Lubin Scholars and Lubin Mentors
Lubin Scholars include some of the nation's most promising early career investigators. Each Lubin Scholar is pursuing cancer-relevant basic or translational laboratory-based research, and each has demonstrated the potential to join the next generation of leaders in cancer research. Lubin Scholar Mentors are leaders in their respective scientific fields — providing the scholars with guidance, support, and inspiration.
2026 Lubin Scholars and Mentors
- Scholar Jamie Brett, MD, PhD, and Mentors Marcia Haigis, PhD, and Kimberly Stegmaier, MD
- Scholar Luke Frankiw, MD, PhD, and Mentor Vijay Sankaran, MD, PhD
- Scholar Gunsagar Gulati, MD, PhD, and Mentor Matthew Freedman, MD
- Scholar Mike Wang, MD, MHS, and Mentor William Freed-Pastor, MD, PhD
Read about our 2026 Scholars and Mentors below.
Scholar Jamie Brett, MD, PhD, and Mentors Marcia Haigis, PhD, and Kimberly Stegmaier, MD
Jamie Brett, MD, PhD, did her undergraduate and MD-PhD training at Stanford University, where she studied stem cell aging. Her graduate work explored how regeneration pathways in skeletal muscle stem cells become liabilities during aging, informing lifestyle and pharmacologic strategies to restore stem cell function. She completed internal medicine residency at Massachusetts General Hospital and is currently a medical oncology fellow at Dana-Farber Cancer Institute and Mass General Brigham. In the labs of Kimberly Stegmaier, MD, and Marcia Haigis, PhD, she is researching how metabolism determines cell fate and how to exploit cancer metabolism. Focused on sarcomas, she investigates the metabolic weaknesses generated during tumorigenesis. As a Lubin Scholar, she will study how the fatty acid enzyme FADS2 in Ewing sarcoma generates a redox vulnerability that can be therapeutically targeted.
Marcia Haigis, PhD, is a Professor in the Department of Cell Biology, co-Director of the Paul F. Glenn Center for the Biology of Aging Research, and the Director of Gender Equity for Faculty in Science at Harvard Medical School. She obtained her Ph.D. in Biochemistry from the University of Wisconsin and performed postdoctoral studies at MIT studying mitochondrial metabolism. Dr. Haigis is an active member of the Harvard Cancer Consortium and the Ludwig Center at Harvard Medical School. Her research has made fundamental contributions to our understanding of how mitochondria contribute to human health and diseases of aging. Her studies identified that mitochondria mediate metabolic reprogramming in cancer, including identifying nodes of metabolic vulnerability in cancer, as well as identifying metabolic recycling of ammonia to generate amino acids important for tumor growth. Her work has shed light on our understanding of how diet and obesity regulate anti-tumor immunity. She is the recipient of numerous honors and awards, including the Brookdale Leadership in Aging Award, the Ellison Medical Foundation New Scholar Award, the American Cancer Society Research Scholar Award, the National Academy of Medicine Emerging Leaders in Health and Medicine Program, and the 2023 Samsung Ho-Am Prize in Medicine.
Kimberly Stegmaier, MD, is Chair of the Department of Pediatric Oncology at Dana-Farber Cancer Institute; Associate Chief of the Division of Hematology/Oncology at Boston Children’s Hospital (BCH); the David G. Nathan Professor of Pediatrics at Harvard Medical School; and a principal investigator in Pediatric Oncology at Dana-Farber. She is also an Institute Member of the Broad Institute of Harvard and MIT. She received her BS from Duke University and her MD from Harvard Medical School. She completed her residency at BCH and a post-doctoral pediatric hematology-oncology fellowship at Dana-Farber/BCH. In 2006, she launched her own laboratory effort at the Institute.
Scholar Luke Frankiw, MD, PhD, and Mentor Vijay Sankaran, MD, PhD
Luke Frankiw, MD, PhD, is a pediatric hematology/oncology fellow interested in understanding how inherited immune variation shapes cancer risk in children. He earned his MD at the David Geffen School of Medicine at UCLA and his PhD at the California Institute of Technology. His graduate research in David Baltimore's laboratory revealed how alternative mRNA splicing regulates gene expression during innate immune responses, establishing a novel post-transcriptional mechanism that fine-tunes immune function. During medical school, he investigated antigen loss as a driver of resistance to immunotherapy and contributed to multiomic studies of tumor heterogeneity. He completed a general pediatrics residency at Boston Children's Hospital through the Accelerated Research Pathway. His postdoctoral research in the laboratory of Vijay Sankaran, MD, PhD, integrates functional genomics and immune organoids to define how genetic variation shapes immunity and predisposition to malignancy, with the goal of informing new strategies to prevent and treat childhood cancer.
