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Written by Preidt for Scout 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. son, an assistant professor of medicine at the

University of California, San Diego (UCSD) School of Medicine and director for

Stem Cell Research at the s 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 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, " son 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. " ScoutNews,

LLC.

http://tinyurl.com/27r82ks

_________________________________

FYI

Lottie Duthu

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