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Turning back the Clock in Inherited Anemias
Date:12/4/2008

how it works.

"While it's been demonstrated that increased levels of HbF ameliorate the severity of sickle cell disease and beta-thalassemia, no direct strategies have yet been developed to increase HbF in these diseases," says Sankaran. "By reducing BCL11A expression or activity, we may be able to develop targeted therapies."

Hemoglobin is the protein in red blood cells that carries oxygen to the body's tissues. In sickle- cell disease, hemoglobin is abnormal, forming long chains that make red blood cells stiff and sickle-shaped. In thalassemia, the body's ability to produce hemoglobin is severely compromised. The hallmark of both disorders is anemia that can range from mild to life-threatening. Sickle-cell disease can cause severe pain and eventual organ damage as the abnormal, sickle-shaped cells block blood vessels, robbing tissues of their blood supply; beta-thalassemia requires frequent blood transfusions and then chelation therapy to rid the blood of excess iron that also leads to organ failure.

At birth, HbF comprises between 50 to 95 percent of a child's hemoglobin before the switch to adult hemoglobin production. The fetal form is thought to be an adaptation to the low oxygen in the fetal environment. Fetal hemoglobin has a higher affinity for oxygen, enabling it to pull oxygen more easily from the mother's circulation.

Are there potential side effects from boosting fetal hemoglobin levels? No, the researchers say. "Some people with rare genetic deletions have 100 percent fetal hemoglobin, and they're perfectly normal," says Orkin.

Orkin and Sankaran are conducting further studies to figure out how the switch from fetal to adult hemoglobin production occurs and how to target BCL11A therapeutically. "Improved understanding will permit the design of therapies for reactivation of HbF in patients with sickle-cell disease or thalassemia," says Orkin.

This study was
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