Scientists move a step closer to targeting key cancer process

In collaboration with the Press Association

Scientists in the US are closer to working out how to target cancer cells that are driven by a hyperactive gene called Myc, according to a report in the journal Science.

Researchers estimate that 20-40 percent of all cancers are driven by mutations in this gene, and are often aggressive.

Researchers at Baylor College of Medicine and Harvard Medical School showed that a second cellular process, called SUMOylation, was responsible for allowing cancer cells to survive when their Myc gene was hyperactive.

In a series of lab experiments, they also showed that switching SUMOylation off caused these cells to die, since the stresses that the hyperactive gene caused them were too great.

"The tumours stopped growing and many of them melted away," said Dr Thomas Westbrook, a senior author of the report.

"For 30 years, scientists have tried to attack [the Myc gene]. However, it has not been amenable to the drugs we have", he added.

"Now we have to take advantage of the stresses the oncogene puts on the cancer cell and determine if we can ramp those up to kill the tumour"

Victoria Cowling, a Cancer Research UK-funded scientist at the University of Dundee, said: "Myc is a gene found in every cell in our bodies. Over 20 years ago, researchers discovered that it was hyperactive in cancer cells, and we now know that this hyperactivity is involved in many types of cancer.

"Developing treatments to directly switch off hyperactive Myc is notoriously difficult, so many experimental approaches focus on working out why cancer cells tolerate the stress of having a hyperactive gene rather than die off. For a cell to survive with high levels of Myc and divide uncontrollably - i.e. become cancerous - it must adapt.

"This early lab research found that human breast cells can only cope with high levels of Myc if they also switch on a process called SUMOylation, which alters the behaviour of many cellular proteins. Significantly, by stopping this process, the researchers switched off Myc's cancer-causing activity, but did not affect healthy cells.

"It will be exciting if this approach can be developed into a way to treat people whose cancers are driven by hyperactive Myc genes. Although this is a long way off, it could one day prove a powerful weapon against cancer."

Copyright Press Association 2011

References

  • Kessler, J. et al. (2011). A SUMOylation-Dependent Transcriptional Subprogram Is Required for Myc-Driven Tumorigenesis Science DOI: 10.1126/science.1212728