Literature DB >> 23684619

Efficacy of ponatinib against ABL tyrosine kinase inhibitor-resistant leukemia cells.

Seiichi Okabe1, Tetsuzo Tauchi, Yuko Tanaka, Kazuma Ohyashiki.   

Abstract

Because a substantial number of patients with chronic myeloid leukemia acquire resistance to ABL tyrosine kinase inhibitors (TKIs), their management remains a challenge. Ponatinib, also known as AP24534, is an oral multi-targeted TKI. Ponatinib is currently being investigated in a pivotal phase 2 clinical trial. In the present study, we analyzed the molecular and functional consequences of ponatinib against imatinib- or nilotinib-resistant (R) K562 and Ba/F3 cells. The proliferation of imatinib- or nilotinib-resistant K562 cells did not decrease after treatment with imatinib or nilotinib. Src family kinase Lyn was activated. Point mutation Ba/F3 cells (E334V) were also highly resistant to imatinib and nilotinib. Treatment with ponatinib for 72h inhibited the growth of imatinib- and nilotinib-resistant cells. The phosphorylation of BCR-ABL, Lyn, and Crk-L was reduced. This study demonstrates that ponatinib has an anti-leukemia effect by reducing ABL and Lyn kinase activity and this information may be of therapeutic relevance.
Copyright © 2013 Elsevier Inc. All rights reserved.

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Year:  2013        PMID: 23684619     DOI: 10.1016/j.bbrc.2013.05.022

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  7 in total

1.  The BCR-ABL inhibitor ponatinib inhibits platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling, platelet activation and aggregate formation under shear.

Authors:  Cassandra P Loren; Joseph E Aslan; Rachel A Rigg; Marie S Nowak; Laura D Healy; András Gruber; Brian J Druker; Owen J T McCarty
Journal:  Thromb Res       Date:  2014-11-18       Impact factor: 3.944

2.  Efficacy of the polo-like kinase inhibitor rigosertib, alone or in combination with Abelson tyrosine kinase inhibitors, against break point cluster region-c-Abelson-positive leukemia cells.

Authors:  Seiichi Okabe; Tetsuzo Tauchi; Yuko Tanaka; Juri Sakuta; Kazuma Ohyashiki
Journal:  Oncotarget       Date:  2015-08-21

3.  ABCB1 Overexpression Is a Key Initiator of Resistance to Tyrosine Kinase Inhibitors in CML Cell Lines.

Authors:  Laura N Eadie; Timothy P Hughes; Deborah L White
Journal:  PLoS One       Date:  2016-08-18       Impact factor: 3.240

4.  BIRC6 mediates imatinib resistance independently of Mcl-1.

Authors:  Denis O Okumu; Michael P East; Merlin Levine; Laura E Herring; Raymond Zhang; Thomas S K Gilbert; David W Litchfield; Yanping Zhang; Lee M Graves
Journal:  PLoS One       Date:  2017-05-16       Impact factor: 3.240

Review 5.  Targeting mTOR in Acute Lymphoblastic Leukemia.

Authors:  Carolina Simioni; Alberto M Martelli; Giorgio Zauli; Elisabetta Melloni; Luca M Neri
Journal:  Cells       Date:  2019-02-21       Impact factor: 6.600

6.  Combining the ABL1 kinase inhibitor ponatinib and the histone deacetylase inhibitor vorinostat: a potential treatment for BCR-ABL-positive leukemia.

Authors:  Seiichi Okabe; Tetsuzo Tauchi; Shinya Kimura; Taira Maekawa; Toshihiko Kitahara; Yoko Tanaka; Kazuma Ohyashiki
Journal:  PLoS One       Date:  2014-02-28       Impact factor: 3.240

7.  Combination of the ABL kinase inhibitor imatinib with the Janus kinase 2 inhibitor TG101348 for targeting residual BCR-ABL-positive cells.

Authors:  Seiichi Okabe; Tetsuzo Tauchi; Seiichiro Katagiri; Yuko Tanaka; Kazuma Ohyashiki
Journal:  J Hematol Oncol       Date:  2014-04-28       Impact factor: 17.388

  7 in total

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