The Kim Lab investigates how vascular dysfunction drives disease progression in cancer and neurodegenerative disorders. Our research focuses on pathological angiogenesis, vascular remodeling, and barrier disruption, with particular emphasis on how vascular destabilization promotes metastasis, therapeutic resistance, and immune suppression. We also study the role of angiopoietin-TIE2 signaling in blood-brain barrier dysfunction and neuroinflammation in Alzheimer’s disease. By integrating in vivo models with translational approaches, we aim to uncover vascular mechanisms that can be therapeutically targeted.
“Targeting tumor vascularization to control liver metastasis.”
We investigate how vascular remodeling shapes the liver metastatic niche and drives immune suppression and therapeutic resistance in pancreatic neuroendocrine tumors. Using mouse models and human specimens, we aim to develop more effective strategies to delay metastatic progression by targeting the tumor vasculature.
“Vascular control of immune exclusion and immunotherapy resistance.”
We study how abnormal tumor vasculature drives T-cell exclusion and immune evasion in melanoma, thereby limiting anti-tumor immunity and responses to immunotherapy. With a focus on the ANGPT2–TIE2 pathway, we aim to identify novel vascular targets that enhance immune activation.
“Blood-brain barrier dysfunction in Alzheimer’s disease.”
We investigate the mechanisms underlying blood-brain barrier disruption and its role in promoting neuroinflammation and disease progression in Alzheimer’s disease, using mouse models, human specimens, and human datasets.