Chronic myeloid leukemia with variant e13a3 (b2a3) <i>BCR-ABL1</i> as an ABL1 tyrosine kinase inhibitor-sensitive subtype

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  • 良好なABL1チロシンキナーゼ阻害薬感受性を示したバリアントe13a3（b2a3）<i>BCR-ABL1</i>慢性骨髄性白血病
  • 良好なABL1チロシンキナーゼ阻害薬感受性を示したバリアントe13a3(b2a3)BCR-ABL1慢性骨髄性白血病
  • リョウコウ ナ ABL1 チロシンキナーゼ ソガイヤク カンジュセイ オ シメシタ バリアント e13a3(b2a3)BCR-ABL1 マンセイ コツズイセイ ハッケツビョウ

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Abstract

<p>We report the case of a 26-year-old male patient with chronic myelogenous leukemia in the chronic phase with the e13a3 (b2a3) variant of BCR-ABL1 fusion. Despite the presence of Philadelphia chromosome and fluorescence in situ hybridization-detectable BCR-ABL1 fusion signals, quantitative measurement of BCR-ABL1 on the ABL1 using a reverse primer in exon 2 of ABL1 failed to detect the fusion transcripts. PCR direct sequencing analysis with a sense primer for exon 13 of BCR and an antisense primer for exon 3 of ABL1 revealed the e13a3 variant of BCR-ABL1 fusion. The variant fusion transcript level was successfully monitored by the TaqMan assay using a forward primer and probe both in exon 13 of BCR and a reverse primer in exon 3 of ABL1. The patient responded extremely well to imatinib treatment, similar to previously reported e13a3 cases. The patient achieved a molecular response (undetectable e13a3 transcripts) after 12 months of treatment.</p>

Journal

  • Rinsho Ketsueki

    Rinsho Ketsueki 62 (3), 180-185, 2021

    The Japanese Society of Hematology

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