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

Highlights • Five SEPT9-ABL1 isoforms with different N-termini were identified in a T-PLL case. • Each SEPT9-ABL1 isoform exhibited different biological activities. • The intracellular distribution of SEPT9-ABL1 varied among the isoforms. • SEPT9-ABL1 isoforms provided IL-3 independency in 32D cells...

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Veröffentlicht in:	Leukemia research 2014-12, Vol.38 (12), p.1451-1459
Hauptverfasser:	Kawai, Hidetsugu, Matsushita, Hiromichi, Suzuki, Rikio, Sheng, Yin, Lu, Jun, Matsuzawa, Hideyuki, Yahata, Takashi, Tsuma-Kaneko, Mitsuyo, Tsukamoto, Hideo, Kawada, Hiroshi, Ogawa, Yoshiaki, Ando, Kiyoshi
Format:	Artikel
Sprache:	eng
Schlagworte:	ABL1 fusion gene Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Animals Drug Resistance, Neoplasm HEK293 Cells Hematology, Oncology and Palliative Medicine Humans Leukemia, Prolymphocytic, T-Cell - drug therapy Leukemia, Prolymphocytic, T-Cell - enzymology Leukemia, Prolymphocytic, T-Cell - genetics Mice Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncogene Proteins, Fusion - antagonists & inhibitors Oncogene Proteins, Fusion - genetics Oncogene Proteins, Fusion - metabolism Phosphorylation - drug effects Protein Isoforms - genetics Protein Isoforms - metabolism Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins c-abl - antagonists & inhibitors Proto-Oncogene Proteins c-abl - genetics Proto-Oncogene Proteins c-abl - metabolism SEPT9-ABL1 Septins - antagonists & inhibitors Septins - genetics Septins - metabolism STAT5 Transcription Factor - genetics STAT5 Transcription Factor - metabolism Tyrosine kinase inhibitors
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Zusammenfassung:	Highlights • Five SEPT9-ABL1 isoforms with different N-termini were identified in a T-PLL case. • Each SEPT9-ABL1 isoform exhibited different biological activities. • The intracellular distribution of SEPT9-ABL1 varied among the isoforms. • SEPT9-ABL1 isoforms provided IL-3 independency in 32D cells to varying degrees. • 32D cells with SEPT9-ABL1 were TKI-resistant despite not having mutations in ABL1.
ISSN:	0145-2126 1873-5835
DOI:	10.1016/j.leukres.2014.08.015