Myeloproliferative Neoplasms: Diagnosis and Treatment

Circulating hematopoietic stem and progenitor cells in myeloproliferative neoplasms

This study profiles circulating hematopoietic stem and progenitor cells in MPN patients, identifying transcriptional signatures and quantitative readouts to distinguish MF from other MPNs and predict progression.

Fibronectin silencing remodels the fibrotic bone marrow niche

This study shows that silencing fibronectin reduces fibrotic bone marrow niche remodeling and stromal activation in myelofibrosis models.

Characterization of Congestive Heart Failure Phenotype in a Murine Model of JAK2V617F-positive Myeloproliferative Neoplasm

This study characterizes heart failure in Tie2FF1 mice, showing left ventricular dilation, microvascular remodeling, and pulmonary/hepatic congestion without obstructive coronary disease.

Basophilic Erythroblast Emerges as the Key Turning Point in Polycythemia Vera

The paper identifies basophilic erythroblasts as the critical stage in polycythemia vera where the JAK2V617F mutation becomes transcriptionally active and treatment-responsive.

Melatonin nanoparticles inhibit mutant hematopoiesis and restore bone marrow architecture in myeloproliferative neoplasms

This study shows that melatonin nanoparticles reduce myeloproliferative neoplasm symptoms by targeting metabolic, inflammatory, and fibrotic pathways.

Plasma proteome screen of individuals with elevated blood counts to identify diagnostic signatures and biomarkers inherent to patients with myeloproliferative neoplasms

The paper identifies plasma proteome biomarkers distinguishing myeloproliferative neoplasms from non-MPN individuals with elevated blood counts, finding TFRC as a specific marker for polycythemia vera.

A comprehensive analysis of calreticulin mutants reveals distinct biophysicochemical proprieties with a potential for refined targeted therapies

This study analyzes 76 CALR exon 9 variants to refine their classification based on charge architecture, revealing subgroups within Type-1-like variants and linking tail chemistry to receptor activation.

Therapy-Induced Clonal Selection as a Driver of Response to JAK Inhibitors in Myelofibrosis

This study investigates clonal dynamics in myelofibrosis patients responding to JAK inhibitors, finding that mutation acquisition order and co-mutation status influence treatment sensitivity and disease persistence.

Linezolid Acts as a Selective Inhibitor of the JAK2V617F Mutation

This paper shows linezolid selectively inhibits JAK2V617F mutant cells in PV models, reducing disease burden without affecting wild-type cells.

A humanized ossicle model of myelofibrosis reveals THPO-driven fibrosis, osteosclerosis and SPP1-dependent microenvironmental remodeling

This paper develops a humanized myelofibrosis model to show THPO drives fibrosis, osteosclerosis, and SPP1-dependent niche remodeling, suggesting SPP1 as a therapeutic target.

Targeting TPO/MPL Signaling to Mitigate JAK2V617F-driven Cardiac Microvascular Disease

This study shows that JAK2V617F-mutant hematopoiesis causes cardiac microvascular disease, and blocking MPL signaling in endocardial endothelial cells improves cardiac function.

Platelets Outperform Leukocytes in Transcriptomic Liquid Biopsy Profiling of Myeloproliferative Neoplasms

This study compares platelet and leukocyte transcriptomes in MPN patients, finding platelets better capture myelofibrosis signatures and provide more accurate diagnosis.

PITPβ Drives JAK2 V617F-Mediated Myeloproliferative Neoplasms by Promoting PtdIns(3,4)P2-Dependent AKT Hyperactivation

This study identifies PITPβ as a critical driver of JAK2 V617F-mediated myeloproliferative neoplasms by promoting PtdIns(3,4)P2-dependent AKT hyperactivation, suggesting therapeutic targeting of this pathway.

Oncodevelopmental plasticity of the skeleton in myeloid neoplasms

This study identifies a novel mechanism in myelofibrosis where a single mutation drives both bone formation and resorption, revealing THBS1 as a therapeutic target.

