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Letters to the Editor
derived oxidative phosphorylation and subsequent reduced tumor burden. While it is likely that daratumum- ab functions through a number of mechanisms of action, here we show in an NSG mouse model lacking functional B cells, T cells and natural killer cells, that inhibition of mitochondrial transfer can be added to the list of mecha- nisms of action for this drug in AML. These data support the further investigation of daratumumab as a therapeu- tic approach for the treatment of mitochondrial-depen- dent tumor growth.
Jayna J. Mistry,1,2 Jamie A. Moore,1 Prakrit Kumar,1 Christopher R. Marlein,1 Charlotte Hellmich,1,3 Genevra Pillinger,1 Aisha Jibril,1 Federica Di Palma,1,2 Angela Collins,3 Kristian M. Bowles1,3
and Stuart A Rushworth1
1Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich; 2Earlham Institute, Norwich Research Park, Norwich and 3Department of Haematology, Norfolk and Norwich University Hospitals NHS Trust, Norwich, UK
Correspondence:
KRISTIANBOWLES- k.bowles@uea.ac.uk STUART RUSHWORTH - s.rushworth@uea.ac.uk
doi:10.3324/haematol.2019.242974
Disclosures: KMB and SAR received funding from Jannsen Pharmaceuticals for this study.
Contributions: KMB and SAR designed the research; JJM, JAM, CRM, CH, GP, PK, AJ and SAR performed the research; AC, FDP, and KMB provided essential reagents and knowledge; JJM, KMB and SAR wrote the paper.
Acknowledgments: the authors also thank Allyson Tyler,
Dr. Ian Thirkettle and Karen Ashurst from the Laboratory Medicine Department at the Norfolk and Norwich University Hospital for technical assistance.
Funding: the authors wish to thank the Norwich Medical School, the United Kingdom National Health Service, the Big C and the Rosetrees Trust for funding, and the Norwich Biorepository (UK)
for help with sample collection and storage. pCDH-Lucferase-T2A- mCherry was kindly gifted by Prof. Irmela Jeremias, MD, from Helmholtz Zentrum München, Munich, Germany. KMB and SAR receive research funding from Janssen.
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