Investigating fundamental mechanisms of immune surveillance during cancer development and therapy
Ma Lab investigates the fundamental mechanisms of immune surveillance during cancer development and therapy. We focus on understanding how DNA damage responses, mutagenesis processes, and epigenetic disruptions shape tumor immunogenicity and influence treatment resistance, with the ultimate goal of developing novel cancer vaccines, TCR therapies, and combination treatments that maximize the potential of the immune system.
Our previous research demonstrated that DNA damage repair deficiencies lead to accumulation of immunogenic mutations, fundamentally alter the tumor immune microenvironment, and enhance tumor sensitivity to immune checkpoint blockade therapy. However, the complex interplay between DNA damage response pathways and immune surveillance mechanisms in cancer requires deeper investigation to fully understand and therapeutically exploit.
Epigenetic dysregulation is a hallmark of cancer progression and drug resistance development. This dysregulation can also drive aberrant expression of non-canonical tumor antigens, potentially creating immunological vulnerabilities that may be targeted for therapeutic benefit.
Our research employs diverse experimental approaches including cellular and animal models, patient samples and clinical cohorts, synthetic biology tools, and computational immunogenomic analyses to investigate these fundamental questions.
Cellular and animal models to study immune-tumor interactions and therapeutic responses
Patient samples and clinical data to validate findings and identify biomarkers
Engineering tools for neoantigen discovery and TCR therapy development
Immunogenomic analyses of large-scale genomic and immunologic datasets
Bridging basic discoveries to clinical applications and therapeutic development
Interdisciplinary partnerships with clinicians, computational biologists, and industry