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Frequent ASXL2 mutations in acute myeloid leukemia patients with t(8;21)/RUNX1-RUNX1T1 chromosomal translocations. 2014
Jean-Baptiste Micol, and
Nicolas Duployez, and
Nicolas Boissel, and
Arnaud Petit, and
Sandrine Geffroy, and
Olivier Nibourel, and
Catherine Lacombe, and
Helene Lapillonne, and
Pascaline Etancelin, and
Martin Figeac, and
Aline Renneville, and
Sylvie Castaigne, and
Guy Leverger, and
Norbert Ifrah, and
Hervé Dombret, and
Claude Preudhomme, and
Omar Abdel-Wahab, and
Eric Jourdan
Hematology Department, INSERM Unité Mixte de Recherche 1009, Gustave Roussy Cancer Campus Grand Paris, Villejuif, Paris-Sud University, Orsay, France; Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical College, New York, NY;
Acute myeloid leukemia (AML) with t(8;21) (q22;q22) is considered to have favorable risk; however, nearly half of t(8;21) patients are not cured, and recent studies have highlighted remarkable genetic heterogeneity in this subset of AML. Here we identify somatic mutations in additional sex combs-like 2 (ASXL2) in 22.7% (25/110) of patients with t(8;21), but not in patients with inv(16)/t(16;16) (0/60) or RUNX1-mutated AML (0/26). ASXL2 mutations were similarly frequent in adults and children t(8;21) and were mutually exclusive with ASXL1 mutations. Although overall survival was similar between ASXL1 and ASXL2 mutant t(8;21) AML patients and their wild-type counterparts, patients with ASXL1 or ASXL2 mutations had a cumulative incidence of relapse of 54.6% and 36.0%, respectively, compared with 25% in ASXL1/2 wild-type counterparts (P = .226). These results identify a high-frequency mutation in t(8;21) AML and identify the need for future studies to investigate the clinical and biological relevance of ASXL2 mutations in this unique subset of AML.
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