Beneficial tyrosine kinase inhibitor therapy in a patient with relapsed BCR - ABL1 -like acute lymphoblastic leukemia wi
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CASE REPORT
Beneficial tyrosine kinase inhibitor therapy in a patient with relapsed BCR‑ABL1‑like acute lymphoblastic leukemia with CCDC88C‑PDGFRB fusion Shuki Oya1 · Satoshi Morishige1 · Hidetoshi Ozawa1 · Kensuke Sasaki2 · Yuichiro Semba2 · Yoshitaka Yamasaki1 · Takayuki Nakamura1 · Kazutoshi Aoyama1 · Ritsuko Seki1 · Fumihiko Mouri1 · Koichi Osaki1 · Toshihiro Miyamoto2 · Takahiro Maeda3 · Koji Nagafuji1 Received: 3 August 2020 / Revised: 4 September 2020 / Accepted: 10 September 2020 © Japanese Society of Hematology 2020
Abstract BCR-ABL1-like acute lymphoblastic leukemia (ALL) is a neoplasm of lymphoblasts committed to the B-cell lineage that lack the BCR-ABL1 translocation but show a pattern of gene expression very similar to that seen in ALL with BCR-ABL1 with poor prognosis. A 22-year-old female was diagnosed with common-B-cell-ALL positive for CD10, CD19, CD22, CD79a, CD34, HLA-DR, and TdT in January 2017, and achieved complete remission (CR) with induction therapy, followed by consolidation therapy and maintenance therapy. In March 2020, 6 months after the completion of maintenance therapy, she relapsed. Inotuzumab ozogamicin (IO) was administered, and on day 28, bone marrow evaluation showed a morphologic CR. She had an HLA-identical sibling, and transplantation in her 2nd CR was planned. Because her ALL had been identified as BCR-ABL1-like ALL with CCDC88C-PDGFRB fusion, she was treated with imatinib for 2 months accompanied by 2 intrathecal methotrexate therapies, and 1 course of l-asparaginase, vincristine, and prednisolone in an outpatient setting. MRD analysis revealed potent efficacy of 2 months imatinib therapy; IgH MRD decreased from 1 × 10−2 to 1 × 10−3, and CCDC88C-PDGFRB/104ABL from 37.3 to 0. It is earnestly desired that well-designed clinical trials of TKI in ABL classmutant BCR-ABL1-like ALL be conducted in Japan. Keywords Acute lymphoblastic leukemia · BCR-ABL1-like · PDGFRB · Tyrosine kinase inhibitor · Imatinib
Introduction
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12185-020-03006-5) contains supplementary material, which is available to authorized users. * Koji Nagafuji [email protected]‑u.ac.jp 1
Division of Hematology and Oncology, Department of Medicine, Kurume University School of Medicine, 67 Asahi‑machi, Kurume 830‑0011, Japan
2
Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka 812‑8582, Japan
3
Center for Cellular and Molecular Medicine, Kyushu University Hospital, Fukuoka 812‑8582, Japan
BCR-ABL1-like acute lymphoblastic leukemia (ALL) is a neoplasm of lymphoblasts committed to the B-cell lineage that lack the BCR-ABL1 translocation but show a pattern of gene expression very similar to that seen in ALL with BCRABL1 with poor prognosis [1, 2]. Patients with BCR-ABL1like ALL is characterized by rearrangements, sequence mutations, and copy number alterations that activate tyrosine kinase or cytokine receptor signaling and are potentially amen
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