UK scientists find new target for cancer drugs

The discovery relates to the activity of telomeres - thimble-like caps that are added to the ends of chromosomes in order to protect DNA from damage. Each time a cell divides, the telomere gets smaller and eventually disappears, giving the cell a signal that it is time to die.

Cancer cells are thought to rely on DNA capping for their remarkable ability to grow and divide eternally - ignoring the normal constraints on lifespan. And overcoming this process could provide a new treatment approach for up to 10 per cent of tumours, according to the researchers.

Many cancer cells achieve immortality by using an enzyme called telomerase to rebuild their telomeres. But this is not the only factor, because malignant cells can achieve immortality without it.

In the new study, the scientists used a immunofluorescence technique to light up various molecules within cancer cells and see precisely where they were operating. One particular molecule, called RAD51D, appeared time and again at the site of the telomeres, suggesting it was interacting in some way with the timer mechanism.

When researchers blocked the activity of RAD51D using a second technique called RNA interference, they found substantial damage to the telomeres and other parts of the genome.

RAD51D is known to play a role in repairing DNA, but the authors suggest that is has a second role - as supplier of a protective cap for the telomeres. This could lead to a new target for cancer, but also ageing, as the process by which elderly cells slide into decrepitude appars to be the same.

Dr Madalena Tarsounas, leading the study at the Cancer Research UK London Research Institute and funded by both Breast Cancer Campaign and Cancer Research UK, said: "Cancer has an amazing ability to shake off the shackles of ageing and death, which is one of the reasons why it can be so hard to treat."​

Having a stable telomere is important to prevent a cell's genetic material from becoming unstable. Researchers believe that in normal cells, RAD51D may stabilise the telomeres without interfering with the timer that limits their lifespan. But in cancer cells RAD51D may be over-active, stopping the clock and allowing the cells to grow and divide indefinitely.

Drugs to block the action of RAD51D could potentially be effective against many different tumours, by stripping cancer cells of their immortality.

Dr Tarsounas adds: "We think as many as 10 per cent of tumours may be heavily reliant on the new mechanism to keep their cells alive and these may also be highly susceptible to drugs targeted against it. "