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Mutation may help cause acute myeloid leukemia

ed to inhibit aml1-eto and tyrosine kinase receptors might one day be used to control this disease."

Tyrosine kinases power chemical reactions in cells, particularly those involved in cell division. Normally, these molecules are carefully regulated to keep a tight lid on cell growth. But they can lose that regulation when tyrosine kinase genes mutate. Instead of powering reactions only when appropriate, for example, the tel-pdgfrb protein runs constantly, like an engine that won't shut off.

"Mutations in tyrosine kinases can push cells to divide," says Grisolano. "If this is combined with a mutation that blocks cells from maturing, as does the aml1-eto gene, it can lead to cancer."

For example, mutations in a gene known as flt3 (pronounced flit 3), also in the tyrosine-kinase gene family, are among the most common mutations in people with AML. Drugs that block flt3 are being developed as a possible treatment for AML. Tel-pdgfrb is closely related to flt3.

"This study further supports the idea that tyrosine kinases may be highly worthwhile targets for new drugs to treat AML," says Tomasson.


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Contact: Darrell E. Ward
wardd@msnotes.wustl.edu
314-286-0122
Washington University School of Medicine
1-Aug-2003


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