Comprehensive mutational profiling of core binding factor acute myeloid leukemia

Author:

Duployez Nicolas12,Marceau-Renaut Alice12,Boissel Nicolas3,Petit Arnaud4,Bucci Maxime1,Geffroy Sandrine12,Lapillonne Hélène5,Renneville Aline12,Ragu Christine4,Figeac Martin6,Celli-Lebras Karine3,Lacombe Catherine7,Micol Jean-Baptiste89,Abdel-Wahab Omar9,Cornillet Pascale10,Ifrah Norbert11,Dombret Hervé3,Leverger Guy4,Jourdan Eric12,Preudhomme Claude12

Affiliation:

1. Biology and Pathology Center, Laboratory of Hematology, Centre Hospitalier Universitaire (CHU) Lille, Lille, France;

2. Cancer Research Institute, INSERM Unité Mixte de Recherche (UMR)–S 1172, Lille, France;

3. Department of Hematology, Saint Louis Hospital, Assistance Publique–Hôpitaux de Paris (AP-HP), Paris, France;

4. Department of Pediatric Hematology and Oncology, Trousseau Hospital, AP-HP, Paris, France;

5. Laboratory of Hematology, Trousseau Hospital, AP-HP, Paris, France;

6. Functional and Structural Genomic Platform, Lille University, Lille, France;

7. Goelamsthèque, Cochin Hospital, AP-HP, Paris, France;

8. Department of Hematology, Gustave Roussy Institute, INSERM UMR 1170, Villejuif, France;

9. Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical College, New York, NY;

10. Laboratory of Hematology, CHU Reims, Reims, France;

11. Department of Hematology, CHU Angers, Angers, France; and

12. Department of Hematology, CHU Nîmes, Nîmes, France

Abstract

Key Points Recurrent mutations in chromatin modifiers and cohesin were observed in t(8;21) AML, but not inv(16) AML. t(8;21) AML patients with mutations in kinase signaling plus chromatin modifiers or cohesin members had the highest risk of relapse.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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