My clinical specialty is pediatric oncology. I’m particularly interested in solid tumors, liver tumors and cancer predisposition. My research focuses on pediatric liver cancer, developmental tumorigenesis and cancer genetics and genomics.
While my interest in combining cancer research with patient care developed early through my undergraduate studies and research experiences, I was drawn to pediatrics and pediatric oncology during my clinical rotations in medical school. As a physician-scientist, I was particularly inspired by the advances made in treating childhood cancers while recognizing the persistent challenges and opportunities to apply my scientific training to improve care for this vulnerable patient population.
For my PhD in the laboratory of Dr. Titia de Lange at Rockefeller University, I studied telomeres, the repetitive sequences found at the ends of linear chromosomes and the associated proteins that protect chromosome ends from being recognized as sites of DNA damage. While my predoctoral training focused on mechanisms by which genomic instability and mutations give rise to cancer as individuals age, my training in pediatric oncology led me to realize the vast biological differences between the spectrum of cancers that develop in children and those that occur in adults. As a clinical and postdoctoral fellow, I joined Dr. Roel Nusse's laboratory at Stanford University to gain further training in developmental biology. There, I directed my research focus to pediatric liver cancer—specifically hepatoblastoma, a solid tumor that arises most commonly in infancy—to understand better how cancers develop in children.
I’m particularly interested in how tumors initiate and grow during specific developmental time windows and how these processes differ when they occur during development as opposed to adulthood. My lab focuses on the most common primary liver cancer in children, hepatoblastoma, using patient-derived tumor organoids and by engineering new mouse models that more faithfully recapitulate tumorigenesis during the developmental period. Our studies aim to identify new strategies for treating liver and other pediatric cancers and to uncover broad paradigms that underlie the unique mechanisms of tumorigenesis during embryonic and early postnatal development.
I’m honored to have received several awards, including the Burroughs Wellcome Fund Career Award for Medical Scientists (2024-2029), the William Guy Forbeck Research Foundation Scholar Award (2022), the Damon Runyon-Jake Wetchler Award in Pediatric Innovation (2021) and the Damon Runyon-Sohn Pediatric Cancer Fellowship Award (2019-2023).
PhD: Cell Biology & Genetics, The Rockefeller University, New York, NY, 2012.
MD: Weill Cornell Medical College, New York, NY, 2013.
Residency: Pediatrics, UCSF School of Medicine, San Francisco, CA, 2016.
Fellowship: Pediatric Hematology/Oncology, Stanford University School of Medicine, Palo Alto, CA, 2019.
Certifications: American Board of Pediatrics, 2017; ABP Pediatric Hematology/Oncology, 2023.
Pediatric oncology; pediatric liver tumors
Cancer and Blood Diseases, Cancer Blood Disease Institute
Pediatric liver tumors; developmental biology; cancer genetics and genomics
Oncology
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A developmental biliary lineage program cooperates with Wnt activation to promote cell proliferation in hepatoblastoma. Nature Communications. 2024; 15:10007.
Current Approaches in Hepatoblastoma-New Biological Insights to Inform Therapy. Current Oncology Reports. 2022; 24:1209-1218.
3D Culture of Primary Patient-Derived Hepatoblastoma Tumoroids. Methods in Molecular Biology. : Springer US; Springer US; 2022.
Abstract B024: Single cell transcriptomics and patient-derived tumoroids reveal that hepatobiliary lineage programs cooperate with Wnt pathway mutations to drive cell proliferation in hepatoblastoma. Cancer Research. 2024; 84:b024.
DNA-PK and the TRF2 iDDR inhibit MRN-initiated resection at leading-end telomeres. Nature Structural and Molecular Biology. 2023; 30:1346-1356.
Intermittent fasting induces rapid hepatocyte proliferation to restore the hepatostat in the mouse liver. eLife. 2023; 12:e82311.
Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade. Proceedings of the National Academy of Sciences of USA. 2022; 119:e2203849119.
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