Acute myeloid leukemia ontogeny is defined by distinct somatic mutations

Author:

Lindsley R. Coleman1,Mar Brenton G.2,Mazzola Emanuele3,Grauman Peter V.4,Shareef Sarah4,Allen Steven L.5,Pigneux Arnaud6,Wetzler Meir7,Stuart Robert K.8,Erba Harry P.9,Damon Lloyd E.10,Powell Bayard L.11,Lindeman Neal12,Steensma David P.1,Wadleigh Martha1,DeAngelo Daniel J.1,Neuberg Donna3,Stone Richard M.1,Ebert Benjamin L.4

Affiliation:

1. Department of Medical Oncology, Division of Hematological Malignancies,

2. Department of Pediatric Oncology, and

3. Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston MA;

4. Division of Hematology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA;

5. Hofstra North Shore–LIJ School of Medicine, Hempstead, NY;

6. Hôpital Haut-Leveque, Centre Hospitalier Universitaire Bordeaux, Pessac, France;

7. Roswell Park Cancer Institute, Buffalo, NY;

8. Hollings Cancer Center, Medical University of South Carolina, Charleston, SC;

9. Division of Hematology and Oncology, University of Alabama, Birmingham, Birmingham, AL;

10. Helen Diller Family Comprehensive Cancer Center, The University of California, San Francisco, CA;

11. Comprehensive Cancer Center of Wake Forest University, Winston Salem, NC; and

12. Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA

Abstract

Key Points The presence of a mutation in SRSF2, SF3B1, U2AF1, ZRSR2, ASXL1, EZH2, BCOR, or STAG2 is highly specific for secondary AML. Secondary-type mutations define an s-AML–like disease within t-AML and elderly de novo AML that underlies clinical heterogeneity.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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