Abstract
AbstractWe have defined a new type of δ-thalassemia in which δ-globin chain synthesis is incompletely suppressed. Homozygotes have unusually low HbA2 levels, and double heterozygosity for this δ-thalassemia gene and β-thalassemia normalizes the HbA2 level. The δ-thalassemia occurs on a chromosome that is identifiable using polymorphic restriction endonuclease sites. We call this condition δ+-thalassemia, to distinguish it from the previously described δ0-thalassemia syndromes in which no δ-globin chain synthesis occurs.
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