The Kim Lab investigates how vascular dysfunction drives disease progression in cancer and neurodegenerative disorders. In cancer, we study how pathological angiogenesis, vascular remodeling, and barrier disruption promote metastasis, immune suppression, and resistance to therapy. In Alzheimer’s disease, we examine how blood–brain barrier dysfunction contributes to neuroinflammation and disease progression.

By integrating in vivo models with translational approaches, we aim to uncover the vascular mechanisms underlying these diseases and identify new therapeutic targets.

Diagram illustrating vascular control of liver metastasis showing tumor cells, hepatocytes, and blood vessels with vascular remodeling, along with labels and a text box about mechanisms and targets to control metastasis.

“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.

Diagram showing how tumor vasculature contributes to immune suppression, with T cells attempting to attack tumor cells outside the bloodstream and immune exclusion occurring due to abnormal blood vessels.

“Vascular control of immune exclusion and immunotherapy resistance.”

We study how abnormal vasculature drives T-cell exclusion and immune evasion in melanoma, thereby limiting anti-tumor immunity and responses to immunotherapy. Focusing on the ANGPT2-TIE2 pathway, we aim to identify novel vascular targets that enhance immune activation.

Diagram showing the connection between broader disease links to vascular dysfunction, specifically highlighting organ-specific vascular beds, Alzheimer's plaques, and compromised blood-brain barrier (BBB), with a caption about molecular understanding of BBB breakdown in Alzheimer's disease.

“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.