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Promising new therapies for deadly form of leukemia

Fresh from successes in the development of the cancer-fighting drug Gleevec, researchers are now setting their sights on a form of acute myelogenous leukemia (AML) that carries a bleak prognosis. They have identified two new drugs that inhibit a specific enzyme that drives development of the deadliest form of AML.

It is hoped that the two drugs -- and others now in clinical trials -- will pack the same potent punch that has made Gleevec (STI571) so effective against chronic myelogenous leukemia.

The scientists reported on studies of the new drugs, called PKC412 and CT53518, in two articles that will be published in the June 18, 2002, issue of the journal Cancer Cell. The articles received immediate early publication status and were published online May 31, 2002. Howard Hughes Medical Institute investigator D. Gary Gilliland at Harvard Medical School and Brigham and Women's Hospital is one of the senior authors of the articles.

According to the American Cancer Society, AML accounts for about 90 percent of all adult leukemias, with about 10,600 new cases in the United States each year. The five-year, disease-free survival rate is about 14 percent, and there are about 7,400 deaths from AML each year in the United States, said Gilliland.

AML is caused by a defect in bone marrow cells, which become "frozen" in an early stage of development. The immature cells cannot differentiate normally and they interfere with blood cell production, causing anemia, hemorrhaging and disruption of organ function. Most adults who develop AML will die from complications related to their disease or from complications of intensive chemotherapy.

According to Gilliland, a deadly form of AML that occurs in about one-third of patients is caused by a mutation in an enzyme called the FLT3 receptor. This receptor is a type of protein called a receptor tyrosine kinase that is embedde
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
7-Jun-2002


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