Targeting Ibrutinib Resistance Pathways with miR-28 in ABC-DLBCL

Background

Diffuse large B-cell lymphoma, or DLBCL, is the most common type of aggressive non-Hodgkin lymphoma. It can often be treated successfully with R-CHOP immunochemotherapy, but outcomes are less favorable in the activated B-cell, or ABC, subtype. ABC-DLBCL is driven in part by chronic B-cell receptor signaling and related survival pathways, which make the disease harder to treat.

One important targeted therapy in this setting is ibrutinib, a Bruton tyrosine kinase, or BTK, inhibitor. By blocking BTK, ibrutinib can disrupt signaling that supports lymphoma cell growth and survival. However, as with many targeted therapies, some tumors eventually adapt and become resistant. Acquired resistance remains a major obstacle to durable benefit.