Figure 5
Association of miR-155 with rituximab resistance and target identification. (A) Association of miR-155 expression with EFS in DLBCL. (B) GEP analysis of miR-155-regulated genes and western blot detection of cyclin-dependent kinase inhibitor 1A (CDKN1A) (p21) (only downregulated genes are shown). (C) Cell-cycle analysis in miR-155 overexpressing DHL16 cells. (D) miR-155-expressing cells were more sensitive to AKT IV inhibition, compared with other inhibitors. (E) The 3-gene miR-155 signature was predictive of treatment failure in DLBCL in the entire cohort (upper) and in the ABC-DLBCL subgroup, but not in GCB-DLBCL (lower). EFS is shown using expression quartiles (Q) of the 3-gene signature in the entire cohort, but divided in halves in subgroup analysis.

Association of miR-155 with rituximab resistance and target identification. (A) Association of miR-155 expression with EFS in DLBCL. (B) GEP analysis of miR-155-regulated genes and western blot detection of cyclin-dependent kinase inhibitor 1A (CDKN1A) (p21) (only downregulated genes are shown). (C) Cell-cycle analysis in miR-155 overexpressing DHL16 cells. (D) miR-155-expressing cells were more sensitive to AKT IV inhibition, compared with other inhibitors. (E) The 3-gene miR-155 signature was predictive of treatment failure in DLBCL in the entire cohort (upper) and in the ABC-DLBCL subgroup, but not in GCB-DLBCL (lower). EFS is shown using expression quartiles (Q) of the 3-gene signature in the entire cohort, but divided in halves in subgroup analysis.

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