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Mutant Genes in High-Risk Childhood Leukemias Identified
Date:5/19/2009

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The new study builds on the researchers' previous genetic analysis of the leukemic cells from pediatric ALL patients.

"The findings from our previous studies have hinted that some high-risk ALL cases might arise from mutations in genes that produce enzymes called kinases, which function as biological on-off switches in cells," said Charles Mullighan, M.D., Ph.D., assistant member in the St. Jude Department of Pathology and a co-first author of the study. "Such mutations would cause those kinases to be stuck in the on position, triggering the uncontrolled proliferation of white blood cells that is seen in leukemia."

Thus, the researchers began to analyze the genetic sequences of many kinases known to be components of the proliferation machinery of white blood cells. The team analyzed the leukemic cells from 187 patients with high-risk ALL. That analysis revealed mutations in about 10 percent of the cases in a family of protein kinases called JAK, whose members were also known to be mutated in other types of leukemias and related diseases.

"Further studies of these mutant JAK proteins revealed that the changes in their molecular structures could switch them on to drive the blood cell proliferation that is characteristic of ALL," said Stephen Hunger, M.D., chairman of the COG ALL committee and a co-senior author of the study. "What's more, in test tube studies, we found that drugs blocking the activation of the mutant JAK kinases prevented uncontrolled growth suggesting that drugs that target JAK proteins might be effective in this subtype of ALL."

The researchers discovered, in some high-risk ALL patients, that mutations in JAK appeared to work in concert with another mutation -- in the gene IKZF1 -- which they had earlier found to underlie such cases.

"Our studies of these leukemia subtypes indicate that leukemia is not necessarily a single-cause disease," said Cheryl
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SOURCE St. Jude Children's Research Hospital
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