Mutant calreticulin knockin mice develop thrombocytosis and myelofibrosis without a stem cell self-renewal advantage

Author:

Li Juan12,Prins Daniel12,Park Hyun Jung12,Grinfeld Jacob123,Gonzalez-Arias Carlos123,Loughran Stephen12,Dovey Oliver M.4,Klampfl Thorsten12,Bennett Cavan25,Hamilton Tina L.12,Pask Dean C.12,Sneade Rachel12,Williams Matthew12,Aungier Juliet12,Ghevaert Cedric25,Vassiliou George S.34,Kent David G.12,Green Anthony R.123

Affiliation:

1. Cambridge Institute for Medical Research and Wellcome Trust/Medical Research Council Stem Cell Institute and

2. Department of Haematology, University of Cambridge, Cambridge, United Kingdom;

3. Department of Haematology, Addenbrooke’s Hospital, Cambridge, United Kingdom;

4. Wellcome Trust Sanger Institute, Cambridge, United Kingdom; and

5. National Health Service Blood and Transplant, Cambridge, United Kingdom

Abstract

Key Points Mutant CALR drives ET and MF in knockin mice. Mutant CALR expression results in expansion of phenotypic HSCs without a self-renewal advantage.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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