Gene mutation may explain deadly form of leukemia

WASHINGTON, April 14 (Xinhua) -- A new study indicates that mutations in the Ikaros gene play a role in triggering acute lymphoblastic leukemia (ALL), an aggressive, treatment-resistant form of cancer.

Researchers at St. Jude Children's Research Hospital in Tennessee reported this week in the magazine Nature that they hoped the find would lead to new ways to tackle the disease.

A chromosomal rearrangement called the Philadelphia chromosome causes chronic my elogenous leukemia (CML), a cancer of blood cells that patients can live with for years and generally recover from with treatment. But the same defect is also found in a small percentage of patients with ALL, which can be fatal in a matter of months and is difficult to treat.

Researchers have long wondered what differentiates the two diseases. One possible culprit is Ikaros. Children with mutations in the gene, but do not have the Philadelphia chromosome develop ALL.

To find out if Ikaros also plays a role in Philadelphia chromosome-associated ALL, researchers looked at ALL patients who also had the Philadelphia chromosome, including 21 children and 22adults.

The majority of the patients had a flawed copy of the gene, with mutations occurring in 76.2 percent of the children and 90.9 percent of the adults. The Ikaros mutations were not found in 23 adults with CML, confirming the role of this gene in triggering ALL in those with the Philadelphia chromosome.

Ikaros codes for a transcription factor protein that is essential for normal development of white blood cells called lymphocytes, but it is not yet clear how the mutations lead to cancer. One possibility is that the faulty protein produced by the mutations leads to abnormal lymphocytes that turn cancerous, researchers said.