Could the DNA-PKcs Protein Unlock the Code to Curing Cancer?

There is a distinct difference between cancer cells and normal cells, but cancer treatments don’t often differentiate. This means that healthy cells can become damaged from common cancer therapies – which can cause further harm to your wellbeing – but now German researchers have discovered a way to exploit the differences between cancer cells and normal cells, and this could lead to new treatments.

The results of the study, published in the journal Science Translational Medicine, show that targeting a protein called DNA-PKcs could be particularly effective for the wellness of cancer patients whose tumours bear a specific fault. Although this needs testing in clinical trials, scientists at University Hospital of Cologne found that this type of ATM protein is crucial, as it is normally involved in directing a cell’s response to damage, and so their study focused on cancer cells that lack this protein.

According to Dr Mark O’Driscoll, a Cancer Research UK-funded DNA repair expert at Sussex University who was not involved in the research, ‘Normally, ATM is a molecular “triage nurse” inside our cells, assessing damage, stopping cells dividing, then repairing damaged DNA. But if the damage is too severe, ATM can also trigger damaged cells to commit suicide. But in about one in ten cancers, ATM is missing or damaged, meaning that the cells can keep growing despite damage from drugs or radiotherapy.’

In a series of lab experiments, the team showed that disrupting DNA-PKcs in cells that lacked ATM had a lethal effect, triggering the suicide pathway. O’Driscoll explained, ‘Much of the recent research into DNA repair mechanisms – which can drive cancer development and help cancers become resistant to treatment – have focused on blocking a molecule called PARP. So it’s good to see these researchers focusing on a second pathway involving the ATM protein. If drugs that safely and effectively target cancer cells that lack this protein can be developed, the potential to use them in combination with other therapies could be vast.  Ultimately, this could lead to the development of new, more personalised ways to treat some of the most aggressive forms of cancer, and we’ll be keenly following future developments.’

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