Yong Wan
PhD
A leading expert in posttranslational modifications and cancer biology, Dr. Wan studies mechanisms of breast carcinogenesis and identifies novel targets for therapeutic development.
Specialty
Recent studies led by Dr. Wan have identified promising new strategies to improve the efficacy of immunotherapy in patients with triple-negative breast cancer.
Titles and Roles
- Professor, Department of Pharmacology and Chemical Biology
- Emory University School of Medicine
- Professor, Department of Hematology & Medical Oncology
- Emory University School of Medicine
- Director for Basic Research, Glenn Family Breast Center
- Winship Cancer Institute of Emory University
- Research Program
- Cell and Molecular Biology
Biography
Yong Wan, PhD, is a professor in the Department of Pharmacology and Chemical Biology with a secondary appointment in the Department of Hematology and Medical Oncology at Emory University School of Medicine. Wan, a leading expert in posttranslational modifications and cancer biology, serves as director for basic research for the Glenn Family Breast Center at Winship Cancer Institute of Emory University.
Dr. Wan joined Emory from the Feinberg School of Medicine at Northwestern University in Chicago. There, he served as professor of obstetrics and gynecology in the Division of Reproductive Science in Medicine, professor of pharmacology, and co-director of the Breast Cancer Program for the Robert Lurie Comprehensive Cancer Center. Prior to joining Northwestern, he served on the faculty of the Department of Cell Biology at the University of Pittsburgh School of Medicine and Hillman Comprehensive Cancer Center.
Education
Dr. Wan received his PhD from Cornell University in Ithaca, New York. He completed his postdoctoral training as a Helen Hay Whitney fellow at Harvard Medical School in Cambridge, Massachusetts.
Research
Dr. Wan studies mechanisms of breast carcinogenesis and identifies novel targets for therapeutic development. Particularly, he seeks address how defects in the ubiquitin-proteasome system and other posttranslational modifiers such as protein methyltransferase, poly (ADP-ribose) polymerase and glycosyltransferase would result in deregulated tumor immune checkpoint function, genomic instability, and aberrant signaling that predispose otherwise normal cells to become cancerous tumor cells or promote cancer progression and metastasis.
Publications
Publications Publication Date