SOMATIC MUTATION IN PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA

The mutation, occurring in a hematopoietic stem cell, creates an eryth rocyte clone deficient in proteins capable of blocking complement-medi ated lysis. The precise defect lies, however, in the biosynthesis of a nchors to tether the proteins. Future research may explain how the clo ne gains a growth advantage (perhaps shedding light on aplastic anemia ). Meanwhile, there remains the challenge of optimal diagnosis and man agement.