Byunggil Yoo

1 Introduction Thiopurines, including thioguanine (6TG) and mercaptopurine (6MP), are the cornerstone of therapy for pediatric acute lymphoblastic leukemia (ALL). In the complex thiopurine metabolic pathway, 6TG and 6MP are methylated by thiopurine methyltransferase (TPMT) to an inactive metabolite, leaving less parent drug available for formation of active thioguanine nucleotides (TGNs), which cause leukemia cell death and myelosuppression [1, 2].

, , , et al., “ Severe Thiopurine-Induced Myelosuppression in a Pediatric Acute Lymphoblastic Leukemia Patient With the NUDT15 *1/*6 Genotype: A Brief Report,” Clinical and Translational Science 19, no. 6 (2026): e70639, https://doi.org/10.1111/cts.70639. In the article cited above, the data points in Figure 2 are not visible beneath the green and red bars. We apologize for this error.

Abstract Gene fusions are common primary drivers of pediatric leukemias and are the result of underlying structural variants (SVs). Current clinical workflows to detect such alterations rely on a multimodal approach, which often increases analysis time and overall cost of testing. In this study, we used long-read sequencing (lrSeq) as a proof-of-concept to determine whether clinically relevant (cr) SVs could be detected within a small (n = 17) pediatric leukemia cohort.