Although hematopoietic stem cell transplantation is the only curative treatment for some pediatric leukemia patients, chronic graft-versus-host disease (cGVHD) is a potentially life-threatening immune complication of stem cell transplantation. Li’s research aims to mitigate the effects of cGVHD by enhancing the activity of regulatory T cells (Tregs), which are immunosuppressive T lymphocytes. Specifically, she is studying the effect of a novel class of drugs called thalidomide analogs on Treg survival and function. Li will use genetic screens, cell culture and mouse models to elucidate the mechanisms by which thalidomide analogs alter Treg activity and to determine whether treatment with thalidomide analogs can mitigate cGVHD severity. She hopes that these studies will identify methods to strengthen Treg function and inform novel strategies to improve therapies for cGVHD. Li received her PhD from the Massachusetts Institute of Technology, her MD from Harvard Medical School, Boston, and her BA from Harvard University, Cambridge.
Acute myeloid leukemia (AML) is a type of blood cancer that affects children and is treated with intense chemotherapy. Unfortunately, if this cancer recurs, it is difficult to treat with chemotherapy. More than half of children with recurrent AML die from the disease. Patients with recurrent AML are typically treated with immunotherapy, a type of treatment that leverages the body’s immune system to kill cancer. Phillips studies a type of natural killer cell called memory-like natural killer cells, which have an enhanced ability to kill AML. Her project aims to help memory-like natural killer cells better recognize AML cells by outfitting them with one of two receptors, chimeric antigen receptors or natural killer cell engagers, to target common markers on the surface of AML cells. She hopes one or both methods can be translated into a clinical trial to treat children with chemotherapy-resistant AML. Phillips received her MD from the Medical College of Wisconsin and her BS from the University of Wisconsin-Madison.
Subyeta is a graduate of the Macaulay Honors College at Hunter College, New York, where she earned a BA in Biological Sciences with a minor in Public Health. Born and raised in New York City, Subyeta’s personal medical experiences exposed her to the profound impact of medicine and scientific discovery. These experiences, coupled with clinical volunteer work in hospitals and nursing homes, solidified her aspiration to pursue a career that intersects both cancer research and medicine. She explored this passion through research experiences in Dr. Ross Levine’s lab at Memorial Sloan Kettering Cancer Center, where she contributed to projects focused on acute myeloid leukemia. In the summer of 2024, she deepened her research experience as a Harvard-Amgen Scholar at Boston Children’s Hospital, studying clonal hematopoiesis in the lab of Dr. Vijay G. Sankaran, current Sponsor to a Damon Runyon Fellow and Damon Runyon-St. Jude Fellow. Subyeta’s research efforts were recognized with the Horace W. Goldsmith Scholar Award from Macaulay Honors College. In her free time, she enjoys exploring New York City, building Legos, and unwinding with a good movie.
Milen [National Mah Jongg League Scholar] was born and raised in Nashville, Tennessee, to parents who emigrated from Eritrea. As an undergraduate at Harvard College, where she majored in Neuroscience and minored in Global Health and Health Policy, she became interested in the phenomena of neurodevelopment and neuroplasticity. Seeking deeper insight into these processes, she joined the lab of Dr. Michael E. Greenberg at Harvard Medical School (HMS) and conducted research under Dr. Xin Gu (who was a Damon Runyon Fellow at that time). There, she investigated the function of the protein midnolin and explored its structural, spatial, and physiological properties, elucidating its regulation of key neuronal proteins. This research earned her the HMS “Outstanding Undergraduate Research Award in the Lefler Center” and the Harvard “Herchel Smith Undergraduate Science Fellowship.” Working in Dr. Gu’s independent lab at Dana-Farber Cancer Institute, her scientific interests have widened from neuroscience to the broader processes of cellular growth, development, and death. She is drawn to the field of cancer biology not only for its scientific complexity but also for its human urgency and its therapeutic potential to prevent people’s stories from being cut too short. Outside of the lab, Milen immerses herself in the arts through volunteer work with local museums, creates her own art, and serves as paint charge for several student-run theatrical productions.