Vijay Sankaran, MD, PhD, is the Jan Ellen Paradise, MD Professor of Pediatrics at Harvard Medical School, an Investigator of the Howard Hughes Medical Institute, an attending physician in the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center, and an associate member of the Broad Institute. Sankaran's lab seeks to understand the influence of human genetic variation on blood and immune cell production in health and disease. Their work has resulted in a number of therapies for blood diseases, including work that led to the development of Casgevy for sickle cell disease and beta-thalassemia. Sankaran has received a number of awards for his work including the 2019 Seldin-Smith Award for Pioneering Research from the American Society of Clinical Investigation, the 2022 E. Mead Johnson Award from the Society for Pediatric Research, and the 2024 Paul-Gallin Trailblazer Prize from the Foundation for the National Institutes of Health. He is an elected member of the Association of American Physicians and the American Society of Clinical Investigation.
Scholar Gunsagar Gulati, MD, PhD, and Mentor Matthew Freedman, MD
Gunsagar Gulati, MD, PhD, completed his undergraduate degree at Harvard College and his MD/PhD at Stanford University, where his doctoral research focused on cancer transcriptomics, stem cell biology, and computational frameworks to infer cellular differentiation states from single-cell data. He went on to complete his clinical training in internal medicine at Brigham and Women’s Hospital and is currently a hematology/oncology fellow at Dana-Farber Cancer Institute. As a postdoctoral fellow, he develops computational and experimental approaches to study cancer epigenomics from circulating cell-free nucleic acids. His work focuses on understanding how chromatin organization and nucleosome architecture encode transcriptional activity and how these features are preserved outside the cell. His research aims to enable mechanistically grounded, noninvasive inference of tumor gene expression, monitor tumor state and therapeutic response over time, and uncover non-genetic mechanisms of cancer progression and resistance.
Matthew Freedman, MD, is the David Goldstein Chair and a Professor of Medicine at Harvard Medical School. He trained as a human geneticist and medical oncologist. He received his MD from the University of Michigan where he spent a year in the laboratory of Francis Collins, MD, PhD. His internal medicine training was at the Hospitals of the University of Pennsylvania. He then trained in Medical Oncology at the Dana-Farber and was a post-doctoral fellow with David Altshuler, MD, PhD. The interests of Freedman’s group can be traced back to the observation that the vast majority of inherited variants associated with cancer risk are located outside of protein coding regions. Thus, his group has been interested in annotating and functionally characterizing the noncoding genome by applying principles from the fields of genomics and epigenomics. They performed one of the first genome wide association studies (GWAS) and identified the 8q24 region as being associated with prostate cancer. They have also pioneered cistrome wide studies and characterized the prostate cancer epigenome across state transitions, such as tumorigenesis and progression. This work identified a novel and functionally relevant, highly recurrent somatically acquired enhancer of the androgen receptor in advanced prostate cancer. Most recently, his group has developed and applied methods to detect circulating cell free epigenetic analytes that capture the biology and dynamics of tumor evolution.
Scholar Mike Wang, MD, MHS, and Mentor William Freed-Pastor, MD, PhD
Mike Wang, MD, MHS, completed his undergraduate degree in Molecular Genetics and Microbiology at the University of Toronto, followed by his MD and a concurrent Master of Health Sciences from Yale School of Medicine. He completed his residency in Internal Medicine at Massachusetts General Hospital and is currently a Hematology/Oncology Fellow at Dana-Farber Cancer Institute. As a postdoctoral fellow in the laboratory of William Freed-Pastor, MD, PhD, his research investigates how oncogenic RAS signaling and RAS inhibition reprogram cellular translation to generate noncanonical HLA class I-presented peptides in pancreatic ductal adenocarcinoma. His work aims to identify novel cancer antigens targetable by cancer vaccines and engineered T-cell therapies, with the goal of rationally combining RAS-targeted agents with antigen-specific immunotherapies to improve outcomes for patients with this devastating disease.
William Freed-Pastor, MD, PhD, is a medical oncologist and physician-scientist at Dana-Farber Cancer Institute, specializing in gastrointestinal oncology and immuno-oncology. He is an investigator within the Division of Molecular and Cellular Oncology and the Hale Family Center for Pancreatic Cancer Research. He is an assistant professor of Medicine at Harvard Medical School and Associate Member at the Broad Institute. Through sophisticated preclinical and patient-derived models, CRISPR-based in vivo genetic engineering, T-cell receptor discovery, and immunopeptidomics, the Freed-Pastor laboratory is focused on dissecting the mechanisms of immune escape and tumor-immune crosstalk in pancreatic cancer, with the overarching goal of using these insights to guide therapeutic advances for pancreatic cancer patients.