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Mutation may help cause acute myeloid leukemia

St. Louis, Aug. 1, 2003 -- Researchers at Washington University School of Medicine in St. Louis have found that a chromosome defect often seen in human acute myeloid leukemia (AML) can cause the same disease in mice when combined with a genetic defect in a molecule known as a tyrosine kinase receptor. The study is published online and in the Aug. 5 issue of the Proceedings of the National Academy of Sciences.

"The findings indicate that tyrosine kinases may be an important class of cancer-causing genes in leukemia," says principal investigator Michael H. Tomasson, M.D., assistant professor of genetics and of medicine. "It further suggests that drugs designed to inhibit these molecules might provide effective new treatments for this deadly disease."

AML is a cancer of immature white blood cells. It can lead to severe anemia and immune deficiency and often is fatal. Although AML accounts for less than 3 percent of all cancers, it is the leading cause of cancer death among Americans under age 35. It also strikes older people, in whom it can be difficult to treat.

About 12 percent of AML patients have a chromosomal abnormality that fuses a piece of chromosome 21 to chromosome 8. The genetic mutation leads to production of an abnormal protein known as aml1-eto. But this change alone isn't enough to cause AML in humans or animals.

Tomasson and colleagues examined mice transplanted with bone-marrow cells some of which contained both the aml1-eto defect and a defect in a tyrosine kinase receptor gene known as tel-pdgfrb. With these two mutations, the mice developed AML; mice with only the aml1-eto fusion gene did not develop the disease.

"This is the first study to show that an activated tyrosine kinase receptor can cooperate with aml1-eto to produce AML in laboratory animals," says first author Jay L. Grisolano, Ph.D., a post-doctoral fellow in Tomasson's laboratory. "It raises the possibility that a combination of therapies design
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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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