2021–2022 Cohort

I grew up in Germany and graduated with a BSc and MSc degree in Molecular Biotechnology from Heidelberg University. During my studies, I was able to experience different scientific environments in Germany, while working in the Department of Applied Tumor Biology at Heidelberg University Hospital, the Department of Cellular Biophysics at the Max Planck Institute for Medical Research, and the Zeller Lab at EMBL Heidelberg.

However, I also had the opportunity to spend a year in Boston with research stays in the Naxerova Lab at Massachusetts General Hospital and the Weinberg Lab at Whitehead Institute. Experiencing the scientific communities at Harvard and MIT, has motivated me to pursue a PhD in Biological and Biomedical Sciences within the Harvard Division of Medical Sciences, where I want to continue working on my major research interest: cancer.

As a first-year PhD student in the Biological and Biomedical Sciences Program, I am still rotating in different research labs and have not committed to joining a lab yet. However, in the future, I am interested in studying how evolutionary processes shape the development of normal tissues and tumors. In particular, I want to explore how the insights gained might be leveraged to improve patient care and develop new, early-stage therapeutic strategies.

I was excited when learning that I was named a Fujifilm Fellow and I am very grateful for the decision to support my studies and research. Fujifilm’s commitment to supporting the life sciences community at Harvard is extraordinary and helps significantly to drive forward innovative strategies aimed at addressing some of the world’s major health problems.

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!

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.

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.

I was born in Hong Kong but mostly grew up in California, which is where I also pursued my undergraduate studies at UC Berkeley. I majored in Molecular and Cell Biology and first got involved in research in Jeremy Thorner's laboratory, where I studied signal transduction mechanisms in yeast. Thanks to the encouragement of my mentors, I decided to apply to graduate school and chose to study at Harvard because of its community of cutting-edge research and supportive mentors and scientists. 

The ubiquitin-proteasome system is responsible for the degradation of unwanted or damaged proteins in the cell. A broad and diverse family of proteins called E3 ligases recognize the target protein that is to be ubiquitinated, which marks it for proteasomal degradation. Over 600 E3 ligases have been identified, however many remain enigmatic in their mode of substrate recognition. An emerging strategy in drug discovery relies on the use of small molecule ligands to recruit a therapeutically relevant protein to an E3 ligase, leading to the ubiquitination and degradation of the recruited protein, which offers advantages over classic inhibitors. My research focuses on understanding the molecular mechanism in which a novel E3 ligase gets recruited by a degrader and how that affects recruitment of substrates. By biochemically and structurally characterizing the interactions between ligase, degrader, and substrate, my research will contribute to therapeutic innovation by expanding the prospects for the design of new targeted protein degraders. 

I was incredibly surprised and honored to learn that I was named a Fujifilm fellow! I've heard of the company throughout my life and it is an honor to receive support from them for my scientific research. 

I grew up in Vancouver, Washington, and attended the University of Washington in Seattle where I studied microbiology and global health. During this time, I worked on a variety of research projects spanning from vegetation modeling to vaccine adjuvant production and finally to host-pathogen interactions during liver stage malaria. For my PhD, I made the move to the east coast for the cutting-edge, collaborative research being conducted at Harvard. In particular, I was drawn to the supportive scientific environment in the BPH program and its strong emphasis on translational research.

Malaria is the third leading infectious disease killer after Covid-19 and tuberculosis, with over 200 million cases each year worldwide. It is caused by Plasmodium parasites and transmitted by Anopheles mosquitoes, and current strategies for malaria control focus on treating infected individuals with antimalarial drugs and killing mosquitoes to prevent transmission in the first place. However, growing insecticide resistance threatens the efficacy of our current vector control strategies and has contributed to a recent plateau in malaria cases after many years of progress. My project focuses on identifying parasite targets that are amenable to drug perturbation during the mosquito stages of its life cycle. This research helps us understand critical Plasmodium biology during its understudied vector stages. Moreover, the application of this novel approach would enable the development of control methods that can kill parasites within its vector, thereby preventing transmission even in areas of high mosquito insecticide resistance. This holds exciting promise for a novel way of combating one of humanity’s oldest diseases.

I was completely honored and excited to learn that I was named a Fujifilm Fellow. It is incredibly heartening to know that Fujifilm is invested not only in my thesis work, but in supporting the advancement of incredible therapeutic research broadly.

I'm originally from Princeton, New Jersey but have so far never lived anywhere for more than four years. I studied Applied Mathematics and Physics at Emory University and then transitioned into biology while working as a computational scientist at the University of California, San Francisco (UCSF) after my graduation. I came to HMS to start my PhD having become interested in pursuing biomedical research as a career from my time at UCSF. 

My research sits at the intersection of virology, genetics, and infectious disease; I currently study the ways in which host biology and genetics influence the variation we see in responses to infection. This type of research can help us understand the molecular basis of disease, how particular genetic variants might influence resistance to disease, and how the dynamics of host and viral factors determine observed clinical outcomes. Together, these findings can inspire novel therapeutics by guiding us to develop medical countermeasures that directly interfere with early molecular pathogenesis, mirror natural mechanisms of resistance which have been selected for over thousands of years, and more accurately predict disease course in the clinic.

I was quite surprised at first, as I did not know about the existence of the fellowship or that I was under consideration. But I quickly became excited as I learned about the work that Fujifilm is doing in the space of pharmaceuticals and biotechnology, and honored to have been selected. 

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.

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.

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.