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. Author manuscript; available in PMC: 2016 May 18.
Published in final edited form as: Leukemia. 2015 Jul 23;29(12):2328–2337. doi: 10.1038/leu.2015.196

Figure 1. β-catenin protein expression is upregulated in CML cells under conditions of TKI resistance.

Figure 1

a–c. Immunoblot analyses revealed increased levels of β-catenin protein in TKI-resistant K562R (a, n=6), AR230R (b, n=4), and CML CD34+ cells from TKI-resistant patients lacking BCR-ABL1 kinase domain mutations (c, n=3), all of which exhibit BCR-ABL1 kinase-independent TKI resistance (left). β-catenin protein levels are also maintained in parental K562S (a, n=3) and AR230S (b, n=3) cells, as well as CML CD34+ cells from newly diagnosed patients (c, n=3), when cultured in direct contact (DC) with HS-5 bone marrow (BM) stromal cells in the presence of 2.5 μM imatinib (right), but not when cultured in HS-5 conditioned medium (CM) (middle).