Kobe City Hospital Organization Kobe City Medical Center General Hospital

Kōbe-shi, Japan

Kobe City Hospital Organization Kobe City Medical Center General Hospital

Kōbe-shi, Japan
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Shimomura Y.,Kobe City Hospital Organization Kobe City Medical Center General Hospital | Mitsui H.,Otemae Hospital | Yamashita Y.,Otemae Hospital | Kamae T.,Otemae Hospital | And 8 more authors.
Cancer Science | Year: 2016

We present an acute promyelocytic leukemia (APL) patient with two subtypes of IRF2BP2–RARA, in which the IRF2BP2 gene showed completely new breakpoints. Bone marrow examination revealed morphologic features indicative of APL. However, promyelocytic leukemia–RARA fusion was not detected. A paired-end mRNA sequencing followed by RT-PCR and direct sequencing revealed two types of fusion transcripts between exon 1B of IRF2BP2 and exon 3 of RARA. The patient received all-trans retinoic acid and conventional chemotherapy, but showed resistance. This is the second report of IRF2BP2 involvement in APL, and we describe various breakpoints for the IRF2BP2–RARA fusion gene. © 2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.


PubMed | Kobe City Hospital Organization Kobe City Medical Center General Hospital, Hiroshima University, Otemae Hospital, Osaka University and Kumamoto University
Type: Case Reports | Journal: Cancer science | Year: 2016

We present an acute promyelocytic leukemia (APL) patient with two subtypes of IRF2BP2-RARA, in which the IRF2BP2 gene showed completely new breakpoints. Bone marrow examination revealed morphologic features indicative of APL. However, promyelocytic leukemia-RARA fusion was not detected. A paired-end mRNA sequencing followed by RT-PCR and direct sequencing revealed two types of fusion transcripts between exon 1B of IRF2BP2 and exon 3 of RARA. The patient received all-trans retinoic acid and conventional chemotherapy, but showed resistance. This is the second report of IRF2BP2 involvement in APL, and we describe various breakpoints for the IRF2BP2-RARA fusion gene.


PubMed | Kobe City Hospital Organization Kobe City Medical Center General Hospital
Type: | Journal: International journal of hematology | Year: 2016

Abnormal platelet-derived growth factor receptor (PDGFR)-mediated signaling may cause hematologic neoplasm. The PDGFR beta (PDGFRB) gene, located at chromosome band 5q31-33, forms a fusion gene as a result of chromosome translocation. Although patients with PDGFRB rearrangement mostly present with myeloproliferative neoplasm and eosinophilia, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) have also been reported in this population. Treatment with imatinib mesylate alone has been shown to have excellent long-term efficacy against myeloproliferative neoplasms; however, its long-term effects on ALL and AML have not been elucidated. A 75-year-old man was diagnosed with acute myeloid leukemia having the PDGFRB and cGMP-dependent protein kinase 2 fusion gene with additional genetic abnormalities. Continuous therapy with single-agent imatinib mesylate resulted in cytogenetic remission and decreased molecular burden for 9months; however, the leukemia subsequently recurred, and the patient died 1year after initiation of treatment. This case report supports the importance of cytogenetic analysis during patient screening.

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