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Fig. 2 | Biomarker Research

Fig. 2

From: Leukemia cutis with IDH1, DNMT3A and NRAS mutations conferring resistance to venetoclax plus 5-azacytidine in refractory AML

Fig. 2

The clone progression following mulitple chemodrugs and venetoclax treatment. Schematic of a possible model clone evolution inferred from next-generation sequencing data combined with the percentage of blasts detected by flow cytometry and visualized using fishplot R packages [11]. Here, we found the variate allele frequence (VAF) of DNMT3A is higher than that of IDH1 mutation at daignosis, implying IDH1 mutations occurring later than DNMT3A mutations. Following the intensive chemotherapy, RUNX1 mutated clone disappeared, but IDH1 and DNMT3A mutated clones still survived. Notably, the leukeiam cutaneous with additional NRAS mutations did not resolve during VA regimens. Thus, these clones in skin can persist over the time of the intensive chemotherapy and obtain resistance to targeted therapy, leading to further clonal expansion and eventually causing recurrent disease in the blood and bone marrow

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