterizing gene mutations from each tumor clone and understanding each clone’s role in tumor formation would allow us to develop effective combination treatments to treat cancer systematically.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I cannot believe it! I learned that Fujifilm Fellowship only provides funding to the most promising PhD students across the nine HMS-based life sciences PhD program. I am truly honored to be selected among all of the excellent candidates.

  • Where are you from, where did you study prior to this, and what brought you to HMS?

    I am a second-year graduate student in the virology program. I grew up in Hong Kong and pursued my undergraduate studies in The Hong Kong University of Science and Technology (HKUST), where I majored in biotechnology and minored in bioengineering. I continued with a research master at The University of Hong Kong (HKU), where my research focused on understanding the lytic reactivation mechanism of Epstein-Barr virus (EBV). I joined the virology program at Harvard to continue researching on viruses because of its highly collaborative and supportive environment.

  • How does your research hold promise for therapeutic innovation?

    EBV is an oncovirus that persistently infects >95% of adults worldwide. It is associated with multiple human malignancies, with nearly 200,000 cancers attributable to EBV each year worldwide. These include Burkitt lymphoma, Hodgkin lymphoma, HIV-associated lymphomas, post-transplant lymphoproliferative diseases, immune-senescence-associated lymphomas, nasopharyngeal, and gastric carcinomas. Upon infection of primary B lymphocytes, EBV enters a state of viral latency but is hardly quiescent. Rather, EBV expresses oncogenic membrane proteins, transcription factors, and microRNAs that efficiently transform resting B-lymphocytes into rapidly growing lymphoblasts. Although there has been a lot of research since its discovery, there are still many unknowns in the field. By constructing the inter- and intra- viral-host protein interactome, we could explore the functions of each of the viral proteins and understand how they lead to tumorigenesis, thus fostering the development of therapeutics against EBV-specific tumor cells.

  • What was your reaction when you learned you were named a Fujifilm Fellow?

    I was very excited and honored to be named as a Fujifilm Fellow. It is very encouraging, and I am looking forward to future research experiences and to share my findings with the community.