Responses to 2009 H1N1 vaccine in children 3 to 17 years of age.

n engl j med 362;4 nejm.org january 28, 2010 370 180 unselected patients with chronic-phase polycythemia vera or essential thrombocythemia. Among the five patients with IDH mutations, three harbored an IDH1 R132C substitution and two harbored a novel IDH2 R140Q mutation affecting a residue conserved in mouse, yeast, and plant homologues. In Patient 2, an IDH2 R140Q mutation was detected in erythroid colonies with a JAK2 mutation as well as in leukemic blasts (Fig. 1A), indicating that this alteration was acquired early during the progression to leukemia and is not responsible for the block in cellular differentiation that occurs in acute leukemia. Leukemic cells arising from myeloproliferative neoplasms with a JAK2 mutation are commonly JAK2 wild-type,4 although the mechanism by which they become wild-type is unknown. Among the five samples of leukemia cells carrying an IDH mutation, three samples lacked the JAK2 mutation. In two of these three samples, an IDH mutation was present in leukemic blasts with wild-type JAK2 but absent from progenitor colonies with a JAK2 mutation (Fig. 1B), establishing the presence of two separate clonal expansions in each patient. In these cases, the separate JAK2-mutant and IDH-mutant clones may represent the shared progeny of an ancestral abnormal clone or the coexistence of two distinct disorders with independent origins.5