Mesenchymal stromal cells (MSCs) are multipotent progenitor cells that contribute to the structure and function of the bone marrow (BM) niche, controlling homing, self-renewal, differentiation and proliferation of hematopoietic stem/progenitor cells (HSPCs). 1 Recently, genetic and functional alterations of MSCs have been reported to occur in patients affected by myelodysplastic syndromes (MDS) and acute leukemias, 2–4 in keeping with the experimental notion that MSC dysfunction can affect relevant functions of leukemic blasts and induce MDS and leukemia in murine models. 5 Philadelphia-negative myeloproliferative disorders (Ph-neg MPNs) encompass polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF) and post-PV or-ET myelofibrosis. Very little is known about BM-derived MSCs of patients with MPNs apart from the absence of the V617FJAK2 mutation, 6 the molecular marker of hematopoietic cells in a great proportion of MPN patients.

We have functionally and genetically characterized MSCs from 38 Ph-neg MPN patients and 15 healthy donors (HDs)(Figure 1a) for clinical and epidemiological characteristics. The study was approved by the institutional review board of IRCSS Policlinico San Matteo Foundation; patients and HDs gave written informed consent. MSCs were isolated either from BM aspirates or/and from trephine bone fragments (TBF) digested with collagenase, 7 expanded and immunophenotypically characterized as described. 8 No significant differences were observed between BM or TBF-expanded MSCs (not shown), as already reported. 7 Both patient and HD MSCs displayed similar morphology, and