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Bone Marrow May Give Rise to Blood Cancers

The birthplace of blood cells could be a source of malignancy, research suggests


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FRIDAY, June 15 (HealthDay News) -- Defects in bone marrow can lead to abnormal blood cells that cause precancerous blood diseases in mice, two new studies find.

Blood cells are produced in the bone marrow. It was previously thought that red blood cells themselves were the source of these precancerous diseases, which can sometimes progress to leukemia.

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In humans, these precancerous conditions can be difficult to treat, because not much is known about what causes the blood cells to become abnormal, explained researcher Louise Purton, who is affiliated with the Peter MacCallum Cancer Center in Australia, as well as Massachusetts General Hospital and the Harvard Stem Cell Institute in Boston.

Purton said her team found "that the bone marrow microenvironment can make the blood cells become abnormal, like a type of pre-leukemic disease."

The second study was conducted by a team led by Stuart Orkin, a Howard Hughes Medical Institute investigator at Children's Hospital Boston and chairman of pediatric oncology at the Dana-Farber Cancer Institute.

"The defect we see isn't intrinsic to the blood cells themselves. It's a result of the interaction of the blood and support cells in bone marrow. We didn't predict that at all," Orkin said in a prepared statement.

The findings from the two studies, published in the June 15 issue of the journal Cell, could help in the development of new treatments for precancerous blood diseases.

"At the moment, most doctors focus on the blood cell as being the cause of the disease. Hopefully, the (bone marrow) microenvironment will now also be considered as a potential cause, which might lead to better treatments for these patients in the future," Purton said.

More information

The American Society of Hematology has more about blood diseases.



-- Robert Preidt

Copyright © 2007 ScoutNews, LLC. All rights reserved.
Last updated 6/15/2007

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SOURCE: Cell Press, news release, June 14, 2007


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