Scientists edge closer to targeting an 'undruggable' cancer gene
Cancers caused by a hyperactive faulty gene called Myc seem to depend on a protein called ARK5 to survive, according to scientists from the University of Wuerzburg in Germany.
Developing treatments to target the protein could be a novel way to kill these cancers, say the researchers in an article published in the journal Nature.
Myc is a so-called oncogene, a gene that under normal circumstances governs how cells divide, but that can also cause cancer if it is damaged or hyperactive.
Dr Martin Eilers and colleagues analysed Myc-driven liver cancers in mice and found that the ARK5 protein had a major influence on the tumour's ability to survive. Loss of the protein caused the cancer cells to die off.
It is notoriously difficult to target Myc in cancer patients, but this study indicates scientists could try to find a way to block ARK5 to help kill tumours that rely on Myc to survive.
Dr Victoria Cowling, a Cancer Research UK-funded scientist at the University of Dundee, described the findings as "exciting".
She said: "For years we've known that hyperactive Myc gives cancer cells all sorts of advantages, allowing them to grow and divide rapidly. Yet this rapid growth rate also gives cells vulnerabilities.
"Finding a way to shut down hyperactive Myc in cancer patients would be huge, as it's involved in many tumours.
"The authors made their discovery by focussing on what makes a Myc-driven cell vulnerable. They studied how cells with hyperactive Myc are able to use so much energy, and found that they depend on a 'kinase' protein called ARK5. Crucially, they showed that you can successfully treat Myc-driven cancer cells and tumours in mice by blocking ARK5.
"We already have drugs that target kinases, so this may be an important early step towards a way to treat patients with Myc-driven tumours.
"This research hasn't yet moved beyond the lab - so treating patients is a long way off - but this is a fascinating approach to targeting this so-far 'undruggable' gene."
Copyright Press Association 2012