Carol Leung
PhD
Junior Group Leader
I studied the immune responses against the tumour-causing Epstein-Barr virus (EBV) during my PhD at the University of Birmingham (UK). Following this, I moved to the University of Zurich to work on EBV vaccine development before returning to the UK. I am experienced in the preclinical development of cancer vaccines, contributing to the clinical testing of innovative cancer vaccines.
A major breakthrough in cancer immunotherapy is the clinical success of immune checkpoint inhibitors in treating advanced cancer. However, only a subset of patients benefit from this treatment, partly due to the lack of pre-existing anti-tumour T-cell responses. Cancer vaccines can induce anti-tumour T cells, offering a promising approach to cancer treatment. Yet, substantial challenges and numerous unresolved questions need to be addressed before these vaccines can be widely used. The Leung lab aims to develop the next-generation cancer vaccines that can induce robust cytotoxic T-cell responses; assess their safety, efficacy, and potential mechanisms of action. Additionally, the lab is interested in studying other treatments and the tumour microenvironment that can influence therapeutic responses and resistance, with the goal of improving the efficacy of tumour immunotherapies.
Recent publications
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Unlocking cancer vaccine potential: What are the key factors?
Journal article
Grant M. et al, (2024), Human vaccines & immunotherapeutics, 20
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Intravenous heterologous prime-boost vaccination activates innate and adaptive immunity to promote tumor regression.
Journal article
Ramirez-Valdez RA. et al, (2023), Cell reports, 42
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Heterologous prime-boost viral vector cancer vaccines have protective effects against a syngeneic mouse model of glioblastoma
Poster
Steffke EE. et al, (2023), JOURNAL OF IMMUNOLOGY, 210
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Heterologous primeboost viral vector vaccines for the treatment of a P1A-expressing BGL1 glioblastoma model
Conference paper
Steffke EE. et al, (2023), CANCER RESEARCH, 83
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Human ZBP1 induces cell death-independent inflammatory signaling via RIPK3 and RIPK1.
Journal article
Peng R. et al, (2022), EMBO reports, 23