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Scientists Gain Insight Into Blood Cancer's Progression
Date:2/20/2009

Findings for chronic myeloid leukemia may have wider implications, researchers say

FRIDAY, Feb. 20 (HealthDay News) -- U.S. researchers say they've spotted a mechanism by which chronic myeloid leukemia (CML) progresses into a deadlier stage.

The finding may improve patient outcomes, they said.

The researchers found that when a molecular off-switch called glycogen synthase kinase (GSK) 3 beta becomes faulty in chronic stage CML cells, it fails to turn off another protein called beta-catenin. This enables pre-leukemia stem cells to develop into leukemia stem cells and increase their numbers, leading to the more dangerous "blast crisis" state of CML.

"If we can predict when a patient is moving from the chronic phase in CML to the blast crisis stage, then we can hopefully intervene before it's too late," study co-leader Dr. Catriona H.M. Jamieson, an assistant professor of medicine at the University of California, San Diego (UCSD) School of Medicine and director for Stem Cell Research at the Moores UCSD Cancer Center, said in a university news release.

Faulty GSK 3 beta also offers a potential treatment target, the researchers said. "This knowledge may enable us to design and develop more effective, personalized therapies for these patients," co-first author and staff research associate Annelie Abrahamsson said in the news release.

The study appears online in this week's issue of the Proceedings of the National Academy of Sciences.

The findings may not be limited to CML, the team noted.

"Downregulating beta-catenin and GSK deregulation may have other implications in many cancers," Jamieson said. "By studying CML, we can understand the molecular evolution of disease and the stepwise progression to cancer. It becomes a useful paradigm for understanding how cancers evolve and the pathways that are essential to escape the normal control mechanisms."

More information

The U.S. National Cancer Institute has more about chronic myeloid leukemia.



-- Robert Preidt



SOURCE: University of California, San Diego, news release, Feb. 16, 2009


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