Functional analysis of the SEPT9-ABL1 chimeric fusion gene derived from T-prolymphocytic leukemia

Hidetsugu Kawai, Hiromichi Matsushita, Rikio Suzuki, Yin Sheng, Jun Lu, Hideyuki Matsuzawa, Takashi Yahata, Mitsuyo Tsuma-Kaneko, Hideo Tsukamoto, Hiroshi Kawada, Yoshiaki Ogawa, Kiyoshi Ando

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)


We analyzed the function of a SEPT9-ABL1 fusion identified in a case of T-prolymphocytic leukemia with tyrosine kinase inhibitor (TKI) resistance. Five isoforms with different N-termini, including SEPT9a-ABL1, SEPT9b-ABL1, SEPT9d-ABL1, SEPT9e-ABL1 and SEPT9f-ABL1, were detected in the leukemic cells. All isoforms except SEPT9d-ABL1 are localized in the cytoplasm, undergo autophosphorylation and phosphorylate the downstream targets, STAT-5 and Crkl, and provided IL-3-independence and in vivo invasiveness to 32D cells. Additionally, these SEPT9-ABL1 isoforms were resistant to TKIs in vitro and in vivo, in comparison to BCR-ABL1. These findings demonstrated that SEPT9-ABL1 had oncogenic activity and conferred resistance to TKIs.

Original languageEnglish
Pages (from-to)1451-1459
Number of pages9
JournalLeukemia Research
Issue number12
Publication statusPublished - 2014 Dec 1
Externally publishedYes


  • ABL1 fusion gene
  • SEPT9-ABL1
  • Tyrosine kinase inhibitors

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research


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