Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms

William Tapper(Salisbury District Hospital), Amy V. Jones(Salisbury District Hospital), Róbert Královics(Austrian Academy of Sciences), Ashot S. Harutyunyan(Austrian Academy of Sciences), Katerina Zoi(Academy of Athens), William Leung(Salisbury District Hospital), Anna L. Godfrey(Addenbrooke's Hospital), Paola Guglielmelli(University of Florence), Alison Callaway(Salisbury District Hospital), Daniel Ward(Salisbury District Hospital), Paula Aranaz(Salisbury District Hospital), Helen White(Salisbury District Hospital), Katherine Waghorn(Salisbury District Hospital), Feng Lin(Salisbury District Hospital), Andrew Chase(Salisbury District Hospital), E. Joanna Baxter(Addenbrooke's Hospital), Cathy MacLean(Addenbrooke's Hospital), Jyoti Nangalia(Addenbrooke's Hospital), Edwin Chen(Addenbrooke's Hospital), Paul Evans(St James's University Hospital), Michael Short(St James's University Hospital), Andrew Jack(St James's University Hospital), Louise Wallis(Royal Bournemouth Hospital), David Oscier(Royal Bournemouth Hospital), Andrew Duncombe(Southampton General Hospital), Anna Schuh(Oxford University Hospitals NHS Trust), Adam J. Mead(University of Oxford), Mike Griffiths(Birmingham Women's Hospital), Joanne Ewing(Heartlands Hospital), Rosemary E. Gale(Cancer Research UK), Susanne Schnittger(Munich Leukemia Laboratory (Germany)), Torsten Haferlach(Munich Leukemia Laboratory (Germany)), Frank Stegelmann(University Hospital Ulm), Konstanze Döhner(University Hospital Ulm), Harald Grallert(Helmholtz Zentrum München), Konstantin Strauch(Helmholtz Zentrum München), Toshiko Tanaka(National Institute on Aging), Stefania Bandinelli(Azienda Sanitaria di Firenze), Andreas Giannopoulos(Academy of Athens), Lisa Pieri(University of Florence), Carmela Mannarelli(University of Florence), Heinz Gisslinger(Medical University of Vienna), Giovanni Barosi(Foundation Center), Mario Cazzola(University of Pavia), Andreas Reiter(University of Mannheim), Claire Harrison(Guy's Hospital), Peter J. Campbell(Wellcome Sanger Institute), Anthony R. Green(University of Cambridge), Alessandro M. Vannucchi(University of Florence), Nicholas C.P. Cross(Salisbury District Hospital)
Nature Communications
April 7, 2015
Cited by 163Open Access
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Abstract

Clonal proliferation in myeloproliferative neoplasms (MPN) is driven by somatic mutations in JAK2, CALR or MPL, but the contribution of inherited factors is poorly characterized. Using a three-stage genome-wide association study of 3,437 MPN cases and 10,083 controls, we identify two SNPs with genome-wide significance in JAK2(V617F)-negative MPN: rs12339666 (JAK2; meta-analysis P=1.27 × 10(-10)) and rs2201862 (MECOM; meta-analysis P=1.96 × 10(-9)). Two additional SNPs, rs2736100 (TERT) and rs9376092 (HBS1L/MYB), achieve genome-wide significance when including JAK2(V617F)-positive cases. rs9376092 has a stronger effect in JAK2(V617F)-negative cases with CALR and/or MPL mutations (Breslow-Day P=4.5 × 10(-7)), whereas in JAK2(V617F)-positive cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia vera (allelic χ(2) P=7.3 × 10(-7)). Reduced MYB expression, previously linked to development of an ET-like disease in model systems, associates with rs9376092 in normal myeloid cells. These findings demonstrate that multiple germline variants predispose to MPN and link constitutional differences in MYB expression to disease phenotype.


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