WASHINGTON (Reuters) - A certain gene abnormality raises the chance of relapse for children with the most common form of childhood cancer, a discovery that could change the way doctors treat them, US researchers said on Wednesday.

Children with acute lymphoblastic leukemia, or ALL, who have abnormalities in a gene called IKZF1 are three times as likely to have a relapse than those who do not, the researchers wrote in the New England Journal of Medicine.

The findings could lead to a genetic test to identify children at high risk of relapse, according to Dr. James Downing of St. Jude Children's Research Hospital in Memphis, Tennessee, one of the researchers.

Those children might then get more aggressive treatment than usual, such as intensified chemotherapy, in a bid to ward off a relapse, Downing said.

"These are children. Once cured, they're going to live a full and long life," Downing said in a telephone interview. "If they don't need to be treated aggressively, don't treat them aggressively. But you want to cure them."

The gene produces a protein that regulates the activity of many other genes and plays an important role in the development of lymphocytes. These white blood cells are the ones that undergo changes to give rise to pediatric ALL.

The cure rate with existing treatment for children with ALL is about 80 percent. About a quarter suffer a relapse, and 30 percent of those children only survive up to five years.

Doctors have been unable to determine which children are more likely to relapse. If they could predict that, those children might receive more intense treatment.

Doctors hesitate to routinely use intensified chemotherapy because of its toxicity, but knowing a child has this genetic abnormality might outweigh the risk, Downing said.

The researchers looked at genetic information from 221 child patients, comparing their cancer cells to their own normal cells to spot any changes. They confirmed the findings in a second group of 258 children with ALL.

About three-quarters of those with abnormalities relating to the gene relapsed, Downing said.

The study identified a series of abnormalities in the gene that increased relapse risk. For example, some children had no working copies of the gene, some had one working copy and in some cases an abnormal copy interfered with a good one.