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‘Surprising’ imbalance in cell growth could help oesophageal cancers form

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by In collaboration with PA Media Group | News

22 August 2016

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Scientists working at a computer.

Oesophageal cancers could stem from more than just cells growing out of control, according to research from the Wellcome Trust Sanger Institute.

“The next important step will be finding out whether the same is true in patients with the disease” – Dr Justine Alford, Cancer Research UK

Scientists found that cells from certain types of oesophageal cancer do not divide faster than neighbouring normal cells, which had been previously assumed. 

The unexpected discovery instead revealed that precancerous cells produced a greater number of dividing cells than their healthy counterparts. This tipped the balance towards more dividing cells, and caused tumours to form in mice.

The researchers believe their discovery could pave the way for research into new treatments for cancers that do not respond to therapies that target fast-growing cells. 

When normal cells divide they typically produce a balance of dividing and non-dividing ‘daughter’ cells. 

But the new study in mice, published in the journal Nature Cell Biology, shows that when cells from a particular type of oesophageal cancer divide they do so in an ‘unbalanced’ way, producing more daughter cells that are able to grow and form a tumour. 

Dr Justine Alford, Cancer Research UK’s senior science information officer, said the findings were ‘surprising’, and that further studies would be needed to see if the same imbalance in cell growth happens in people with oesophageal cancer.

“If scientists can unpick the biology causing the imbalance, then it may lead to new treatments for this hard to treat type of cancer and boost the number of people surviving,” she added.

Balancing the number of dividing and non-dividing cells in the body is crucial for maintaining healthy tissues. Tissues can change the ratio of dividing and non-dividing cells when, for example, healing a wound. But this imbalance tends to stop once the wound is healed.

Typically, for every 100 normal cells, half will divide and half won’t. But the Sanger team found that for the same number of precancerous cells, the balance becomes slightly skewed in favour of dividing cells, with 52 going on to divide. 

Dr Philip Jones, lead researcher from the Sanger Institute, said it’s this ‘marginal gain’ of cells with the potential to divide that can lead to tumours forming.

Looking at one type of oesophageal cancer, the researchers found that as different cells became cancerous, they evolved differently with some producing a greater proportion of dividing daughters. This leads to a group of cells in the developing tumour dominating and out-competing the other cells.

Dr Julia Frede, also from the Sanger Institute and who led the study, said that because these cancer cells don’t divide more rapidly than normal cells, this could explain why treatments such as radiotherapy that target fast-dividing cells aren’t effective against all cancers.

Frede added that further research will need to focus on what causes the imbalance in dividing cell numbers.

The study was funded by Cancer Research UK, the Medical Research Council and the Wellcome Trust.

  • Frede, J., et al. (2016). A single dividing cell population with imbalanced fate drives oesophageal tumour growth. Nature Cell Biology. DOI: 10.1038/ncb3400