To explore the risk factors of thrombosis in patients with JAK2V617F‐mutated myeloproliferative neoplasms (MPNs), a cohort of 1537 Chinese patients with JAK2V617F‐mutated MPN was retrospectively analyzed. The Kaplan‐Meier method and multivariate Cox analysis were used to study the risk factors of thrombosis in patients with JAK2V617F‐mutated MPN. Among the 1537 MPN patients, 931, 468, and 138 had polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), respectively. The median follow‐up time was 7 years (range 1‐47), and 12.8% of patients (197/1537) died during this period. A total of 16.8% (259/1399) of PV and ET patients had secondary myelofibrosis, and 2.5% (38/1537) of patients developed acute myeloid leukemia (AML). Thrombotic events occurred in 43.9% (675/1537) of patients, among which 91.4% (617/675) were arterial thrombosis and 16.6% (112/675) were venous thrombosis. The number of thrombotic events in PV, ET, and PMF patients was 439 (47.2%), 197 (42.1%) and 39 (28.2%), respectively. The multivariate analysis indicated that age ≥60 years old, HCT ≥48%, at least one cardiovascular risk factor, a history of thrombosis, and JAK2V617F allele burden (V617F%) ≥50% are risk factors for thrombosis in JAK2V617F‐mutated MPN. According to the results of the multivariate analysis, a risk model of thrombosis was established and comprised low‐risk (0 points), intermediate‐risk (1 points) and high‐risk (≥2 points) groups, among which the incidence of thrombosis was 9.1%, 33.7% and 72.9%. For elderly patients with JAK2V617F‐mutated MPN and a history of thrombosis, reducing the V617F%, controlling HCT and preventing cardiovascular risk factors are necessary measures to prevent thrombosis.

Bone marrow stromal cells (BMSCs) represent an important cellular component of the bone marrow microenvironment, which play an important role in supporting and regulating the proliferation and differentiation of hematopoietic stem/progenitor cells (HSPCs). We have previously reported that the ability of BMSCs derived from CMML patients (CMML-BMSCs) in supporting the expansion of cord blood (CB) CD34+ cells was significantly reduced compared to BMSCs derived from healthy donors (HD-BMSCs). In addition, CMML-BMSCs led to a skewed differentiation of CB CD34+ cells favoring myeloid lineage compared with HD-BMSCs. To assess whether the altered cytokine secretion was one of the mechanisms to mediate the impaired hematopoietic supportive activity of CMML-BMSCs, a transwell coculture followed by cytokine array was performed. We showed that noncontacted coculture with CMML-BMSCs preferentially promoted the differentiation of CB CD34+ cells toward myeloid lineage. The expression levels of multiple cytokines (IL-6, IL-8, and GRO-β) were markedly reduced in CMML-BMSCs compared with HD-BMSCs. By supplementing IL-6, IL-8, or GRO-β, the hematopoietic supportive activity of CMML-BMSCs was partially restored. These results suggested that BMSCs may contribute to the pathogenesis of CMML by altering their cytokine secretion, which will shed light on the further investigation to develop novel therapeutic strategies for CMML patients.