Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells.

Tyrosine kinase inhibitor (TKI) resistance is a major problem in chronic myeloid leukemia (CML). We generated a TKI-resistant K562 sub-population, K562-IR, under selective imatinib-mesylate pressure. K562-IR cells are CD34-/CD38-, BCR-Abl-independent, proliferate slowly, highly adherent and form int...

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Bibliographic Details
Main Authors: Seda Baykal-Köse, Eda Acikgoz, Ahmet Sinan Yavuz, Öykü Gönül Geyik, Halil Ateş, Osman Uğur Sezerman, Güner Hayri Özsan, Zeynep Yüce
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2020-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0229104