Enasidenib induces acute myeloid leukemia cell differentiation to promote clinical response

Author:

Amatangelo Michael D.1,Quek Lynn2,Shih Alan3,Stein Eytan M.3,Roshal Mikhail3,David Muriel D.4,Marteyn Benoit5,Farnoud Noushin Rahnamay6,de Botton Stephane7,Bernard Olivier A.4,Wu Bin8,Yen Katharine E.8,Tallman Martin S.3,Papaemmanuil Elli69,Penard-Lacronique Virginie4,Thakurta Anjan1,Vyas Paresh2,Levine Ross L.3610

Affiliation:

1. Celgene Corporation, Summit, NJ;

2. Medical Research Council Molecular Hematology Unit, Oxford Comprehensive Biomedical Research Centre, Weatherall Institute of Molecular Medicine, and Department of Hematology, Oxford University Hospital National Health Service Foundation Trust, University of Oxford, Oxford, United Kingdom;

3. Department of Medicine, Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY;

4. Gustave Roussy, Université Paris-Saclay, Villejuif, France;

5. Unité de Pathogénie Microbienne Moléculaire, Institut Pasteur, Paris, France;

6. Center for Hematologic Malignancies, Memorial Sloan Kettering Cancer Center, New York, NY;

7. Hématologie Clinique, Gustave Roussy, Université Paris-Saclay, Villejuif, France;

8. Agios Pharmaceuticals, Inc., Cambridge, MA;

9. Center for Molecular Oncology and Department of Epidemiology and Biostatistics, and

10. Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY

Abstract

Key Points Enasidenib inhibits mIDH2, leading to leukemic cell differentiation with emergence of functional mIDH2 neutrophils in rrAML patients. RAS pathway mutations and increased mutational burden overall are associated with a decreased response rate to mIDH2 inhibition.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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