Thrombo-inflammatory endothelial signatures in <i>JAK2</i> -mutated myeloproliferative neoplasms
ECFCs from patients with JAK2-mutated MPN display functional and transcriptomic signatures of endothelial dysfunction in the absence of detectable driver mutations. These findings support a model in which a primed, thrombo-inflammatory endothelium cooperates with clonal hematopoiesis to promote the heightened thrombotic risk characteristic of MPN.
Authors
- Nikolai Alexandrovich Podoltsev (ORCID: https://orcid.org/0000-0002-3657-778X)
- David Štegner
- Anish V. Sharda (ORCID: https://orcid.org/0000-0003-3856-4277)
- Lourdes Mendez (ORCID: https://orcid.org/0000-0002-5922-2877)
- Salma A.S. Abosabie
- Mohammed Ali
- Alexandra Boye-Doe
Institutions
- University of Würzburg (DE)
- Yale Cancer Center (US)
- Yale University (US)
- Universitätsklinikum Würzburg (DE)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-02-18
- DOI
- https://doi.org/10.64898/2026.02.16.706250
- Primary Topic
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00