Overview
The overall goal of the Lee lab is to improve the therapeutic window of radiation therapy and the survivorship of cancer patients by minimizing the acute and late effects of radiation. The lab studies mechanisms underlying radiation-induced tissue injury and regeneration to develop novel medical countermeasures and predictive biomarkers. The Lee lab is supported by active NIH grants studying radiation-induced oral mucositis (R01DE033404), gastrointestinal acute radiation syndrome (U01AI186969 and R21AI193496), radiation-induced intestinal fibrosis (U01AI183940), and radiation-induced heart disease (U01AI189426).
Current Appointments & Affiliations
Associate Professor in Radiation Oncology
·
2024 - Present
Radiation Oncology,
Clinical Science Departments
Assistant Professor in Pathology
·
2020 - Present
Pathology,
Clinical Science Departments
Member of the Duke Cancer Institute
·
2018 - Present
Duke Cancer Institute,
Institutes and Centers
Recent Publications
Wild-Type p53 Protein Enhances APR-246-Induced Cytotoxicity in Acute Myeloid Leukemia and Normal Hematopoietic Stem/Progenitor Cells.
Journal Article Int J Mol Sci · May 30, 2026 APR-246 (Eprenetapopt) is a small-molecule drug that restores the activity of dysfunctional p53 proteins caused by missense mutations that affect the DNA-binding domain. However, recent studies suggest that APR-246 can also induce cell death in cancer cell ... Full text Link to item CiteChromosomal instability induced by CRISPR/Cas9: implications for pancreatic cancer therapy.
Journal Article J Clin Invest · May 15, 2026 Clinical management of pancreatic cancer (PC) remains severely limited, primarily due to the complex tumor microenvironment. Emerging DNA damage-targeted strategies have demonstrated considerable therapeutic potential in PC. In this issue of the JCI, Teh e ... Full text Link to item CiteMis-splicing drives loss of function of p53E224D point mutation.
Journal Article PLoS One · 2025 BACKGROUND: The tumor suppressor p53 (Trp53), also known as p53, is the most commonly mutated gene in cancer. Canonical p53 DNA damage response pathways are well characterized and classically thought to underlie the tumor suppressive effect of p53. Challen ... Full text Link to item CiteRecent Grants
Serum pro-N-cadherin as an early biomarker of radiation-induced heart disease
ResearchPrincipal Investigator · Awarded by National Institutes of Health · 2025 - 2030Mitigation of gastrointestinal acute radiation syndrome by promoting clusterin-mediated intestinal regeneration
ResearchPrincipal Investigator · Awarded by National Institute of Allergy and Infectious Diseases · 2024 - 2029Radioprotective effect of p53 against oral mucositis
ResearchPrincipal Investigator · Awarded by National Institute of Dental and Craniofacial Research · 2023 - 2028View All Grants
Education
Duke University ·
2012
Ph.D.