Isabella [National Mah Jongg League Scholar] was born and raised in Puyallup, Washington. She graduated from Pacific Lutheran University, Tacoma, with a BS in Biological Sciences with minors in Chemistry and Business Administration. Her motivation to pursue cancer research stems from her own health struggles, which sparked a strong interest in human health and biology from an early age. Over time, that interest has evolved into a deep intellectual curiosity about the molecular mechanisms of cancer. During her undergraduate studies, she had the opportunity to work as a summer intern in the laboratory of Christina M. Termini, PhD, where she investigated how inhibiting isoprenoid production impacts hematopoietic stem cell (HSC) maintenance, expansion, and survival. Her ultimate goal is to contribute meaningfully to improving patient outcomes by developing safe, accessible, and effective cancer treatments. Outside the lab, she enjoys being outdoors, cooking, dancing, and spending quality time with her family.
Dr. Chan’s [Sijbrandij Foundation Fellow] research focuses on gamma delta T cells, an unusual and understudied population of immune cells. While gamma delta T cells have strong antitumor activity, they are most highly stimulated not by cancer cells but by signals produced by microorganisms. Dr. Chan’s work examines the mechanisms by which gamma delta T cells detect and respond to leukemia versus pathogenic microorganisms, and how infection with these microorganisms subsequently impacts the trajectory of leukemia. This is particularly relevant to patients undergoing conventional cancer treatments (e.g., chemotherapy) that suppress the immune system, rendering them susceptible to infection. Furthermore, gamma delta T cells are capable of both rapid and long-term responses against their targets, which positions them as a tool to treat initial cancer as well as prevent disease recurrence. Dr. Chan received her PhD from Yale University, New Haven, and her BS from the University of California, Los Angeles.
Acute myeloid leukemia (AML) is an aggressive blood cancer, diagnosed in about 20,000 people in the U.S. each year. New targeted therapies have greatly expanded treatment options, particularly for older adults who cannot tolerate chemotherapy, but despite these advances, most patients with AML will experience relapse. Research has identified that mutations in the RAS signaling pathway are associated with relapse after targeted therapies. Dr. Anandappa aims to establish a role for RAS inhibitors in treating AML and elucidate the role of inflammation in RAS-mutated AML. She will use CRISPR to study over 300 genes involved in inflammatory signaling and determine if blocking them will increase response to treatment with a RAS inhibitor. The outcomes of this project will ultimately guide the design of combination regimens for the treatment of RAS-mutated AML.
Dr. Gu’s [Sijbrandij Foundation Breakthrough Scientist] lab studies how cells regulate the destruction of proteins without using the typical "ubiquitin" tag, which signals that a protein should be transported to the proteasome for digestion and recycling of amino acids. The lab has discovered a new pathway, the midnolin-proteasome pathway, that helps degrade key proteins involved in cancer, including several linked to blood cancers like multiple myeloma. The lab’s goal is to understand this pathway better and explore how it might be used to develop new treatments, especially for blood cancers, by targeting specific proteins that drive disease.
Hematopoietic stem cells, which are found in the bone marrow and give rise to all other blood cells, maintain lifelong blood production and immune function. Due to their remarkable ability to regenerate the entire blood system, medical uses of HSCs have provided cures for many previously incurable diseases, including blood cancers. However, several unanswered questions limit our ability to full harness their therapeutic potential for cancer treatment. What regulates HSC regeneration? Why does their function decline with age? How does HSC behavior vary in healthy individuals? Using cutting-edge single-cell analyses and computational biology, Dr. Gao [HHMI Fellow] aims to identify the molecular and cellular factors involved in HSC regeneration, as well as possible targets for enhancing their regenerative potential. This work could enable significant improvements in stem cell-based therapies for cancer treatment. Dr. Gao received his PhD from Harvard University, Cambridge and his BS from Washington University, St. Louis.
The cellular response to DNA damage is coordinated by an enzyme known as ATM kinase. Mutations in ATM are found in approximately 1% of the population and contribute to an increased risk of both hereditary and sporadic cancers, including breast cancer. Dr. Kim’s [Lallage Feazel Wall Fellow] research investigates how ATM suppresses the production of double-stranded RNAs (dsRNAs) in response to DNA damage. These dsRNAs play a critical role in tumor progression. Dr. Kim aims to identify the key molecular players involved in ATM-mediated suppression of dsRNAs and elucidate how the loss of ATM function triggers inflammatory responses through dsRNA sensing pathways. By uncovering these mechanisms, Dr. Kim aims to deepen our understanding of how ATM mutations drive cancer development and uncover novel therapeutic strategies for ATM-associated cancers. Dr. Kim received his PhD and BS from the Ulsan National Institute of Science and Technology, Ulsan.