Inflammation and cancer: Till death tears them apart

- Inflammation plays a key role in cancer initiation and propagation.
- Chronic and subclinical inflammation increases cancer risk.
- Cytokines, chemokines and reactive species support tumour initiation, progression and metastasis.
- Signalling pathways that mediate the pro-tumourigenic effects of inflammation are often subject to positive feedback loops.
- Specific therapies or therapeutic strategies for veterinary species should be designed around this new understanding.

Advances in biotechnology have enabled the collection of an immeasurable amount of information from genomic, transcriptomic, metabolomic and proteomic studies of tumours within their microenvironments. The dissection of cytokine and chemokine networks has provided new clues to the interactions between cancer cells and their surrounding inflammatory landscape. To bridge the gap between chronic inflammation and cancer, dynamic participants in the tumour microenvironment have been identified, including tumour-associated macrophages (TAMs) and regulatory T cells (Tregs). Both of these cell types are notable for their ability to cause immunosuppressive conditions and support the evasion of tumour immune surveillance. It is clear now that the tumour-promoting inflammatory environment has to be included as one of the major cancer hallmarks. This review explores the recent advances in the understanding of cancer-related inflammation and how this is being applied to comparative oncology studies in humans and domestic species, such as the dog.