Case Study: Cancer cells and the inflammatory response

When the body encounters an infectious agent such as a virus or bacterium, comes up close with irritants such as chemical agents or uv light, or finds damaged cells in its tissues, its first reaction is protection. The affected area becomes inflamed: painful, itchy, swollen - like a sunburn or an allergic reaction to stinging nettles. Inflammation is the body’s way of getting rid of damaged and dead cells and beginning the repair process

When the body encounters an infectious agent such as a virus or bacterium, comes up close with irritants such as chemical agents or uv light, or finds damaged cells in its tissues, its first reaction is protection. The affected area becomes inflamed: painful, itchy, swollen - like a sunburn or an allergic reaction to stinging nettles. Inflammation is the body’s way of getting rid of damaged and dead cells and beginning the repair process.

In the case of cancer cells, the inflammatory response can go two ways: it can either kill newly born cancer cells, or nurture them. We don’t yet know how these inflammatory cells find and interact with these cancer cells, and how the cancer cells go on to multiply in tissues (creating a malignant tumour).

Here at the University of Bristol Professor Paul Martin and his team have identified some of the first signals that attract these inflammatory, or immune, cells to the early cancer cells. Inflammatory cells feasting on pre-tumour cells have been filmed; but it was also observed that pre-tumour cells with no interaction with immune cells grow at a slower rate. This suggests it is the immune cells that deliver the growth signals to the pre-tumour cells. We have now shown that one of these growth signals is prostaglandin, a hormone-like substance that plays an important role with a range of bodily functions including inflammation.

This observation may explain recent studies that have shown how low-dose aspirin can hold off the onset of gut and other cancers – because it blocks prostaglandin synthesis.

We think that local inflammation might drive the formation of polyps – the precursors of most bowel cancers – and we’re working with cancer clinician Dr Tom Creed, to investigate.

We’re also investigating the inflammatory response of wounds as they heal after surgery by watching – using zebrafish models - how the natural inflammatory response of a wound attracts immune cells to nearby newly transformed cancer cells, and what the consequences of that might be.

Why Zebrafish?

These fish are invaluable in our cancer research because they’re translucent, which means we are able to watch – live, in realtime – the interactions between cancer cells and immune cells. It is impossible to watch these interactions in tissues that aren’t translucent, and by watching the interplay between cells we’re able to better understand the role inflammation has in cancer cell growth.

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