Researchers now think tumours evolve in a Darwinian fashion

“Cancer starts when a single cell in our body starts dividing out of control.”

We repeat this statement so often it would be banal, were it not for its implications.

But after a single, initial, malignant cell division, what happens to the two resulting ‘daughter’ cells? Are they identical to their parents? And what about their daughters? And their daughters’ daughters?

And what about the offspring that split off and travel around the body? After all, it’s usually cancer’s tendency to spread that makes it dangerous, rather than the initial tumour itself. But why is it that advanced cancer is so hard to treat?

Today, a team of some of the UK’s most exciting young researchers, funded by Cancer Research UK, University College London Cancer Institute, the Medical Research Council and the Wellcome Trust, has published results of a three-year analysis of kidney cancer samples.

Sequencing billions of ‘letters’ of DNA, the researchers looked in unprecedented detail at the relatedness of different regions of patients’ tumours, and between the patients’ primary tumour and the more distant secondaries, or ‘metastases’.

Their findings are stark: whichever way they looked at the data, no two samples from the same patient were genetically identical – not even samples next to each other in the original tumour. And the secondaries were significantly different from their parent tumour.

Their findings are the most compelling evidence yet that, like populations of animals in an ecosystem, tumours adapt as they grow, obeying the fundamental evolutionary laws laid down by Charles Darwin over a century ago. It seems this evolutionary aptitude may foster their ability to spread, and to become resistant to almost every treatment we can throw at them.

This heterogeneous nature of cancer has big implications for the way we think about the disease, and for how we continue to improve the way we treat it.

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