Dr Kelvin Tuong

Advance Qld Early Career Fellow

The University of Queensland Diamantina Institute
Faculty of Medicine
z.tuong@uq.edu.au
+61 7 344 36980

Overview

Dr Kelvin Tuong completed his PhD in the laboratories of Professor Jennifer Stow and Professor George Muscat at the Institute for Molecular Bioscience (IMB), The University of Queensland. His PhD research topic revolved around the nuclear hormone receptor RORα and its role in macrophages and fat/lipid metabolism in the context of obesity and diabetes.

Dr Kelvin Tuong is currently undertaking post-doctoral training in laboratory of Professor Ian Frazer, Faulty of Medicine, Diamantina Insitute, The University of Queensland. He is conducting studies looking into factors that influence HPV-related cancer development and skin cancer development using molecular cell biology, immunology and next-generation sequencing approaches. He is particularly interested in how antigen presenting cells control the immunological dynamics within a cancer-like microenvironment and how that can be translated for better design towards effective immunotherapy.

Research Interests

  • How HPV subverts the immune program in premalignant epithelial conditions
    The risk of persistent HPV infection is highly associated with cancers in the anogenital region. However, not all infections result in cancer, highlighting that sufficient immunological control exists to prevent the progression of the disease in some patients. It is still not adequately understood why these mechanisms fail in certain individuals, resulting in cancer formation. I'm interested in applying single-cell technology to individually profile the cells that participate in the immunological dynamics within a HPV-associated pre-malignant environment. The aim is to discover whether we can target molecular switches in individual cells and sufficiently alter the immune cellular heterogeneity within this environment to favour the clearance of HPV, so that we can consistently prevent the progression of the disease when HPV is involved.
  • Single-cell RNA-seq of antigen presenting cells
    There are at least 4 main classes of antigen presenting cells present in mouse and human skin. The 4 classes has been typically associated with specific function, e.g. cross-presenting CD103+ dendritic cells. However, conventional classification approaches can be ill-describing the effects and i'm interested in using state-of-the-art single-cell technology to characterize this interesting type of cells.
  • Immunology of the skin
    The skin contains a plethora of immune cells that act in unison to protect the body against undesired pathogens and danger. However, these processes are altered during cancer and we still do not understand why. I'm interested in how T cells and antigen presenting cells cope with a developing epithelial cancer environment and what we can do help the immune system fight off the cancer.

Qualifications

  • Doctor of Philosophy, The University of Queensland

Publications

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Grants

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Supervision

  • Doctor Philosophy

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Available Projects

  • Mice that express the high-risk HPV16 E7 oncoprotein display characteristic eptihelial hyperplasia similar to that of human lesions infected with HPV. Interstingly, this effect is accompanied with a marked immunosuppressive immune cell infiltrate. We still do not understand the mechanisms underlying this phenomenon and how it may interfere with the innate and adaptive immunity.

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Publications

Journal Article

Conference Publication

Other Outputs

Grants (Administered at UQ)

PhD and MPhil Supervision

Current Supervision

  • Doctor Philosophy — Joint Principal Advisor

    Other advisors:

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • Mice that express the high-risk HPV16 E7 oncoprotein display characteristic eptihelial hyperplasia similar to that of human lesions infected with HPV. Interstingly, this effect is accompanied with a marked immunosuppressive immune cell infiltrate. We still do not understand the mechanisms underlying this phenomenon and how it may interfere with the innate and adaptive immunity.