Research

Current Research Topics

How Tumors Rewire Cell Interactions to Progress and Resist Therapy 

Cancer cells evade immunity, withstand treatment, and progress by rewiring their interactions with immune and stromal cells and reorganizing the tumor’s spatial architecture. We map these changes to reveal vulnerabilities for precision intervention. 
Our current studies probe these vulnerabilities through tumor antigenicity and cancer vaccines, macrophage reprogramming and CAR-macrophage therapy, therapy-induced senescence, and phosphorylation-driven signaling networks. 

Selected papers from our lab on this topic: 
Nature Communications. 11, 951 (2020) - We developed a deep-learning framework to identify clinically relevant neoantigens and immune-evasion mutations, linking tumor antigenicity to immune escape and personalized vaccine and immunotherapy strategies.   
Clinical and Translational Medicine. 12, e714 (2022) - We showed that genes essential for tumor survival also shape neoantigen immunoediting, linking tumor fitness and immune pressure to the evolution of immune escape.
Nature Communications. 15, 10164 (2024) - Using deep proteogenomics, we mapped NSCLC into distinct tumor–immune ecosystem states and identified coordinated tumor and microenvironmental programs associated with prognosis and therapeutic vulnerabilities. 

How Metabolic Stress Rewires Cells in Cancer, Obesity, and Aging 

We trace how nutrient transport and metabolic stress reshape cell states and tissue interactions in cancer, obesity, and aging, aiming to uncover mechanisms that drive immune dysfunction, therapy resistance, and disease progression.
Current studies focus on SLC-mediated nutrient transport, tumor immunometabolism and immune evasion, obesity-associated inflammatory remodeling, and age-related macrophage metabolic changes linked to inflammaging.

Selected papers from our lab on this topic:

Science Advances. 12(41), eaeh2362 (2026) - We showed that SLC39-driven zinc uptake rewires colorectal cancer cells and their interactions with myeloid cells, creating an immune-suppressive ecosystem and revealing a targetable metabolic–immune vulnerability.  

How Early Environmental Exposures Reprogram Immunity and Shape Allergic Disease 

Prenatal and early-life exposures can leave lasting epigenetic marks that reprogram developing immune cells and alter later susceptibility to allergic disease. 
Our work examines air-pollution and chemical exposures, placental and fetal immune programming, and their links to childhood asthma and atopic dermatitis. 

Selected papers from our lab on this topic:
Clinical and Translational Medicine. 11, e562 (2021) - We integrated human and experimental multi-omics to define disease-associated molecular programs driven by exposure, establishing a framework for moving from exposure associations to mechanism. 
Environmental Pollution. 366, 125471 (2024) - We showed that prenatal particulate-matter exposure leaves epigenetic signatures in the placenta linked to childhood asthma, supporting a developmental connection between early environmental signals and later disease susceptibility.  
Nature Communications. 17, 9531 (2026) -  We identified persistent FCER1G dysregulation in fetal macrophages connecting prenatal PM2.5 exposure to macrophage states associated with atopic dermatitis, demonstrating a lasting immune imprint of early exposure. 

How DNA and RNA Structures Shape Immune Cell Fate and Aging 

We investigate the effects of noncanonical DNA and RNA structures—and the helicases that regulate them—on gene regulation, immune-cell state, development, and function across aging.
Current work focuses on G-quadruplexes, R-loops, and DHX9-dependent chromatin and RNA regulation, together with their roles in immune-cell survival, differentiation, and age-related functional change, while extending these studies to cancer.  

Selected papers from our lab on this topic:
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