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Eliminating Influence of Hyperactive Genes That Help Regulate Cell Development Shows Potential as Additional Target Therapy for Chronic Myelogenous Leukemia
Date:11/12/2007

Researchers at Cincinnati Children's Zero In on Rac1, Rac2 Genes as

Molecular Targets

CINCINNATI, Nov. 12 /PRNewswire/ -- In a study published in the Nov. 13 issue of Cancer Cell, researchers at Cincinnati Children's Hospital Medical Center reported that they have discovered that targeting and inactivating two genes can inhibit the onset and spread of chronic myelogenous leukemia (CML) in mice.

When these genes, Rac1 and Rac2, become hyperactive, they prompt a protein linked to leukemia to stimulate the onset and spread of CML, a cancer that originates in blood marrow stem cells. But targeted inactivation of those genes, or using a molecule to nullify their hyperactivity, inhibits the onset of leukemia due to the 'Philadelphia chromosome' fusion protein called BCR-ABL, according to David Williams, M.D., director of Experimental Hematology at Cincinnati Children's and the study's senior author.

These findings are significant given the increase in patients with CML in the United States. According to the National Cancer Institute, 4,500 new cases of CML will be diagnosed in the U.S. by the end of 2007, and about 21,000 U.S. residents currently live with the disease -- a number that has been increasing largely due to treatment advances, including bone marrow transplant (which is only appropriate for about 25 percent of patients) and tyrosine kinase inhibitors. These inhibitors are designed to block the tyrosine kinase enzyme's ability to stimulate cellular pathways that lead to the growth of cancer cells.

Despite the success of these treatment advances, the BCR-ABL protein remains persistent in its stimulation of CML onset in some patients, says Dr. Williams. "The persistence of the BCR-ABL protein at the molecular level and development of resistance to this therapy suggest that inhibiting this kinase activity alone is not sufficient to eliminate all leukemic cells," he said. "Our data support the hypothesis
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SOURCE Cincinnati Children's Hospital Medical Center
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