Myeloproliferative Neoplasm

This study provides one of the first extensive characterizations of PV in southern Colombia, confirming internationally recognized clinical features, including advanced age at diagnosis, increased prevalence of cardiovascular comorbidities, and a predominance of high-risk classification. The low rate of finding JAK2 mutations suggests that molecular testing may not be as easy to get as it could be. Even if the treatment followed the guidelines, the risk of recurrence and thrombosis remained, showing that PV is a long-term and worsening condition. These findings highlight the urgent need to expand access to molecular diagnostics, develop tailored risk-adapted medicines, and initiate prospective multicenter studies in Latin America to optimize outcomes and quality of life in PV.

Management of thromboembolic event requires cytoreductive therapy and, depending on the site of thrombosis, antiplatelet therapy, and/or anticoagulation. Our review provides an overview of essential thrombocythemia, polycythemia vera, and primary myelofibrosis, as well as the hemostatic disorders associated with these conditions, focusing on diagnostic approaches and the prophylaxis and management of thromboembolic and bleeding complications.

This study provides a genetics-guided map of shared and subtype-specific molecular features in ET and PV, highlighting potential therapeutic pathways and molecular signals distinguishing the two diseases.

We describe a 71-year-old man with JAK2-positive polycythemia vera (PV) whose hematologic parameters remained suboptimally controlled under hydroxycarbamide treatment...This case demonstrates that additional mutated clones can significantly influence phenotype and disease evolution, highlighting the limitations of stepwise molecular testing. Comprehensive profiling of clonal architecture is essential to refine diagnosis and prognosis, in the NGS era.

P2, N=30, Not yet recruiting, Stanford University

P2, N=25, Completed, H. Lee Moffitt Cancer Center and Research Institute | Active, not recruiting --> Completed

After ruxolitinib therapy, he later developed leukocytosis and 2% circulating blasts. Repeat marrow demonstrated ≥ 15% ring sideroblasts. Retrospectively, the initial biopsy fulfills ICC 2022 criteria for MDS/MPN-SF3B1-T, highlighting the diagnostic value of genetics-integrated classification in fibrotic marrows.

We propose a simple 0-8-point composite algorithm that combines key HF and MPNs variables (natriuretic peptides or troponins, HF risk scores, driver mutations, leukocytosis/thrombocytosis, LDH) to identify high-risk HF-MPNs phenotypes across ACC/AHA HF Stages A-C, suitable for structured cardio-oncology follow-up. Prospective validation of this hybrid algorithm in dedicated cardio-oncology cohorts and the development of MPNs-adapted HF guidelines are key future priorities.

P2, N=15, Not yet recruiting, Zhongshan Hospital (Xiamen), Fudan University

Treatment strategies included supportive care, interferon, hydroxyurea, and ruxolitinib. PMF and SMF demonstrate distinct clinical phenotypes despite sharing bone marrow fibrosis as a common endpoint. The mutational landscape highlights the genetic heterogeneity of MF and underscores the importance of integrating clinical, pathological, and molecular information to improve disease characterization and guide individualized management.

This suggests that direct sensing of basal levels of type-I IFNs by NK cells is essential for attenuating disease progression, emphasizing a critical role for NK cells in immune surveillance of MPN. These findings offer new insights into type-I IFN-mediated immune modulation in MPN and highlight the potential of NK cell activation to improve therapeutic outcomes.

In patient-derived xenograft models of PTPN11-mutant JMML, dual NLRP3/PTGS2 inhibition combined with MEK blockade most effectively reduced leukemic burden, decreased human CD45⁺ engraftment, and depleted leukemic CD34⁺CD38⁺ progenitors and GMPs while restoring MEP populations, resulting in significantly improved overall survival. Together, these findings establish IL-17A/PTGS2/NLRP3 signaling as a central driver of immune suppression and myeloid expansion in PTPN11-mutant JMML and highlight combinatorial anti-inflammatory targeting as a promising therapeutic strategy for this high-risk disease.