Figure 3.
Figure 3. The clonal architecture of HLA-A3101−granulocytes in case 2. (A) Changes in the VAF of the DNMT3A mutation during the last 6-year study (7-12 years after the diagnosis). (B) The composition of HLA-A3101− granulocytes, as revealed by HLA-A allelic sequencing. 6pLOH−A*31:01mut− cells accounted for 64% of the total HLA-A3101− granulocytes. (C) The chronological changes in the GPI-AP− granulocytes and HLA-A3101− granulocytes. (D) The genotypes of 4 colonies derived from PB non-T–nonadherent cells. Whether individual colonies are positive or negative for the amplified product of A*31:01 and mutated DNMT3A (top panel) and their summary (bottom panel) are shown. (E) The results of HUMARA for HLA-A3101− granulocytes. The S score was as low as 1.17, and was in line with the results of HLA-A–allelic sequencing, which showed the presence of >2 HLA-A3101− HSPC clones. NSAA, nonsevere aplastic anemia.

The clonal architecture of HLA-A3101granulocytes in case 2. (A) Changes in the VAF of the DNMT3A mutation during the last 6-year study (7-12 years after the diagnosis). (B) The composition of HLA-A3101 granulocytes, as revealed by HLA-A allelic sequencing. 6pLOHA*31:01mut cells accounted for 64% of the total HLA-A3101 granulocytes. (C) The chronological changes in the GPI-AP granulocytes and HLA-A3101 granulocytes. (D) The genotypes of 4 colonies derived from PB non-T–nonadherent cells. Whether individual colonies are positive or negative for the amplified product of A*31:01 and mutated DNMT3A (top panel) and their summary (bottom panel) are shown. (E) The results of HUMARA for HLA-A3101 granulocytes. The S score was as low as 1.17, and was in line with the results of HLA-A–allelic sequencing, which showed the presence of >2 HLA-A3101 HSPC clones. NSAA, nonsevere aplastic anemia.

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