II. Therapy of DLBCL based on genomics

摘要

The activated B-cell-like (ABC) and germinal centre B-cell-like (GCB) subtypes of diffuse large B-cell lymphoma (DLBCL) were defined by their apparent derivation from different stages of B-cell differentiation and their differential response to chemotherapy [1]. With current chemotherapy supplemented with Rituximab, the ABC DLBCL subtype remains less curable [2,3], necessitating new approaches to its treatment.The view that the ABC and GCB subtypes represent molecularly distinct diseases has been underscored by studies of translocations, genomic copy number changes and somatic mutations (reviewed in ref. [4]). Transloca-tion of BCL2 is restricted to GCB DLBCL, whereas translocation of BCL6 is three times more common in ABC DLBCL. ABC DLBCL is characterized by recurrent deletions of the INK4a/Arf, PRDM1 and TNFAIP3 loci and gain/amplification of the SPIB and BCL2 loci.