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. 2018 May 2;2(9):1000–1012. doi: 10.1182/bloodadvances.2017013953

Figure 2.

Figure 2.

The clonal expansion of HLA-A24−granulocytes associated with secondary somatic mutations in case 1. (A) The somatic mutations detected in both HLA-A24− and HLA-A24+ granulocytes and their VAFs. The numbers of nucleotide positions where mutation occurred and the resultant amino acid replacement are shown at the bottom. (B) The changes in the percentages of GPI-AP− granulocytes and HLA-A24− granulocytes during the 10-year observation period. (C) The genotypes of 21 colonies derived from PB non-T–nonadherent cells. Positivity for the amplified product of A*24:02, mutated DNMT3A, mutated ZRSR2, and mutated TET2 sequences (top panel) and their summary (bottom panel) are shown. (D) The results of HUMARA for HLA-A24− and A24+ granulocytes. Similarly skewed XCI patterns were observed in the 2 granulocyte populations in which the S scores (2.58) in HLA-A24− were higher than those in A24+ granulocyte populations (1.48), suggesting the overwhelming expansion of an HLA-A24−DNMT3AmutZRSR2mut HSPC. SAA, severe aplastic anemia.