Bartalucci Niccolò

To the Editor In a recent issue of the journal, Handa S. et al. reported novel 12q14.3 deletions in Myelofibrosis (MF) and Myeloproliferative Neoplasms (MPN)-accelerated/blast phase (AP/BP) patients [1], leading to loss of most exon 5 non-coding regions and MIRLET7 binding sites in 3’UTR of HMGA2, resulting in HMGA2 transcript overexpression.

Abstract Despite increased understanding of the genomic landscape of Myeloproliferative Neoplasms (MPNs), the pathological mechanisms underlying abnormal megakaryocyte (Mk)-stromal crosstalk and fibrotic progression in MPNs remain unclear. We conducted mass spectrometry-based proteomics on mice with Romiplostim-dependent myelofibrosis to reveal alterations in signaling pathways and protein changes in Mks, platelets, and bone marrow (BM) cells.