Association between AID expression and somatic hypermutation of Immunoglobulin m human B cell neoplasms

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Three research articles have been published. [1] In 15 BL (Burkitt lymphoma) cell lines and 5 fresh BL samples, AID expression and SHM (somatic hypermutation) were investigated. AID expression was not detected in only Tree92 and Black93, and no SHM was found in these 2 cell lines. In the other samples, including the 5 fresh samples, AID and SHM was always found. In Tree92, the absence of SHM had been expected based on the phenotype expressing TdT and RAG1/2, while Black93 has a usual phenotype of BL. This work raised a question if AID-negative BL constitutes a significant subset of BL. Furthermore, t(8;14)(q24;q32) can occur at the stage prior to AID expression. (Leukemia & Lymphoma 2004;45:155-160) [2] In 15 cases of FL (follicular lymphoma) and 4 cell lines, the status of SHM and AID expression were investigated. Ten cases of fresh cases and 3 cell lines expressed AID. In the fresh samples, the degree of on-going mutation correlated with the degree of AID expression. In the cell lines, no on-going mutation was found, indicating that some clonal selection had been over, erasing the trace of on-going mutation. The results indicated that SHM starts, proceed and is terminated in the stage counterparting FL. (Leukemia 2004;18:826-831) [3] ALL cases with t(14;18)(q32;q21) have been reported rarely, but the genotypic study has been insufficient. Three cell lines and two frsh samples, including a pair of the fresh and cell line, were investigated. Despite the occasional expression of TdT and Rag1/2, the VH gene showed SHM. The fresh samples showed even on-going mutation. These results were insightful from such viewpoints as the relationship between disease type (ALL versus lymphoma) and derivation stage, the overlapping of the early stage phenotype and the mature genomic characteristics, and the probable relationship between the mechanism of t(14;18)(q32;q21) and the machinery causing SHM.