 |  |  | | | GENE OFFERS NEW CANCER CLUE | | | | |
| |  Dr Stankovic
Release Date: 27th March 2002
UK scientists have uncovered a genetic mistake associated with the most common form of leukaemia in the western world, a discovery that could significantly advance efforts to combat this disease.
More than 2,500 new cases of chronic lymphocytic leukaemia (CLL) are recorded each year in Britain. The finding by Leukaemia Research Fund scientists from the Universities of Birmingham and Liverpool presents a tantalizing clue as to how complex genetic machinery can go wrong in this common cancer.
It has been known for many years that a gene called p53 plays an important role in the majority of human cancers including CLL. Known as the "guardian of the genome", this gene helps to protect the body from cancer. It ensures that cells that have damaged or altered genes are destroyed if they cannot be repaired. Damage to this gene is therefore implicated in a number of cancers.
The LRF scientists have now found for the first time that damage to another gene - dubbed ATM (ataxia telangiectasia mutated) - can have a knock-on effect on the p53 gene. A healthy ATM gene plays a key role in helping the body to detect unwanted damage to DNA.
But a defective ATM gene can interfere with p53 thereby allowing potentially cancerous cells to multiply. "It is almost as if this mutant gene can deactivate the 'cell destruct' button, allowing the rogue cells to multiply," says Dr Tanya Stankovic from the University of Birmingham. She has been collaborating with Dr Andrew Pettitt - who is based at Royal Liverpool Hospital.
"It is well known that p53's protein helps protect us from cancer but this is the first time that scientists have shown that another gene can have a knock on effect on p53 function in tumour cells," she adds.
The researchers found that around 20% of B-cell CLL tumours had a faulty ATM gene, and another 10-15% had an abnormality in the p53 gene representing a third of all B-CLLs. Scientists believe that patients with this mutant ATM gene may have a more aggressive form of CLL which is more difficult to treat with conventional drugs.
Today's new grant of £300,000 from the Leukaemia Research Fund will enable Dr Stankovic and her team to push forward with their pioneering research. "Thanks to this grant from the LRF, we will now be able to see whether this group of patients does indeed have a worse prognosis," Dr Stankovic says.
Dr David Grant, Scientific Director of the Leukaemia Research Fund, said: "These findings should prove to be a key weapon in treating this form of leukaemia. It is vital that we pick out patients with a poor prognosis at an early stage so we can give them more aggressive therapy when they are fitter and in a better position to tolerate it," he adds.
The LRF grant will also enable Dr Stankovic to look for other genes in CLL where ATM can also have a knock-on effect. "It is only by having a full understanding of the way our genetic machinery goes wrong that we will be able to find a way of stopping CLL cells in their tracks," she explains
There are two copies of the ATM gene in all individuals and scientists have found that some CLL patients carry one faulty copy of the gene from birth. With the new funding, they will also see whether a faulty gene at birth confers a high risk of developing B-CLL.
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