The response to Histone deacetylase inhibitor in Imatinib resistant, BCR-ABL independent, K562 variant with high levels of phosphorylated P38

Esther Rabizadeh, Adina Aviram, Inessa Belyaev, Vita Mirkin, Yael Zimra



Background Imatinib mesylate, a TK inhibitor, is the main treatment for CML but patients may develop drug resistance. Mutations within the Abl kinase domain, increased expression of BCR-ABL or other regulatory mechanisms were suggested to be involved. However, recently the importance of Bcr-Abl independent mechanisms in Imatinib resistance was suggested. Exploring the role of proteins involved in Bcr-Abl independent resistance is of great importance in designing new modalities to overcome resistance or potentiate TKI efficacy.

Full Text:



Journal of Hematological Malignancies
ISSN 1925-4024 (Print)   ISSN 1925-4032 (Online)
Copyright © Sciedu Press  
To make sure that you can receive messages from us, please add the '' domain to your e-mail 'safe list'. If you do not receive e-mail in your 'inbox', check your 'bulk mail' or 'junk mail' folders