Hemopoietic stem cell transplantation failure followed by switch to stable production of fetal hemoglobin.

摘要

Sickle cell anemia and beta-thalassemia remain the most common human genetic disorders worldwide. High fetal hemoglobin (HbF) levels are correlated with reduced morbidity and mortality in both diseases. Based on this observation, recent studies provide new insight into the molecular mechanisms of the hemoglobin switching to induce the HbF production in adult hemopoietic cells as a promising therapeutic approach to ameliorate the severity of these two disorders.