Discovered by Karl Landsteiner in 1900, the ABO blood type is the most important blood type for transfusions [1]. For safe blood transfusions, cell type and serum type test results of the patient should match. If the results of the tests are inconsistent, we call it ABO discrepancy. It is essential to resolve ABO discrepancies in clinical laboratories for safe blood transfusion [2]. Weak ABO subgroups are the main cause of ABO discrepancy. Various genotyping methods can be used to con rm the ABO blood group. Recently, next-generation sequencing has been used for blood grouping. However, this technique is expensive [3]. Here, we describe a weak B phenotype harboring B101/O04-variant alleles observed in a Korean family, and suggest a practical algorithm to work-up ABO subgroups without using whole-genome sequencing. The
Dear Editor, ETV6-RUNX1 (previously TEL-AML1) is the most common fusion gene associated with childhood ALL, which occurs in approximately 25% of pediatric ALL patients receiving diagnoses between the ages of 2-10 years and is associated with favorable prognoses [1,2]. ETV6 rearrangement contributes to leukemogenesis in lymphoid neoplasms but is not well described in myeloid leukemia, and very few cases have been reported [3][4][5][6]. We report the first case of AML with the ETV6-RUNX1 fusion gene. The Institutional Review Board of Chonnam National University Hwasun Hospital, Hwasun, Korea, approved this study (CNUHH-2022-013) and waived the need for informed consent.In January 2021, a 66-year-old man presented with newly developed thrombocytopenia and underlying dyslipidemia. Complete blood count showed leukocytosis (13.3 × 10 9 /L) and thrombocytopenia (82×10 9 /L). Peripheral blood smear comprised ~78% abnormal-appearing monocytes and nucleated RBCs. The bone marrow (BM) aspirate showed 63%, 7%, and 7% monoblasts,
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