Dr. Chen completed his MD/PhD training at the Tri-Institutional MD/PhD program. He subsequently completed residency training in internal medicine at the Brigham and Woman’s Hospital and fellowship training in Medical Oncology at MSKCC. During his fellowship, he was mentored in the laboratory of Charles Sawyers where he helped to elucidate the tumorigenic mechanisms of ETS transcription factor overexpresison in prostate cancer and gastrointestinal stromal tumor (GIST).
Dr. Chen is currently an Assistant Member in the Human Oncology and Pathogenesis Program (HOPP), and an Attending Physician in the Department of Medicine at Memorial Sloan Kettering Cancer Center (MSKCC). He is a physician scientist who treats patients with advanced prostate cancer. His laboratory focuses on the interplay between aberrant signaling and dysregulated transcriptional output in tumorigenesis in prostate cancer and uveal melanoma. In prostate cancer, work in his laboratory has led to the understanding of how ETS family transcription factors reinforce androgen receptor signaling and aberrant prostate lineage specification. More recently, his laboratory has identified a prevalent mechanism of how prostate cancer can become resistant to lineage directed androgen deprivation therapy through aberrant expression of GI lineage master regulators. To address the need for in vitro models of human prostate cancer, his laboratory has developed human prostate cancer organoid technology for in vitro culture of both benign and malignant prostate epithelial cells from human and mouse prostates. This technology has been widely adapted for therapeutic and mechanistic studies. In uveal melanoma, his laboratory focuses on the mechanistic and therapeutic studies of aberrantly activated G-alpha q signaling. Work from the laboratory includes the discovery of mutations in the G-protein coupled receptor CYSLTR2 that activate G-alpha q signaling and of a critical pathway by which aberrantly activated G-alpha q signaling that is ubiquitous in this disease leads to activation of Ras signaling.
