Our primary discovery efforts focus on the complexity of the tumour microenvironment (the Tumour Metropolis; Theme 1), because, almost irrespective of mutational load, transformed cells will not form tumours unless the local environment is conducive. The Tumour Metropolis regulates whether the immune system can “see” tumours, underpinning inspiring clinical successes via CD8 and CD4 T-cell recognition of cancer neo-epitopes and tumour-associated antigens. While promoting this approach, our Centre goes much further, being pioneers in identifying axes beyond CD4, CD8 T-cells through which immune cells target cancers. Such axes promise modalities for cancers that respond poorly to current immunotherapies. However, immune responses to cancer can equally well promote tumour growth and spread. To regulate this very delicate balance in the patient’s favour, it is essential to employ innovative ways to understand the Tumour Metropolis. Hence, we have extended our current activities and committed several new faculty positions to a new Centre for Inflammation Biology and Cancer Immunology (CIBCI), which will serve as a hub for tackling the complexity of the Tumour Metropolis, harnessing our established expertise in the genetics, immunobiology, and treatment of inflammatory diseases.

 
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Tumour associated macrophages expressing fibroblast activation protein alpha (FAP) and heme oxygenase-1 (HO-1) are exploited from an innate regenerative wound healing response driven by IL-6 in a collagen-rich microenvironment to facilitate tumour cell metastasis. Frozen tissue sections stained with DAPI (nuclei; blue) and antibodies against CD11b (h) / F4/80 (m) (green/macrophage markers), FAP (yellow) and HO-1 (red) in a murine dermal wound (top) and human breast cancer (bottom). Arrows indicate examples of FAP+ HO-1+ macrophages.

 
 

Research Groups