Fig. 2

Schematic representation of the oncogenesis of B-lineage malignancies. The t(14;18)(q32;q21) rearrangement caused by aberrant D-JH recombination during the pro-B-cell stage plus the acquisition of N-gly sites during the SHM period ultimately leads to FL. The blockade at the pre-B-cell stage to the immature B-cell stage in parallel with the ongoing recombination events promotes the development of ALL. MCL originates from immature B cells with t(11;14)(q13;q32). GCB-DLBCL is transformed from B cells under continuing antigenic pressures in GC characterized by ongoing SHM or is transformed from FL, while the non-GCB subtype originates from plasma cells or memory-like B cells that have completed the GC reaction. MM is caused by an aberrant translocation involving the IGH locus (14q32), which occurs during V(D)J recombination, SHM or CSR. HL derives from surviving cells that escape from apoptosis caused by unfavorable mutations by the activation of oncogenes. N-gly sites, asparagine-X-serine/threonine sites