Cancer self-destructs thanks to new technique © Getty Images

Cancer self-destructs thanks to new technique

Blocking the ATF4 protein in cells and mice caused tumours to die of stress.

Another battle has been won in the war against cancer. Researchers have developed a new way to block the development of multiple cancers, which could lead to new forms of treatment.

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The key is a gene is known as MYC. It’s one of the most commonly affected genes in human cancers, contributing to the cause of at least 40 per cent of tumours. MYC controls normal cell growth, but when it becomes mutated or amplified in cancer, it triggers a chain reaction that causes tumours to grow uncontrollably.

There’s currently no way to target MYC specifically, so research is focused on blocking steps in the chain between the gene and the tumour. Previously, researchers looked at blocking an enzyme called PERK, which is involved in one of the steps along the chain.

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In this new study, however, the same team of researchers showed that knocking out PERK doesn’t always prevent tumour growth, because the MYC gene controls another, parallel, process that can kick in, involving a different enzyme. In other words, the cancer has a choice of paths, and it can switch from one to the other.

“What we’ve learned is that 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,” said Dr Constantinos Koumenis, team leader and oncologist at the University of Pennsylvania’s Perelman School of Medicine.

The researchers looked a couple more steps down the chain reaction, identifying a protein called ATF4. When the researchers blocked ATF4 in cells and mice, the tumour cells produced too much protein, eventually dying as a result of stress. This halted tumour growth in mice with lymphomas and colorectal cancer.

A link was also found between ATF4 and tumours driven by the MYC gene in humans, so these findings could point the way towards a new treatment that involves blocking the synthesis of ATF4.

The researchers now want to find out why ATF4 has the effect it does, which may help them to find other possible targets in the chain.


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