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Dear Editor, There are three types of BCR-ABL1 fusion transcripts that differ on the basis of the breakpoint in the BCR gene [1]. The major type, encoding p210, has two isoforms, b2a2 (e13a2) and b3a2 (e14a2), and is associated with more than 95% of Ph-positive CML cases. The minor type, encoding p190, is e1a2. The micro type, encoding p230, is e19a2. This micro type is rare, and has been associated with a variety of hematologic malignancies including neutrophilic CML (CML-N), all phases of classical CML, essential thrombocythemia (ET), and acute myeloid or lymphoblastic leukemia [2, 3]. Here, we describe the first case of chronic phase CML concurrently expressing e1a2 and e19a2 BCR-ABL1. An 89-year-old woman was referred to our hospital for evaluation of her leukocytosis. She appeared ill, but had no splenomegaly. The complete blood count (CBC) revealed 137.46× 10/L WBC, 10.0 g/dL Hb, and 194×10/L platelets. The blood smear demonstrated 3% blasts, basophilia, and eosinophilia, and bone marrow (BM) aspirate showed a hypercellularity (Fig. 1). The karyotype in BM was 46,XX,t(9;22)(q34;q11.2) [20] and the FISH result using an LSI BCR/ABL probe (Abbott Molecular Inc., Des Plaines, IL, USA) was nuc ish (ABLx3),(BCRx3),(ABL con BCRx2)[200/200]. JAK2 mutation was not detected. The commercial multiplex reverse transcription (RT)-PCR (HemaVision, DNA Diagnostic, Risskov, Denmark) result was positive for BCR/ABL in Master M6 and Split-out M6B PCR, and presented as an atypically thick band overlapping with the control band at 911 bp (Fig. 2A). Additional sequencing from the M6B amplicon revealed the BCR-ABL1 fusion was the micro type (e19a2) (Fig. 2B). Another real-time quantitative PCR for the minor BCR-ABL1 rearrangement indicated positivity (0.04, normalized copy number [NCN]), which was confirmed by sequencing (Fig. 2C). Therefore, it was determined that the patient had a BCR-ABL1 fusion consisting predominantly of the micro isoform (e19a2) with a small amount of the minor isoform (e1a2). The concurrence of those two isoforms might occur as a result of alternative splicing of the primary BCR-ABL1 fusion transcript [4]. The patient could not start any targeted therapy owing to her poor performance status and the potential interaction with her ongoing risperidone treatment. Only hydroxyurea (500 mg/day) was initiated. One month later, her WBC count decreased to 14.23 ×10/L. After 6 months, she showed no complications and her WBC count was 16.60×10/L. The e19a2 BCR-ABL1 fusion transcript can be associated

Concurrence of e1a2 and e19a2 BCR-ABL1 Fusion Transcripts in a Typical Case of Chronic Myeloid Leukemia