title: Anti-leukemic activity of axitinib against cells harboring the BCR-ABL T315I point mutation.
abstract: The BCR-ABL; breakpoint cluster region-Abelson point mutation T315I is resistant to ABL tyrosine kinase inhibitors. However, axitinib, a vascular endothelial growth factor receptor inhibitor, is effective against this mutation. In this study, we investigated axitinib activity against ponatinib-resistant cells and found that axitinib inhibited cellular growth and apoptosis in Ba/F3 T315I-mutant cells and T315I-mutant primary samples, but not in ponatinib-resistant Ba/F3 cells and primary samples. Thus, an alternative strategy may be required to improve the prognosis of Philadelphia-chromosome-positive leukemia patients harboring BCR-ABL point mutations.
authors.affiliation: Department of Hematology, Tokyo Medical University, 6-7-1 Nishi-shinjuku, Shinjuku-ku, Tokyo, 160-0023, Japan. okabe@tokyo-med.ac.jp.
authors.forename: Seiichi
authors.initials: S
authors.lastname: Okabe
authors.affiliation: Department of Hematology, Tokyo Medical University, 6-7-1 Nishi-shinjuku, Shinjuku-ku, Tokyo, 160-0023, Japan. tauchi@tokyo-med.ac.jp.
authors.forename: Tetsuzo
authors.initials: T
authors.lastname: Tauchi
authors.affiliation: Department of Hematology, Tokyo Medical University, 6-7-1 Nishi-shinjuku, Shinjuku-ku, Tokyo, 160-0023, Japan. yukois9@yahoo.co.jp.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Tanaka
authors.affiliation: Department of Hematology, Tokyo Medical University, 6-7-1 Nishi-shinjuku, Shinjuku-ku, Tokyo, 160-0023, Japan. ulie27@yahoo.co.jp.
authors.forename: Juri
authors.initials: J
authors.lastname: Sakuta
authors.affiliation: Department of Hematology, Tokyo Medical University, 6-7-1 Nishi-shinjuku, Shinjuku-ku, Tokyo, 160-0023, Japan. ohyashik@rr.iij4u.or.jp.
authors.forename: Kazuma
authors.initials: K
authors.lastname: Ohyashiki
mesh_terms: D000077784:Axitinib; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D007191:Indazoles / Q000494:pharmacology / Q000627:therapeutic use*; D017354:Point Mutation / Q000235:genetics*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D007093:Imidazoles; D007191:Indazoles; D047428:Protein Kinase Inhibitors; D000077784:Axitinib; D016044:Fusion Proteins, bcr-abl