Journal article
Srsf2P95H initiates myeloid bias and myelodysplastic/ myeloproliferative syndrome from hemopoietic stem cells
MF Smeets, SY Tan, JJ Xu, G Anande, A Unnikrishnan, AM Chalk, SR Taylor, JE Pimanda, M Wall, LE Purton, CR Walkley
Blood | AMER SOC HEMATOLOGY | Published : 2018
Abstract
Mutations in SRSF2 occur in myelodysplastic syndromes (MDS) and MDS/myeloproliferative neoplasms (MPN). SRSF2 mutations cluster at proline 95, with the most frequent mutation being a histidine (P95H) substitution. They undergo positive selection, arise early in the course of disease, and have been identified in age-related clonal hemopoiesis. It is not clear how mutation of SRSF2 modifies hemopoiesis or contributes to the development of myeloid bias or MDS/MPN. Two prior mouse models of Srsf2P95H mutation have been reported; however, these models do not recapitulate many of the clinical features of SRSF2-mutant disease and relied on bone marrow (BM) transplantation stress to elicit the repor..
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Awarded by Victorian Cancer Agency
Funding Acknowledgements
This work was supported by the Leukaemia Foundation (C.R.W., Phillip Desbrow Senior Research Fellow [SRF]; M.W., grant-in-aid; S.Y.T., PhD scholarship); Cancer Council of Victoria (C.R.W., M.W., A. M.C.; APP1126010); National Health and Medical Research Council (NHMRC; J.E.P., APP1024363/APP1102589); Cancer Institute of NSW Translational Cancer Research Network (J.E.P.); South Eastern Area Laboratory Services (J.E.P.), Anthony Rothe Memorial Trust (A.U.); Victorian Cancer Agency Research Fellowship (C.R.W.; MCRF15015); NHMRC SRF (L.E.P.; APP1003339); UNSW International PhD scholarship (G.A.); and Tom Bee Stem Cell Research Fund (G.A.) and in part by the Victorian State Government OIS.