The research investigates the molecular and cellular mechanisms driving advanced myelofibrosis, a progressive blood disorder marked by severe bone marrow scarring. By performing single-cell transcriptomic and epigenetic profiling on surgically removed spleens, the authors reveal that neoplastic extramedullary hematopoiesis in the spleen is characterized by a significant expansion of hematopoietic stem and progenitor cells. The findings demonstrate that these abnormal progenitor cells show a strong bias toward erythroid and megakaryocytic differentiation alongside heightened inflammatory signatures involving NF-κB signaling and interferon responses. Furthermore, the study highlights a profound remodeling of the splenic immune landscape, featuring dysfunctional T cell subsets and inflammatory memory B cells that establish a pro-inflammatory, immune-tolerant environment. Ultimately, this work provides critical insights into how malignant progenitor cells adapt to extramedullary sites, reshaping the microenvironment to promote disease progression while evading immune surveillance.
References:
Austin R, Kowalski M H, Wang X, et al. Splenic extramedullary hematopoiesis in myelofibrosis is shaped by transcriptomic and epigenetic dysregulation[J]. Cell Stem Cell, 2026, 33(9): 1495-1513. e13.
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