Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11) (p21;q23)

DOI PDF PubMed 被引用文献1件
  • Kimihiko Sano
    From the Department of Pediatrics, Kobe University School of Medicine, Kobe, Japan.
  • Akira Hayakawa
    From the Department of Pediatrics, Kobe University School of Medicine, Kobe, Japan.
  • Jin-Hua Piao
    From the Department of Pediatrics, Kobe University School of Medicine, Kobe, Japan.
  • Yoshiyuki Kosaka
    From the Department of Pediatrics, Kobe University School of Medicine, Kobe, Japan.
  • Hajime Nakamura
    From the Department of Pediatrics, Kobe University School of Medicine, Kobe, Japan.

書誌事項

公開日
2000-02-01
DOI
  • 10.1182/blood.v95.3.1066.003k11_1066_1068
公開者
American Society of Hematology

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説明

<jats:p>The mixed lineage leukemia (MLL) gene located at chromosome band 11q23 is frequently rearranged in patients with therapy-related acute monocytic leukemia who received topoisomerase II inhibitors. We have identified a novel fusion partner of MLL(FAB M5b) in a patient who developed t-AML 9 years after treatment for acute lymphoblastic leukemia (ALL). The leukemic cells had a sole karyotypic abnormality of t(3;11) (p21;q23). Screening of a genomic DNA library, prepared from leukemic cell DNA, identified rearranged clones composed of MLL and a novel gene on chromosome 3p21 (AF3p21). The AF3p21 gene encodes a protein of 722 amino acids, which contains an Src homology 3 (SH3) domain, a proline-rich domain, and a bipartite nuclear localizing signal (NLS). RNA analysis demonstrated that exon 6 of the MLLgene fused to exon 2 of the AF3p21 gene. The resulting chimeric protein consists of AT-hooks, methyltransferase, and transcription repressor domains of MLL in addition to the AF3p21 proline-rich domain and NLS but not the AF3p21 SH3 domain.</jats:p>

収録刊行物

  • Blood

    Blood 95 (3), 1066-1068, 2000-02-01

    American Society of Hematology

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