Skip to main content
. 2022 Jun 21;14(13):3045. doi: 10.3390/cancers14133045

Figure 1.

Figure 1

Acquisition of R110G mutation on IGLV3-21*01/04 alleles leads to aggressive CLL. R110G mutation may be acquired through SHM induced by AID overexpression [51] or through defective VL–CL end joining during light-chain gene recombination [74]. The IGLV3-21*01 (depicted in figure) and IGLV3-21*04 alleles contain the K16 residue in the FR1 and two D residues at position 50 and 52 in the CDR2, which, along with the R110 at the VL–CL junction, fulfill all the structural requirements for homotypic BCR–BCR interactions. This in turn induces ligand-independent autonomous BCR activation, leading to proliferation and survival of the malignant cells that ultimately results in severe disease course.