Hyungjin Kim

Hyungjin Kim is an Associate Professor in the Department of Pharmacological Sciences at Stony Brook University's Renaissance School of Medicine and the Cancer Center. His research focuses on elucidating fundamental mechanisms of DNA repair with the goal of developing anti-cancer targets and biomarkers for therapeutic benefits. Dr. Kim received his Ph.D. from Washington University in St. Louis and completed his postdoctoral training at Dana-Farber Cancer Institute, Harvard Medical School. He earned his B.S. from Seoul National University in South Korea.

Dr. Kim's research primarily investigates DNA repair mechanisms associated with DNA replication, with a particular focus on proteolysis in regulating these steps. His laboratory studies genome instability as a pervasive characteristic of cancer, examining how defective DNA repair contributes to the pathogenesis of both hereditary and sporadic cancers. The lab's work centers on two main areas: the Fanconi anemia (FA) pathway, which resolves stalled replication forks in response to DNA interstrand cross-links, and DNA replication stress response mechanisms. Dr. Kim's team investigates how proteolytic mechanisms control the activity of the FA core complex and how various genome surveillance factors preserve replication fork integrity through PCNA interaction and ubiquitin signaling.

Analysis of Dr. Kim's recent publications reveals a strong focus on replication stress response mechanisms, particularly involving TIMELESS, SDE2, and the Fanconi anemia pathway. His work demonstrates how these proteins protect stalled replication forks and maintain genome stability, with direct implications for cancer therapeutics. The research shows increasing emphasis on developing targeted therapies that exploit DNA repair vulnerabilities in cancer cells, including synthetic lethality approaches. His publications span high-impact journals in molecular biology, DNA repair, and cancer research, reflecting the interdisciplinary nature of his work.

Dr. Kim leads an active research laboratory investigating the molecular mechanisms of DNA repair and replication stress response. His lab employs cellular, biochemical, and genetic approaches to study how DNA repair systems function as tumor suppressor networks to preserve genomic integrity. The research has direct translational implications for cancer treatment, particularly in developing strategies to exploit DNA repair deficiencies in tumors. Dr. Kim's work connects basic molecular mechanisms with potential clinical applications, especially in understanding how to target replication stress vulnerabilities in cancer cells.