Looking at skin cells the researchers demonstrated that damaged, non-dividing cells were able to send signals to neighbouring cells telling them to divide and form the beginnings of a tumour.
Cancers are characterised by faulty cells dividing uncontrollably – rapidly building a mass of cells. Because of this it is generally assumed cancers only arise from dividing cells, such as stem cells, with genetic faults called mutations.
Instead, non-dividing cells are able to contribute to the beginnings of tumour formation through the inflammatory response – chemicals sent out by cells in response to damage.
In response to damage, the non-dividing cells that switch on a gene called MEK1 recruit adjacent cells that are able to divide to help form the bulk of the tumour.
But this alone is not enough to initiate a tumour. The damage also releases a molecule from skin cells called IL1 that helps speed up tumour development by stimulating cells to divide and helping tumours to form their own blood supply.
This molecule in turn attracts inflammatory cells, including macrophages, which contribute to tumour formation. They encourage the tumour’s blood supply to grow and suppress the tumour-fighting responses of the immune system.
Individually these steps do not start tumours but the researchers have shown that collectively, in response to damage, they can lead to cancer.
Professor Fiona Watt , lead researcher and deputy director of Cancer Research UK’s Cambridge Research Institute, said: “Since a hallmark of cancer is uncontrolled cell growth, it is widely assumed that tumours only arise from dividing cells.
In contrast, our studies show that cells that do not divide can still contribute to tumour formation. These results suggest new therapeutic approaches to treating certain cancers.”
Dr Lesley Walker, director of cancer information at Cancer Research UK, said: “These intriguing results could really change our understanding of how cancers develop.
The more we understand about the development of cancers, the more opportunities we have to design new treatments to block and prevent cancers progressing further.”
Source: Cancer Research UK Cambridge Research Institute