“For three decades biomedical researchers have hypothesized that fetal hemoglobin could be turned off if the mechanism of hemoglobin switching could be understood.”
On October 13, 2011 the Howard Huges Medical Institute (HHMI) published an article that explains how turning on fetal hemoglobin can reverse sickle cell anemia (SCA). An HHMI study led by Dr. Stuart Orkin of Children’s Hospital Boston, Dana Farber Cancer Institute and Harvard Medical School has shown that silencing a protein known as BCL11A can reactivate fetal hemoglobin production in adult mice. In fact, their research demonstrates that BCL11A is one of the primary factors involved in turning off hemoglobin production. In regard to methods of the study Dr. Orkin’s and his team used a genetic manipulation of a mouse model of SCD. A detailed review of the findings, that should further reveal methods used, will be published by Dr. Orkin and his team.
BLC11A could serve as a target for treating SCD and related blood disorders. Of his research Dr. Orkin says: “I think we’ve demonstrated that a single protein in the cells is a target that, if interfered with, would provide enough fetal hemoglobin to make patients better.” However, further research is needed into the working of BCL11A, to determine a model of transference from a mouse model of SCD to a human one.