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Research from Nuffield Department of Orthopaedics, Rheumatology & Musculoskeletal Sciences (NDORMS) shows how IL-22 interacts with KRAS mutant tumours to promote excessive growth in colorectal cancer

Cancer attacking a cell in the colon © Shutterstock

Colorectal cancer (CRC) is the third most common cancer worldwide and the fourth leading cause of cancer-related deaths. For patients, current therapy primarily entails surgical removal of the tumour and chemotherapy, to which tumours are variably responsive.

The immune system can be a double-edged sword in cancer because it can both combat and contribute to tumour development. The Powrie Group at the Kennedy Institute of Rheumatology (NDORMS) were interested understanding the role of molecule IL-22, produced by immune cells, and to identify mechanisms by which it might influence CRC.

Their research published in Clinical Cancer Research found a link between the receptor for IL-22 and a mutation in the gene KRAS, showing that they work cooperatively to promote excessive growth and division of tumour cells. This is hypothesised to explain why prognosis is significantly worse for patients whose tumours have both a mutation in KRAS and high expression of the IL-22 receptor.

The full article is available on the NDORMS website