There has been a major breakthrough in finding a cure for cancer as Greek Professor Constantinos Koumenis and his team of scientists at the University of Pennsylvania announced they have identified its ‘Achilles Heel’, forcing tumour cells to over stress and self-destruct.

The technique worked on a range of human forms of the disease and mice with bowel and blood cancer, with experiments showing it can block a specific protein that fuels tumours and kills them off.

And there are already drugs that block the chemical called ATF4, offering hope of the fast-tracking of a revolutionary therapy.

Co-senior author Professor Constantinos Koumenis said, “What we’ve learned is we need to go further downstream to block tumour growth in a way that cancer cells can’t easily escape, and our study identifies the target to do just that.”

Dr Koumenis did this by homing in on ATF4 in human bowel, breast and lymphoma cells grown in the lab – and rodents genetically engineered to develop lymphoma.

For years scientists have been trying to target a gene called MYC. It’s known to drive cell growth and allow cancer to take over if it’s mutated or over-expressed.

Now Dr Koumenis, an oncologist at Pennsylvania University, and colleagues have found ATF4 controls a chemical pathway that works in tandem with the gene.

Stopping it in its tracks causes cancer cells to produce too much protein and die, say the researchers and now the findings published in Nature Cell Biology could open the door to a completely fresh approach.

Normal versions of MYC control healthy cell growth. But when it is mutated – or there is too much – it sets off a chain reaction that helps tumors develop and spread.

There is currently no specific way to target it, so the focus has increasingly been on other ways to stop the process indirectly.

Dr Koumenis’ team found in some tumors ATF4 is activated by an enzyme known as PERK.

But blocking this protein does not always work because MYC actually controls a second enzyme called GCN2 that can function in parallel – making PERK redundant.

The alternative approach is to target ATF4 itself since it’s the point where both these signal pathways converge.

This means there’s less built-in protection to allow cancer to survive, explained Dr Koumenis.

This is further evidence suggesting the approach will be successful in patients, said Dr Koumenis.


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