Mucosa-associated lymphoid tissue lymphoma with unusual 18F-FDG hypermetabolism arising at the colorectal anastomosis

Figure 9 Activation of the NF-κB pathway. A: Antigen-dependent aggregation of the BCR induces CBM signalosome formation. The CBM complex activates IKK, which triggers activation of the NF-κB pathway; B: t(11;18)(q21;q21) causes the linkage of BIRC3 gene on chromosome 11 and MALT1 gene on chromosome 18. The BIR domain of BIRC3–MALT1 mediates self-oligomerization, which activates the NF-κB pathway and overexpression of NF-κB target genes; C: t(14;18)(q32;q21) occurring at 14q32 and 18q21 breakpoints involves IgH and MALT1 rearrangements. MALT1 oligomerizes through interaction with BCL10, which promotes the proliferation and antiapoptosis of B cells through the activation of the classic NF-κB pathway; D: t(1;14)(p22;q32) translocation leads to the nuclear overexpression of BCL10 protein. The BCL10 containing a CARD can interact with MALT1 to transfer signals for NF-κB activation.