The scientists say they have uncovered how cells switch a gene called p53, which can block the development of tumours, on and off and their finding has important implications for the treatment and diagnosis of cancer.

The study, carried out by teams of scientists in Singapore and the University of Dundee, Scotland found that the p53 gene, which was first discovered 30 years ago, plays a vital role in keeping the body healthy by ordering damaged cells to commit suicide, or by stopping them dividing while key repair work is carried out.

In many cancers the gene is either damaged or inactive, giving damaged cells a free run in dividing and continuing to form cancers and discovering how it is regulated will have important implications in the development of better drugs and ways to diagnose cancer.

For this latest research the scientists used a genetic trick to make Zebra fish turn green when the p53 gene was switched on in order to explore the way it was regulated and they found that the gene makes not only the well-established p53 protein, but also an alternative "control switch" variation of the p53 protein - known as an isoform.

Zebra fish carry the same p53 gene as humans and can normally survive low doses of radiation, which causes damage to the DNA, because the gene steps in to repair that damage but it was revealed that no such repair took place in zebra fish without the isoform switch, and they died after radiation exposure.

According to the researchers this is proof that the switch plays a crucial role in enabling p53 to do its repair work.

Lead researcher Professor Sir David Lane, says the function of p53 is critical to the way that many cancer treatments kill cells since radiotherapy and chemotherapy act in part by triggering cell suicide in response to DNA damage.

Professor Lane says understanding more about how this gene is controlled in cells is really important for finding ways to prevent cells from turning cancerous.

Experts say the study is exciting because it improves the understanding of how the p53 gene works and discovered how it is regulated, which will have very important implications in the development of better drugs and ways to diagnose cancer.

The study is published in Genes and Development.

"Our study indicated that some patients may have inherited a tendency to return to drinking even after intensive treatment," said Wojnar, "and [may be] more treatment-resistant than other patients. Specifically, we found that a particular type or variant of the gene that codes for BDNF was associated with an increased risk for relapse in alcoholic patients, particularly those with a family history of AD." BDNF is a protein found in the brain that helps nerve cells survive and connect to one another.

"These findings provide further support for the assertion that alcoholic patients are not all alike," said Bauer. "Some possess genetic propensities which may motivate or promote risk for alcoholism as well as risk for treatment failure."

"These patients may have special difficulty in responding well to currently available treatments because of their biological makeup," added Wojnar, "and therefore may need newly constructed intensive programs of therapy that are preferably individualized. This might be a step forward towards 'personalized medicine.'"

Bauer agreed. "During the past 10 years, several new treatments have become available," he said. "However, 'how does one decide among the options?' Genetic differences may eventually help us make the decision. For example, individuals possessing the high-risk-for-relapse variant of the BDNF gene might warrant assignment to the most intensive “ and usually most expensive “ treatment. Individuals with the low-risk variant might not require this level of treatment to have a good outcome."

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