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. 2021 Jan 3;18(1):67–81. doi: 10.21873/cgp.20242

Figure 3. PCR analyses of the pediatric leukemias. (A) Partial sequence chromatogram showing the junction position of exon 9 of the KMT2A with exon 14 of ARHGEF12 in the chimeric transcript. (B) Gel electrophoresis showing the amplified KMT2A-ARHGEF12 genomic DNA fragment using two primer combinations and template DNA extracted from the patient’s bone marrow cells 1,539 days after the initial diagnosis. Lane 1: Primer combination MLL-4116F1/ARHGEF12-1502R1. Lane 2: Primer combination MLL-4202-F1/ARHGEF12-1437-R1. (C) Gel electrophoresis showing the absence of amplified KMT2A-ARHGEF12 cDNA (lane 1) and genomic DNA (lane 3) fragments at diagnosis when the leukemic cells had t(9;11)(p21;q23) and a KMT2A-MLLT3 fusion gene, and the presence of KMT2A- ARHGEF12 in the patient’s bone marrow cells 1,198 days after the initial diagnosis, when the patient had developed ALL with t(14;19)(q32;q13) and rearrangement of the IGH locus (lane 4). For both cDNA and genomic DNA amplifications, the primer combination MLL-4116F1/ARHGEF12-1502R1 was used. Lane 2: Assessment of the quality of cDNA synthesis by amplification of a cDNA fragment of ABL1 using the primer combination ABL1-91F1/ABL1-404R1. Lane 4: Amplification of a genomic KMT2AARHGEF12 DNA fragment in the patient’s bone marrow cells 1,198 days after the initial diagnosis. M, GeneRuler 1 Kb Plus DNA ladder (ThermoFisher Scientific). (D) Partial sequence chromatogram showing the junction position of intron 9 of the KMT2A with intron 13 of ARHGEF12 in the chimeric amplified DNA fragment. The junction of positions 11:118355287-11:120311617 is based on the human genome GRCh37/hg19 assembly.

Figure 3