Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line

Nilotinib is approved for treatment of newly diagnosed chronic myeloid leukemia (CML) and it is shown superiority over imatinib in first-line treatment for patients of CML. In this study, we established a nilotinib-resistant cell line, K562NR, and evaluated the resistance to nilotinib and efficacy o...

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Autores principales: Okabe, Seiichi, Tauchi, Tetsuzo, Tanaka, Yuko, Ohyashiki, Kazuma
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Letter to the Editor
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163636/
https://www.ncbi.nlm.nih.gov/pubmed/21806844
http://dx.doi.org/10.1186/1756-8722-4-32
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author Okabe, Seiichi
Tauchi, Tetsuzo
Tanaka, Yuko
Ohyashiki, Kazuma
author_facet Okabe, Seiichi
Tauchi, Tetsuzo
Tanaka, Yuko
Ohyashiki, Kazuma
author_sort Okabe, Seiichi
collection PubMed
description Nilotinib is approved for treatment of newly diagnosed chronic myeloid leukemia (CML) and it is shown superiority over imatinib in first-line treatment for patients of CML. In this study, we established a nilotinib-resistant cell line, K562NR, and evaluated the resistance to nilotinib and efficacy of dasatinib. We found activation of Lyn plays a dominant role in survival of the nilotinib-resistant cell line. We found dasatinib induces the apoptosis of nilotinib-resistant cells and inhibits Lyn kinase activity. This novel nilotinib-resistant CML cell line may help to explore novel therapy for CML.
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spelling pubmed-31636362011-08-31 Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line Okabe, Seiichi Tauchi, Tetsuzo Tanaka, Yuko Ohyashiki, Kazuma J Hematol Oncol Letter to the Editor Nilotinib is approved for treatment of newly diagnosed chronic myeloid leukemia (CML) and it is shown superiority over imatinib in first-line treatment for patients of CML. In this study, we established a nilotinib-resistant cell line, K562NR, and evaluated the resistance to nilotinib and efficacy of dasatinib. We found activation of Lyn plays a dominant role in survival of the nilotinib-resistant cell line. We found dasatinib induces the apoptosis of nilotinib-resistant cells and inhibits Lyn kinase activity. This novel nilotinib-resistant CML cell line may help to explore novel therapy for CML. BioMed Central 2011-08-02 /pmc/articles/PMC3163636/ /pubmed/21806844 http://dx.doi.org/10.1186/1756-8722-4-32 Text en Copyright ©2011 Okabe et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Letter to the Editor
Okabe, Seiichi
Tauchi, Tetsuzo
Tanaka, Yuko
Ohyashiki, Kazuma
Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line
title Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line
title_full Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line
title_fullStr Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line
title_full_unstemmed Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line
title_short Dasatinib preferentially induces apoptosis by inhibiting Lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line
title_sort dasatinib preferentially induces apoptosis by inhibiting lyn kinase in nilotinib-resistant chronic myeloid leukemia cell line
topic Letter to the Editor
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163636/
https://www.ncbi.nlm.nih.gov/pubmed/21806844
http://dx.doi.org/10.1186/1756-8722-4-32
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