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. Author manuscript; available in PMC: 2009 Sep 22.
Published in final edited form as: Curr Opin Hematol. 2008 Jul;15(4):381–390. doi: 10.1097/MOH.0b013e328302c7df

Figure 1. BCL6 and AID contribute to lymphomagenesis by facilitating genomic instability in GC B-cells.

Figure 1

A: Naïve B-cells are triggered to form germinal centers by T-cell dependent immune responses. B: AID and BCL6 are upregulated as B-cells differentiate into centroblasts. AID mediates somatic hypermutation while BCL6 represses ATR and TP53 to attenuate DNA damage responses, and represses PRDM1 to block further differentiation. C: AID induces genetic lesions that lead to constitutive expression of BCL6, which in turn leads to sustained repression of ATR, TP53 and PRDM1. This forces B-cells to lock in to the GC B-cell phenotype and prevents them from undergoing terminal differentiation (D). E: The combined action of AID and BCL6 result in genomic instability and lymphomagenesis. F: Constitutive expression of BCL6 maintains DLBCL cell survival and may lead to further mutagenesis.