2026-05-22T02:32:08Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/51212025-05-30T06:26:01Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605col_20.500.12105_19607

00925njm 22002777a 4500 dc Bartolome-Izquierdo, Nahikari author de Yebenes, Virginia G author Alvarez-Prado, Angel Francisco author Mur, Sonia M. author Lopez, Juan Antonio author Roa, Sergio author Vazquez, Jesus author Ramiro, Almudena R author 2017 Non-Hodgkin lymphoma comprises a variety of neoplasms, many of which arise from germinal center (GC)-experienced B cells. microRNA-28 (miR-28) is a GC-specific miRNA whose expression is lost in numerous mature B-cell neoplasms. Here we show that miR-28 regulates the GC reaction in primary B cells by impairing class switch recombination and memory B and plasma cell differentiation. Deep quantitative proteomics combined with transcriptome analysis identified miR-28 targets involved in cell-cycle and B-cell receptor signaling. Accordingly, we found that miR-28 expression diminished proliferation in primary and lymphoma cells in vitro. Importantly, miR-28 reexpression in human Burkitt (BL) and diffuse large B-cell lymphoma (DLBCL) xenografts blocked tumor growth, both when delivered in viral vectors or as synthetic, clinically amenable, molecules. Further, the antitumoral effect of miR-28 is conserved in a primary murine in vivo model of BL. Thus, miR-28 replacement is uncovered as a novel therapeutic strategy for DLBCL and BL treatment. Blood. 2017; 129(17):2408-2419 10.1182/blood-2016-08-731166 1528-0020 0006-4971 Blood 28188132 http://hdl.handle.net/20.500.12105/5121 B-CELL LYMPHOMA NF-KAPPA-B INDUCED CYTIDINE DEAMINASE GENOMIC INSTABILITY BURKITT-LYMPHOMA CANCER-THERAPY C-MYC MICRORNAS PATHOGENESIS EXPRESSION miR-28 regulates the germinal center reaction and blocks tumor growth in preclinical models of non-Hodgkin lymphoma