NicheSphere reveals Spp1⁺ macrophages as central hubs coordinating fibrotic remodeling in myeloproliferative neoplasms

This study identifies Spp1⁺ macrophages as key hubs coordinating fibrotic remodeling in myeloproliferative neoplasms using NicheSphere, a novel computational method for cell communication analysis.

Thrombo-inflammatory endothelial signatures in JAK2-mutated myeloproliferative neoplasms

This study identifies thrombo-inflammatory endothelial dysfunction in JAK2-mutated myeloproliferative neoplasms using patient-derived endothelial colony-forming cells.

Inhibition of the EBF1-ITGB8 Axis in Bone Marrow Niche Ameliorates Hallmarks of Myelofibrosis

This study identifies EBF1 and ITGB8 as key regulators of BM fibrosis in myelofibrosis and shows their inhibition reduces disease features in mouse models.

Genome editing for treatment of JAK2 V617F-driven myeloproliferative neoplasms

This study uses CRISPR-Cas genome editing to selectively inactivate JAK2 V617F mutations in patient cells, showing that heterozygous cells are not oncogene addicted while homozygous cells are eradicated, suggesting genome editing as a potential treatment for MPNs.

The V617F mutation in JAK2 renders myeloid cells more sensitive to IL-6-mediated gp130 signaling

This study shows that the JAK2 V617F mutation enhances IL-6 sensitivity by promoting gp130 dimerization and expression in myeloid cells, contributing to chronic inflammation in MPN.

JAK2V617F Myeloproliferative Neoplasms Support Parallel Evolution of Independent Leukemic Clones

This study shows that leukemic clones can evolve independently of JAK2V617F in MPNs and contribute to disease progression through pro-inflammatory environments.

Single JAK2-V617F hematopoietic stem cells can initiate MPN in transplantations into non-conditioned recipient mice

This study shows that single JAK2-V617F mutant HSCs can initiate MPN in non-irradiated mice, demonstrating their competitive advantage over normal HSCs and highlighting species-specific immune recognition differences.

Targeting HMGA1-driven leukemic transformation in myeloproliferative neoplasms with pacritinib

This study identifies HMGA1 as a critical driver of MPN progression to sAML, showing it outperforms existing markers and is targeted by pacritinib to improve survival.

Divergent conformational mechanisms of JAK2V617F and TYK2V678F mutations in Thrombocythemia and related disorders: Molecular Dynamics insights into pathway activation and therapeutic targeting

This study uses molecular dynamics simulations to analyze how JAK2V617F and TYK2V678F mutations sustain JAK-STAT pathway activation through distinct conformational changes, providing insights for therapeutic targeting.

Classical Myelo-Proliferative Neoplasms emergence and development based on real life incidence and mathematical modeling

The paper uses mathematical modeling and real-world data to show that JAK2V617F mutations in MPNs emerge with age-dependent exponential rates and have distinct onset and expansion times between PV and ET.

The Immune-Modulatory Function of Megakaryocytes in the Hematopoietic Niche of Myeloproliferative Neoplasms

This study shows that JAK2V617F mutant megakaryocytes drive immune dysregulation and HSC expansion in MPNs by reprogramming the marrow microenvironment and activating LINE-1 retrotransposons.

Targeting CD38 effectively prevents myelofibrosis in myeloproliferative neoplasms

This study shows that targeting CD38 in monocytes prevents myelofibrosis in MPN models and identifies CD38 as a potential biomarker and therapeutic target.

Inhibition of JAK2V617F-Driven Neoplastic Endothelial Dysfunction by IFNα as a Novel Antifibrotic Mechanism

This study identifies JAK2V617F zygosity-specific vascular changes in MPN and shows IFNα inhibits EndMT, offering a novel antifibrotic mechanism.

In silico analysis of Missense Variants in Human MPL Gene Associated with Essential Thrombocythemia

The paper performs in silico analysis of missense variants in the MPL gene to identify those with potential functional impact on TPO-R structure and function in essential thrombocythemia.

Genetic predisposition to myeloproliferative neoplasms implicates hematopoietic stem cell biology

This study identifies 14 genome-wide significant loci and a polygenic signature for myeloproliferative neoplasms, implicating hematopoietic stem cell function and self-renewal in disease risk.