Single-Cell Analyses Reveal Megakaryocyte-Biased Hematopoiesis in Myelofibrosis and Identify Mutant Clone-Specific Targets

Bethan Psaila(National Institutes of Health), Guanlin Wang(University of Oxford), Alba Rodríguez-Meira(University of Oxford), Rong Li(University of Oxford), Elisabeth F. Heuston(National Institutes of Health), Lauren C. Murphy(University of Oxford), Daniel Yee(University of York), Ian S. Hitchcock(University of York), Nikolaos Sousos(University of Oxford), Jennifer O’Sullivan(University of Oxford), Stacie M. Anderson(National Institutes of Health), Yotis A. Senis(Inserm), Olga K. Weinberg(Boston Children's Hospital), Monica L. Calicchio(Boston Children's Hospital), Deena Iskander(Hammersmith Hospital), Daniel Royston(University of Oxford), Dragana Milojković(Hammersmith Hospital), Irene Roberts(University of Oxford), David M. Bodine(National Institutes of Health), Supat Thongjuea(University of Oxford), Adam J. Mead(University of Oxford)
Molecular Cell
May 1, 2020
Cited by 176Open Access
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Abstract

hematopoietic stem and progenitor cells (HSPCs), single-cell proteomics, genomics, and functional assays. We identified a bias toward megakaryocyte differentiation apparent from early multipotent stem cells in myelofibrosis and associated aberrant molecular signatures. A sub-fraction of myelofibrosis megakaryocyte progenitors (MkPs) are transcriptionally similar to healthy-donor MkPs, but the majority are disease specific, with distinct populations expressing fibrosis- and proliferation-associated genes. Mutant-clone HSPCs have increased expression of megakaryocyte-associated genes compared to wild-type HSPCs, and we provide early validation of G6B as a potential immunotherapy target. Our study paves the way for selective targeting of the myelofibrosis clone and illustrates the power of single-cell multi-omics to discover tumor-specific therapeutic targets and mediators of tissue fibrosis.


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