Ernesto José Cuenca-Zamora, Pedro J Guijarro-Carrillo, María J López-Poveda, María Luz Morales, María Luisa Lozano, Rocío Gonzalez-Conejero, Constantino Martínez, Raúl Teruel-Montoya, Francisca Ferrer-Marín
Emerging evidence shows the crucial role of inflammation (particularly NF-κB pathway) in the development and progression of myelofibrosis (MF), becoming a promising therapeutic target. Furthermore, tailoring treatment with currently available JAK inhibitors (such as ruxolitinib or fedratinib) does not modify the natural history of the disease and has important limitations, including cytopenias. Since recent studies have highlighted the role of miR-146a, a negative regulator of the NF-κB pathway, in the pathogenesis of MF; here we used miR-146a-/- (KO) mice, a MF-like model lacking driver mutations, to investigate whether pharmacological inhibition of JAK/STAT and/or NF-κB pathways may reverse the myelofibrotic phenotype of these mice...
April 22, 2024: American Journal of Hematology